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        <title>Cancer Letters via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Cancer Letters' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Cancer+Letters&t=Cancer+Letters&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 08:41:21 +0100</lastBuildDate>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5647156&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383512000158%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647156</comments>
            <pubDate>Thu, 02 Feb 2012 13:23:04 +0100</pubDate>
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        <item>
            <title>Induced expression of B7-H4 on the surface of lung cancer cell by the tumor-associated macrophages: A potential mechanism of immune escape</title>
            <link>http://www.medworm.com/index.php?rid=5647169&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100718X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: B7-homolog 4 (B7-H4), a recently identified homolog of B7.1/2 (CD80/86), has been described to exert co-stimulatory and immune regulatory functions. We investigated the expression and the functional activity of B7-H4 in lung cancer in vitro and in vivo. Although a lung cancer cell line constitutively expressed B7-H4 mRNA and protein in plasma, primary tumor cell isolated from the transplanted lung carcinoma model expressed B7-H4 on the surface. Interestingly, in transplanted lung carcinoma model, the expression of membrane-bound B7-H4 in tumor cells was increased as prolonging of tumor transformation. Exposure to tumor-associated macrophages strongly induced membrane-bound B7-H4 expression on the lung cancer cell line. To elucidate the functional significance of lung cancer-relat...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647169</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Anti-cancer activity of an acid-labile N-alkylisatin conjugate targeting the transferrin receptor</title>
            <link>http://www.medworm.com/index.php?rid=5628163&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006380%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We have previously reported a series of pH-sensitive imine-linked N-alkylisatin prodrugs that are stable at pH 7.4, but readily cleaved at pH 4.5. Herein, one of the most potent prodrugs, 5,7-dibromo-N-(p-methoxybenzyl)isatin (NAI), was functionalized with a para-phenylpropionic acid linker, and the resulting NAI–imine prodrug conjugated to transferrin (Tf) to form a NAI–imine–Tf conjugate. Cytotoxicity assays revealed the conjugate was equipotent to the free drug against MCF-7 breast cancer cells, with clear selectivity patterns based on TfR levels. These results suggest that this novel isatin-based cytotoxin conjugated to a tumor targeting protein via an acid-labile linker warrants further preclinical testing. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628163</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Intussusceptive microvascular growth in tumors</title>
            <link>http://www.medworm.com/index.php?rid=5628160&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006574%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Intussusception is an alternative to the sprouting mode of angiogenesis. The advantage of this mechanism of vascular growth is that blood vessels are generated more rapidly and the capillaries thereby formed are less leaky. This review article summarizes our current knowledge concerning the role played by intussusceptive microvascular growth in tumor growth. Interestingly, an angiogenic switch from sprouting to intussusceptive angiogenesis occurs after treatment with angiogenesis inhibitors and may be considered as a tumor-protective adaptative response. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628160</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Identification of heat shock protein 90 inhibitors to sensitize drug resistant side population tumor cells using a cell based assay platform</title>
            <link>http://www.medworm.com/index.php?rid=5647167&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006872%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Current cancer therapeutics are identified based on initial tumor regression screens that mostly kill differentiated tumor cells, sparing the rare cancer stem cells (CSCs). Being rare and difficult to characterize, it remains a challenge to identify compounds active against them. Side population (SP) cells identified in multiple cancer cell line panels expressing mitochondrial Cytochrome C-EGFP were evaluated for identifying possible drug candidates utilizing high-throughput imaging. We identified heat shock protein 90 inhibitors as potential agents to sensitize SP cells to anticancer drugs. Hsp90 inhibitors induced down regulation of Akt leading to proteasomal degradation of survivin and consequent mitochondrial apoptosis. A successful screening platform for identifying compound...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647167</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>HS-116, a novel phosphatidylinositol 3-kinase inhibitor induces apoptosis and suppresses angiogenesis of hepatocellular carcinoma through inhibition of the PI3K/AKT/mTOR pathway</title>
            <link>http://www.medworm.com/index.php?rid=5628167&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006549%2Fabstract%3Frss%3Dyes</link>
            <description>This study aimed to clarify the anticancer effect of HS-116 in human hepatocellular carcinoma (HCC). To identify the effect of HS-116 on HCC cells, a PI3K assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and Western blotting were conducted. IC50 of HS-116 for PI3Kα was 31nM, and it effectively suppressed the phosphorylation of PI3K downstream factors such as AKT, mTOR, p70S6K, and 4EBP1. Also, HS-116 induced apoptosis by increasing the proportion of sub-G1 apoptotic cells from 1.8% to 35% and increasing the expressions of Bax, cleaved-caspase-3, and cleaved-PARP as well as decreasing the expression of Bcl-2. In addition, chromatin condensation and apoptotic bodies were detected in HS-116-treated HCC cells. Furthermore, HS-116 decreased prote...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628167</comments>
            <pubDate>Mon, 19 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Overexpression of BMI1 confers clonal cells resistance to apoptosis and contributes to adverse prognosis in myelodysplastic syndrome</title>
            <link>http://www.medworm.com/index.php?rid=5647161&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006902%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we reported that overexpression of BMI1 protein was detected in MDS patients, and inversely correlated with the apoptosis of CD34+ cells. In vitro overexpression of BMI1 facilitated proliferation and inhibited apoptosis of MDS-L cells. The overexpression of BMI1 could downregulate apoptosis sensitivity to cytotoxic agents in MDS-L cells; on the contrary, MDS-L cells could be rendered apoptosis-sensitive by BMI1 knockdown. Overexpression of BMI1 antagonised apoptosis by downregulating several apoptosis-related proteins, such as p16INK4a, phospho-p53 (Ser46) and caspase 3/9. In addition, overexpression of BMI1 was correlated with an elevated IPSS score and a shorter survival. Collectively, overexpression of BMI1 induces resistance to apoptosis and contributes to adverse progno...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647161</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Genome-wide microRNA profiles identify miR-378 as a serum biomarker for early detection of gastric cancer</title>
            <link>http://www.medworm.com/index.php?rid=5628168&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006513%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Recent studies demonstrated that in several human malignancies aberrant expression profiles of circulating microRNAs (miRNAs) anticipate great cancer diagnostic potential. Here we showed that serum miR-378 could serve as a novel noninvasive biomarker in gastric cancer (GC) detection. Genome-wide miRNA expression profiles followed with Real-Time quantitative RT-PCR (qRT-PCR) assays revealed that miR-187*, miR-371-5p and miR-378 were significantly elevated in GC patients. Further validation indicated that miR-378 alone could yields a ROC curve area of 0.861 with 87.5% sensitivity and 70.73% specificity in discriminating GC patients from healthy controls. Collectively, these data support our contention that serum miR-378 has strong potential as a novel noninvasive biomarker in gastr...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628168</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Cryptotanshinone suppresses androgen receptor-mediated growth in androgen dependent and castration resistant prostate cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5581087&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006197%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Androgen receptor (AR) is the major therapeutic target for the treatment of prostate cancer (PCa). Anti-androgens to reduce or prevent androgens binding to AR are widely used to suppress AR-mediated PCa growth; however, the androgen depletion therapy is only effective for a short period of time. Here we found a natural product/Chinese herbal medicine cryptotanshinone (CTS), with a structure similar to dihydrotestosterone (DHT), can effectively inhibit the DHT-induced AR transactivation and prostate cancer cell growth. Our results indicated that 0.5μM CTS effectively suppresses the growth of AR-positive PCa cells, but has little effect on AR negative PC-3 cells and non-malignant prostate epithelial cells. Furthermore, our data indicated that CTS could modulate AR transactivation ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581087</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Copy number status and mutation analyses of anaplastic lymphoma kinase (ALK) gene in 90 sporadic neuroblastoma tumors</title>
            <link>http://www.medworm.com/index.php?rid=5647166&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006914%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we investigated the association of ALK copy number alterations with copy number status 2p24.1 amplicon harboring DEAD box polypeptide 1 (DDX1), MYCN and neuroblastoma-amplified (NAG) genes in 90 primary tumors of sporadic NB cases by multiplex ligation-dependent probe amplification (MLPA). We also performed mutation analysis of ALK gene by directly sequencing the exons 20–28 which cover the region that encodes juxtamembrane and kinase domains. A total of 39 (43.3%) NB cases revealed copy numbers alterations of ALK gene. There was highly significant association of ALK copy number gains with gains of one or more of the genes at 2p24.1 (DDX1, MYCN or NAG) in MYCN unamplified tumors (P (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647166</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5647166</guid>        </item>
        <item>
            <title>Sleeping Beauty – A mouse model for all cancers?</title>
            <link>http://www.medworm.com/index.php?rid=5647157&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006847%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Sleeping Beauty (SB) is a genetically engineered insertional mutagenesis system. Its ability to rapidly induce cancer in SB-transgenic mice as well as the ease of identification of the mutated genes suggest important roles for SB in the discovery of novel cancer genes as well as the generation of models of human cancers where none currently exist. The range of SB-related tumors extends from haematopoietic to solid cancers such as hepatocellular carcinoma. This review follows the refinement of SB for different cancers and assesses its potential as a model for all cancers and a tool for cancer gene discovery. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647157</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5647157</guid>        </item>
        <item>
            <title>Vitamin K3 and K5 are inhibitors of tumor pyruvate kinase M2</title>
            <link>http://www.medworm.com/index.php?rid=5628169&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006562%2Fabstract%3Frss%3Dyes</link>
            <description>This study combined with previous reports supports that VK3 and VK5 have potential as adjuvant for cancer chemotherapy. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628169</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Understanding the role of cytokines in Glioblastoma Multiforme pathogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5628162&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006586%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cytokines play a significant role in cancer diagnosis, prognosis and therapy. The immune system’s failure to recognize the malignant tumor cells and mount an effective response may be the result of tumor-associated cytokine deregulation. Glioblastoma Multiforme (GBM) has a characteristic cytokine expression pattern, and abnormalities in cytokine expression have been implicated in gliomagenesis. Within the heterogeneous GBM microenvironment, the tumor cells, normal brain cells, immune cells, and stem cells interact with each other through the complex cytokine network. This review summarizes the current understanding of the functions of key cytokines on GBM, and highlights potential therapeutic applications targeting these cytokines. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628162</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Mammosphere cells from high-passage MCF7 cell line show variable loss of tumorigenicity and radioresistance</title>
            <link>http://www.medworm.com/index.php?rid=5581092&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006355%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we report that mammospheres derived from MCF-7 sublines after different passage numbers were consistently enriched for CD44+/CD24−/low cells but were not consistently enriched for tumorigenic and radioresistant cells. The tumorigenicity and radioresistance of MSs were associated with their sphere-forming ability, proliferation ability in vitro, and intracellular reactive oxygen species (ROS) levels. The radioresistant MSs showed significant cell cycle arrest in G2/M phase after X-ray irradiation and expressed higher ataxia telangiectasia mutated (ATM) mRNA levels. These results suggest that MSs from high-passage cancer cell lines were not consistently enriched for stem-like cancer cells with higher tumorigenicity and enhanced radioresistance. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581092</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581092</guid>        </item>
        <item>
            <title>Characterization of two mouse models of metastatic pheochromocytoma using bioluminescence imaging</title>
            <link>http://www.medworm.com/index.php?rid=5581091&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006367%2Fabstract%3Frss%3Dyes</link>
            <description>In this study we generated two sensitive luciferase models using bioluminescent pheochromocytoma cells: an experimental metastasis model to monitor tumor spreading and a subcutaneous model to monitor tumor growth and spontaneous metastasis. These models offer a platform for sensitive, non-invasive and real-time monitoring of pheochromocytoma primary growth and metastatic burden to follow the course of tumor progression and for testing relevant antitumor treatments in metastatic pheochromocytoma. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581091</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581091</guid>        </item>
        <item>
            <title>The LIM domain protein, CRIP2, promotes apoptosis in esophageal squamous cell carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5581090&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006379%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, this study shows CRIP2 plays an important role in the development of ESCC. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581090</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>p65-Dependent production of interleukin-1β by osteolytic prostate cancer cells causes an induction of chemokine expression in osteoblasts</title>
            <link>http://www.medworm.com/index.php?rid=5647170&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511007178%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Skeletal metastases are a frequent complication of prostate, breast and lung cancer, and the interactions of tumor cells with bone-forming osteoblasts and bone-resorbing osteoclasts have been suggested to play critical roles in disease progression. We have previously shown that treatment of primary murine osteoblasts with conditioned medium of the human osteolytic prostate cancer cell line PC-3 results in a rapid induction of chemokine expression, thereby providing further evidence for a molecular crosstalk between bone and tumor cells. The aim of our current study was to identify PC-3-derived molecules mediating this effect. Using Affymetrix Gene Chip hybridization followed by qRT-PCR we were able to confirm that the expression of chemokine-encoding genes is markedly induced in ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647170</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Targeting cathepsin S induces tumor cell autophagy via the EGFR–ERK signaling pathway</title>
            <link>http://www.medworm.com/index.php?rid=5647168&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511007154%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, the current study reveals that cathepsin S plays an important role in the regulation of cell autophagy through interference with the EGFR–ERK/MAPK-signaling pathway. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647168</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>SUMOylation in carcinogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5628159&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006537%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: SUMOylation is a post-translational modification characterized by covalent and reversible binding of small ubiquitin-like modifier (SUMO) to a target protein. In mammals, four different isoforms, termed SUMO-1, -2, -3 and -4 have been identified so far. SUMO proteins are critically involved in the modulation of nuclear organization and cell viability. Their expression is significantly increased in processes associated with carcinogenesis such as cell growth, differentiation, senescence, oxidative stress and apoptosis. Little is known about the role of SUMOylation in cancer development. Therefore the present review focuses on possible implications of SUMOylation in carcinogenesis highlighting its impact as an important regulatory cell cycle protein. Moreover, novel opportunities f...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628159</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Newcastle disease virus induces apoptosis in cisplatin-resistant human lung adenocarcinoma A549 cells in vitro and in vivo</title>
            <link>http://www.medworm.com/index.php?rid=5647164&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006860%2Fabstract%3Frss%3Dyes</link>
            <description>This study aims to investigate whether Newcastle disease virus (NDV) exhibits an oncolytic effect on cisplatin-resistant A549 lung cancer cells. We found that NDV induced A549/DDP cell apoptosis via the caspase pathway, particularly involving caspase-9, while the mitogen-activated protein kinase (MAPK) and Akt pathways also contributed to apoptotic induction. Furthermore, NDV displayed oncolytic effects in a mouse A549/DDP lung cancer model. Collectively, our data indicate that NDV could overcome the cisplatin resistance in lung cancer cells in vitro and in vivo. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647164</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Transplacental carcinogenesis with dibenzo[def,p]chrysene (DBC): Timing of maternal exposures determines target tissue response in offspring</title>
            <link>http://www.medworm.com/index.php?rid=5647163&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006884%2Fabstract%3Frss%3Dyes</link>
            <description>This study highlights the importance of developmental stage in susceptibility to environmental carcinogens. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647163</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Insulin-like growth factor binding protein-3 inhibits migration of endometrial cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5647162&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006896%2Fabstract%3Frss%3Dyes</link>
            <description>This study demonstrates that endogenous IGFBP-3 modulates adhesion–migration dynamics in EC cells, implying that it may be important in regulating metastasis in this disease. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647162</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>LCH-7749944, a novel and potent p21-activated kinase 4 inhibitor, suppresses proliferation and invasion in human gastric cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5647160&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006859%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: P21-activated kinase 4 (PAK4), a serine/threonine protein kinase, has involved in the regulation of cytoskeletal reorganization, cell proliferation, gene transcription, oncogenic transformation and cell invasion. Moreover, PAK4 overexpression, genetic amplification and mutations were detected in a variety of human tumors, which make it potential therapeutic target. In this paper we found that LCH-7749944, a novel and potent PAK4 inhibitor, effectively suppressed the proliferation of human gastric cancer cells through downregulation of PAK4/c-Src/EGFR/cyclin D1 pathway. In addition, LCH-7749944 significantly inhibited the migration and invasion of human gastric cancer cells in conjunction with concomitant blockage of PAK4/LIMK1/cofilin and PAK4/MEK-1/ERK1/2/MMP2 pathways. Interest...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647160</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5647160</guid>        </item>
        <item>
            <title>Bortezomib enhances radiation-induced apoptosis in solid tumors by inhibiting CIP2A</title>
            <link>http://www.medworm.com/index.php?rid=5647158&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006719%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Previously, we demonstrated that cancerous inhibitor of protein phosphatase 2A (CIP2A) mediates bortezomib-induced apoptosis in hepatocellular carcinoma cells. Herein, we report that bortezomib sensitizes solid tumor cells to radiation-induced apoptosis. Treatment with a combination of bortezomib and radiation downregulated CIP2A in a dose-dependent manner in solid tumor cells. Knockdown of CIP2A enhanced radiation-induced apoptosis in cancer cells, and ectopic expression of CIP2A in cancer cells abolished radiation-induced apoptosis. Finally, our in vivo data showed that bortezomib and radiation combination treatment decreased tumor growth significantly. Thus, bortezomib sensitized solid tumor cells to radiation through the inhibition of CIP2A. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647158</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5647158</guid>        </item>
        <item>
            <title>Carnosine inhibits KRAS-mediated HCT116 proliferation by affecting ATP and ROS production</title>
            <link>http://www.medworm.com/index.php?rid=5552115&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100437X%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we demonstrate that carnosine inhibits the proliferation of human HCT116 colon cancer cells. In this cell line, the activating KRAS mutation induces mitochondrial ROS, the signaling molecules for cell proliferation. We observed that 50–100mM carnosine decreases ATP and ROS concentration and induces cell cycle arrest in G1 phase. In HCT116 cells these effects are related to decreased ERK1/2 phosphorylation and increased p21waf1 protein. Our findings support the concept that carnosine could inhibit HCT116 cell growth via its antioxidant activity and its ability to affect glycolysis. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552115</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552115</guid>        </item>
        <item>
            <title>P-21 activated kinase 1 knockdown inhibits β-catenin signalling and blocks colorectal cancer growth</title>
            <link>http://www.medworm.com/index.php?rid=5647165&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511007129%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The p21-activated kinase 1 (PAK1) plays important roles in cell growth, motility, and transformation. The aims of this study were to delineate the signalling mechanisms downstream of PAK1, and to investigate the importance of PAK1 for colorectal cancer (CRC) growth and metastasis in vivo. PAK1 knockdown in human CRC cell lines inhibited β-catenin expression, β-catenin/TCF4 transcriptional activity, and the expression of c-Myc. In mouse models PAK1 knockdown suppressed the growth and metastasis of human CRC cells by decreasing proliferation and increasing apoptosis. Our findings demonstrate for the first time the crucial role of PAK1 in CRC progression in vivo. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647165</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5647165</guid>        </item>
        <item>
            <title>Irreversible electroporation shows efficacy against pancreatic carcinoma without systemic toxicity in mouse models</title>
            <link>http://www.medworm.com/index.php?rid=5647159&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006690%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Pancreatic ductal adenocarcinoma (PDAC) therapies show limited success. Irreversible electroporation (IRE) is an innovative loco-regional therapy in which high-voltage pulses are applied to induce plasma membrane defects leading to cellular death. In the present study we evaluated the feasibility of IRE against PDAC. IRE treatment exhibited significant antitumor effects and prolonged survival in mice with orthotopic xenografts. Extensive tumor necrosis, reduced tumor cell proliferation and disruption of microvessels were observed at different days post-IRE. Animals had transient increases in transaminases, amylase and lipase enzymes that normalized at 24h post-IRE. These results suggest that IRE could be an effective treatment for locally advanced pancreatic tumors. (Source: Canc...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5647159</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5647159</guid>        </item>
        <item>
            <title>Synergistic antitumor effect of adenovirus-mediated hING4 gene therapy and 125I radiation therapy on pancreatic cancer</title>
            <link>http://www.medworm.com/index.php?rid=5628170&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006604%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we demonstrated that either ING4 or 125I radiotherapy treatment could induce Panc-1 pancreatic cancer cell growth suppression and apoptosis in vitro. Furthermore, both treatments inhibited tumor growth and angiogenesis of Panc-1 pancreatic cancer subcutaneously xenografted in vivo. Moreover, the combination therapy had a synergistic effect. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628170</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5628170</guid>        </item>
        <item>
            <title>Lipocalin 2 in cancer: When good immunity goes bad</title>
            <link>http://www.medworm.com/index.php?rid=5628161&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006598%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The innate immune molecule Lipocalin 2 (LCN2) was initially shown to combat bacterial infection by binding bacterial siderophores, hence impairing microbial iron sequestration. In recent years, it has become apparent that LCN2 is over-expressed in cancers of diverse histological origin and that it facilitates tumorigenesis by promoting survival, growth, and metastasis. Herein, we discuss emerging evidence that substantiates two functional roles for LCN2 in cancer: promotion of the epithelial-to-mesenchymal transition (EMT) that facilitates an invasive phenotype and metastasis, and sequestration of iron that results in cell survival and tumorigenesis. Further, we present evidence that upregulated LCN2 expression in solid tumors is induced by hypoxia and pro-inflammation, microenvi...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628161</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5628161</guid>        </item>
        <item>
            <title>Thymidine kinase and cancer monitoring</title>
            <link>http://www.medworm.com/index.php?rid=5581086&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006422%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Thymidine kinases (TK) have a key function in the synthesis of DNA. Two isoenzymes have been characterized: TK1 is cell cycle-dependent and present in the cytoplasm whereas TK2 – located in mitochondria – is cell cycle-independent. The diagnostic and prognostic role of TK1 has recently been investigated. TK1 might be helpful for screening and monitoring of human malignancies. TK1 may also serve as a prognostic factor for progression. Herein, we summarize the status of TK1 for cancer monitoring and point out its use as a proliferation marker. A comprehensive overview about the association of TK-1 with various entities is given. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581086</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581086</guid>        </item>
        <item>
            <title>ABCB1/MDR1 contributes to the anticancer drug-resistant phenotype of IPH-926 human lobular breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5552119&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005982%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► The role of ABCB1/MDR1 for breast cancer drug-resistance has been controversial. ► We studied IPH-926 cells, which are derived from a chemo-refractory breast cancer. ► IPH-926 cells were anticancer drug-resistant in vitro. ► Microarray profiling of IPH-926 revealed an endogenous overexpression of ABCB1. ► Inhibition of ABCB1 function by PSC-833 increased drug-sensitivity of IPH-926 cells.Abstract: Contribution of the ABCB1/MDR1/P-glycoprotein drug transporter to breast cancer resistance has been controversial. One issue is that ABCB1-dependent drug-resistance has primarily been investigated in mammary epithelial cell models technically manipulated to overexpress ABCB1, either by gene transfer using appropriate expression vectors or by chronic anticancer drug-selecti...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552119</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552119</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5440375&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511007038%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440375</comments>
            <pubDate>Fri, 25 Nov 2011 01:55:41 +0100</pubDate>
            <guid isPermaLink="false">5440375</guid>        </item>
        <item>
            <title>Inhibition of Plk1 and Pin1 by 5′-nitro-indirubinoxime suppresses human lung cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5581098&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100646X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A novel indirubin derivative, 5′-nitro-indirubinoxime (5′-NIO), exhibits a strong anti-cancer activity against human cancer cells. Here, the 5′-NIO-mediated G1 cell cycle arrest in lung cancer cells was associated with a decrease in protein levels of polo-like kinase 1 (Plk1) and peptidyl-prolyl cis/trans isomerase Pin1. Treatment with Plk1 siRNA or Pin1 inhibitor effectively inhibited the Rb phosphorylation, suggesting their regulatory role at G1 phase. In addition, the overexpression of Plk1 or Pin1 inhibited apoptotic signals following the cleavage of PARP in 5′-NIO-treated cells. These findings suggest that 5′-NIO have potential anti-cancer efficacy through the inhibition of Plk1 or/and Pin1 expression. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581098</comments>
            <pubDate>Thu, 24 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581098</guid>        </item>
        <item>
            <title>ShRNA silencing glycogen synthase kinase-3 beta inhibits tumor growth and angiogenesis in pancreatic cancer</title>
            <link>http://www.medworm.com/index.php?rid=5628166&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006501%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we showed that GSK-3β was aberrantly activated in pancreatic cancer. GSK-3β knockdown resulted in arrested proliferation and increased apoptosis in pancreatic cancer cell lines. Expression of Bcl-2 and vascular endothelial growth factor (VEGF) decreased significantly in a GSK-3β knockdown group. In a xenograft tumor model, GSK-3β knockdown inhibited tumor growth and angiogenesis. Our study showed that GSK-3β may become a promising therapeutic target for human pancreatic cancer. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628166</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5628166</guid>        </item>
        <item>
            <title>IFN-γ combined with targeting of XIAP leads to increased apoptosis-sensitisation of TRAIL resistant pancreatic carcinoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5628165&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006525%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is a specific and potent inducer of apoptosis in cancer cells, but the resistance of many tumour cells to TRAIL still represents a major hurdle for the clinical treatment of tumours with TRAIL. As apoptosis is regulated by the balance of activities of several anti-apoptotic factors and pro-apoptotic factors, we analysed the relative contribution of the two sides and found that down-regulation of Bcl-xL and in particular XIAP, but not c-Flip, sensitised the TRAIL resistant pancreatic cancer cell line Panc-1. A combination of both XIAP and Bcl-xL knock-downs showed no substantial added benefit indicating that both act in the same pathway. Notably, the degree of sensitisation by silencing of anti-apoptotic genes wa...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628165</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5628165</guid>        </item>
        <item>
            <title>Inhibition of activated Stat3 reverses drug resistance to chemotherapeutic agents in gastric cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5552124&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006288%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, these data supported the hypothesis that interruption of Stat3 signaling could reverse resistance to chemotherapy agents in human gastric cancer cells. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552124</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552124</guid>        </item>
        <item>
            <title>Monocyte differentiation induced by co-culture with tumor cells involves RGD-dependent cell adhesion to extracellular matrix</title>
            <link>http://www.medworm.com/index.php?rid=5552118&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005763%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we attempted to induce monocytes to differentiate into TAM-like cells producing matrix metalloproteinases (MMPs) by co-culture with tumor cells. When human monocytes were co-cultured for 3–7days with tumor cell lines, monocytes differentiated to produce MMP-9, accompanied by morphological changes. The in vitro cell invasion of MKN1 human gastric carcinoma cells into Matrigel membranes was promoted in the presence of differentiated monocytes, and the enhancement of cell invasion by differentiated monocytes was correlated with their MMP-9 productivity. The addition of an RGD (Arg-Gly-Asp) peptide to the culture significantly inhibited monocyte differentiation. The MMP-9 production from monocytes was diminished by the depletion of fibronectin from the conditioned media with g...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552118</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552118</guid>        </item>
        <item>
            <title>Recent trends in antibody-based oncologic imaging</title>
            <link>http://www.medworm.com/index.php?rid=5552113&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006343%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Antibodies, with their unmatched ability for selective binding to any target, are considered as potentially the most specific probes for imaging. Their clinical utility, however, has been limited chiefly due to their slow clearance from the circulation, longer retention in non-targeted tissues and the extensive optimization required for each antibody-tracer. The development of newer contrast agents, combined with improved conjugation strategies and novel engineered forms of antibodies (diabodies, minibodies, single chain variable fragments, and nanobodies), have triggered a new wave of antibody-based imaging approaches. Apart from their conventional use with nuclear imaging probes, antibodies and their modified forms are increasingly being employed with non-radioisotopic contrast...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552113</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552113</guid>        </item>
        <item>
            <title>β1 integrin is required for anchorage-independent growth and invasion of tumor cells in a context dependent manner</title>
            <link>http://www.medworm.com/index.php?rid=5628164&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006495%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Recent studies suggest that extracellular matrix (ECM) components within the tumor microenvironment can influence malignant progression, thus we investigated the influence of the ECM binding receptor β1 integrin, on the hallmark properties of tumorigenesis. Small interfering (si) or short hairpin (sh) RNA approaches were used to deplete β1 integrin in cancer cell lines. β1 integrin-depleted cells were then assessed for their growth and invasive capabilities using 2-dimensional (2D) or 3D culture conditions. Depletion of β1 integrin expression did not impact cell growth in 2D assay systems; however, β1 integrin and its ligand fibronectin were required for growth in 3D. β1 integrin-depleted cells also had reduced invasive capabilities, in part due to increased tissue inhibito...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5628164</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5628164</guid>        </item>
        <item>
            <title>miR-21 functionally interacts with the 3′UTR of chemokine CCL20 and down-regulates CCL20 expression in miR-21 transfected colorectal cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5581099&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006483%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: As deregulation of miRNAs and chemokine CCL20 was shown to play a role in colorectal cancer (CRC) pathogenesis, we analyzed the functional interactions of candidate miRNAs with CCL20 mRNA. After target prediction software programs indicated a role for miR-21 in CCL20 regulation, we applied the luciferase reporter assay system to demonstrate that miR-21 functionally interacts with the 3′UTR of CCL20 mRNA and down-regulates CCL20 in miR-21 mimic transfected CRC cell lines (Caco-2, SW480 and SW620). Thus, regulation of CCL20 expression by miR-21 might be a regulatory mechanism involved in progression of CRC. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581099</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581099</guid>        </item>
        <item>
            <title>Selective killing of lung cancer cells using carcinoembryonic antigen promoter and double suicide genes, thymidine kinase and cytosine deaminase (pCEA-TK/CD)</title>
            <link>http://www.medworm.com/index.php?rid=5581089&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100632X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The application of gene therapy in cancer treatment is limited by non-specific targeting. In the present study, we constructed a recombinant plasmid, containing a carcinoembryonic antigen (CEA) promoter and double suicide genes thymidine kinase (TK) and cytosine deaminase (CD), henceforth referred to as pCEA-TK/CD. Our results showed that the CEA promoter can specifically drive target gene expression in CEA-positive lung cancer cells. In the presence of prodrugs 5-flucytosine and ganciclovir, pCEA-TK/CD transfection decreased inhibitory concentration 50 and increased apoptosis and cyclomorphosis. Our result suggests that gene therapy using pCEA-TK/CD may be a promising new approach for treating lung cancer. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581089</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581089</guid>        </item>
        <item>
            <title>Therapeutic approaches targeting midkine suppress tumor growth and lung metastasis in osteosarcoma</title>
            <link>http://www.medworm.com/index.php?rid=5581088&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006306%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Midkine (MK) plays important roles in tumorigenesis, however, the biological function of MK and whether MK can be a therapeutic target in osteosarcoma are unclear. Here, we found that osteosarcoma tissues showed high MK expression. MK knockdown by small interfering RNA significantly induced apoptosis in osteosarcoma cells, whereas recombinant MK increased cell proliferation. Inhibition of MK signaling by anti-MK monoclonal antibody (anti-MK mAb) suppressed growth of osteosarcoma cells both in vitro and in vivo. Moreover, inhibition of MK function significantly suppressed lung metastasis in xenograft transplantation model. Targeting MK by anti-MK mAb may have value in the treatment of osteosarcoma. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581088</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581088</guid>        </item>
        <item>
            <title>Adoptive T-cell therapy of B-cell malignancies: Conventional and physiological chimeric antigen receptors</title>
            <link>http://www.medworm.com/index.php?rid=5581085&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006446%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Hematological malignancies remain incurable diseases because of the high risk of relapse, even after complete remission. Adoptive T-cell therapy (ACT) using modified T cells with chimeric antigen receptors (CARs) targeted to specific tumor-associated antigens expressed by B-cell malignancies represents an attractive approach for cancer immunotherapy. Investigators optimized the design of CARs to enhance receptor mediated T cell signaling and demonstrated that second and third generation CARs, including various costimulatory molecules, resulted in enhanced T-cell persistence and sustained antitumor activity in both in vitro and in vivo mouse models as well as clinical trials. We highlight advances in the use of CARs in the treatment of B-cell malignancies and future challenges in ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581085</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581085</guid>        </item>
        <item>
            <title>Prostate cancer in the senior men from rural areas in east district of China: Contemporary management and 5-year outcomes at multi-institutional collaboration</title>
            <link>http://www.medworm.com/index.php?rid=5552121&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005957%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: In keeping with a lack of prostate-specific antigen (PSA)-based screening, Chinese men present later in life and course of their disease, with over 27% men dying of PCa at five years. Debulking of tumors by surgery and radiation therapy for high grade tumor may provide some survival benefit in the senior men but further study is required to validate these findings. It is important of the annual use of PSA test for men over 50years old to detect the PCa in the early stage in this nation. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552121</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552121</guid>        </item>
        <item>
            <title>Aberrant methylation of the PTPRO gene in peripheral blood as a potential biomarker in esophageal squamous cell carcinoma patients</title>
            <link>http://www.medworm.com/index.php?rid=5552117&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005295%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► We measured PTPRO methylation in primary ESCCs and matched peripheral blood samples. ► PTPRO methylation in blood samples displayed the same alteration as in ESCC tumors. ► No methylated PTPRO was observed in peripheral blood from healthy individuals. ► Demethylation treatment could reverse methylation-mediated PTPRO inactivation. ► Circulating methylated PTPRO may serve as a biomarker for noninvasive diagnosis and disease monitoring.Abstract: Epigenetic inactivation of protein tyrosine phosphatase receptor-type O (PTPRO), a new member of the PTP family, has been described in several forms of cancer. We evaluated PTPRO promoter hypermethylation as a potential biomarker in esophageal squamous cell carcinoma (ESCC). This alteration was observed in 27 (75%) of 36 prima...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552117</comments>
            <pubDate>Fri, 18 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552117</guid>        </item>
        <item>
            <title>NIH-3T3 fibroblasts cultured with plasma from colorectal cancer patients generate poorly differentiated carcinomas in mice</title>
            <link>http://www.medworm.com/index.php?rid=5581096&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006458%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The ability of cells to undergo cellular transitions, in particular, to switch between epithelial and mesenchymal states, might be highly advantageous during the progression of carcinoma. Using histological and immunohistochemical techniques, we here show that the injection into mice of spontaneously transformed NIH-3T3 cells generated fusocellular sarcomas, whereas NIH-3T3 cells that had been transformed by culturing with plasma from colorectal cancer patients gave rise to tumors that phenotypically resembled the carcinomas of the original cancer patients. Thus, plasma from cancer patients is able to transform NIH-3T3 fibroblasts into malignant epithelial-like cells, suggesting that such cells might undergo mesenchymal to epithelial transition during plasma-induced transformatio...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581096</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581096</guid>        </item>
        <item>
            <title>Re-expression of miR-199a suppresses renal cancer cell proliferation and survival by targeting GSK-3β</title>
            <link>http://www.medworm.com/index.php?rid=5552123&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006215%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Recently, we have identified GSK-3 as a new therapeutic target in renal cell cancer (RCC). miR-199a could potentially downregulate GSK-3β expression. Here, we found a decreased miR-199a expression in 59% (32 of 54) of RCCs and it was correlated with higher tumor stage (p (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552123</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552123</guid>        </item>
        <item>
            <title>A novel gain-of-function mutation of TGF-β receptor II promotes cancer progression via delayed receptor internalization in oral squamous cell carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5552120&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005969%2Fabstract%3Frss%3Dyes</link>
            <description>We present a novel gain-of-function mutation of TGF-β receptor II (TβRII) in human oral squamous cell carcinoma. ► This mutation of TβRII enhances TGF-β signaling. ► Mutation of TβRII induces higher migratory and invasive capabilities. ► Enhanced TGF-β signaling by this mutation is due to delayed TβRII internalization.Abstract: We present a novel gain-of-function mutation of TGF-β receptor II (TβRII) found in human oral squamous cell carcinoma (OSCC). Expression of E221V/N238I mutant TβRII enhanced TGF-β signaling. Mutation of TβRII conferred cells higher migratory and invasive capabilities and MMP-2 activity. In mouse tumor model, mutant tumors exhibited poor differentiation and E-cadherin relocalization to the cytosol. Lipid-raft-dependent endocytosis of TβRII was atte...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552120</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552120</guid>        </item>
        <item>
            <title>Requirement of p38 MAPK for a cell-death pathway triggered by vorinostat in MDA-MB-231 human breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5552114&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004575%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Vorinostat-induced apoptosis correlates to hyperacetylation of histone H3 in MDA-MB-231 cells. ► Vorinostat activates the intrinsic apoptotic pathway and caspase-3 cleavage. ► Vorinostat modulates MAPK signaling during apoptosis induction. ► p38 MAPK is essential for the induction of vorinostat-induced apoptosis in MDA-MB-231 cells.Abstract: Vorinostat is a histone deacetylase inhibitor that effectively suppresses cancer-cell proliferation by inducing cell-cycle arrest and/or apoptosis. We now show the involvement of p38 mitogen-activated protein kinase (MAPK) in the regulation of vorinostat-induced apoptosis in MDA-MB-231 human breast cancer cells. Vorinostat induced the hyperacetylation of histone H3, which correlated to apoptosis induction. Vorinostat-induced apopt...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552114</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552114</guid>        </item>
        <item>
            <title>L1 cell adhesion molecule and epidermal growth factor receptor activation confer cisplatin resistance in intrahepatic cholangiocarcinoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5581094&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006410%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Intrahepatic cholangiocarcinoma (ICC) is refractory to conventional chemotherapy. We previously generated chemoresistant ICC (SCKR) cells and showed that AKT and ERK signaling conferred cisplatin resistance. Here, we report that epidermal growth factor receptor (EGFR) signaling and L1 cell adhesion molecule (L1CAM) conferred cisplatin resistance in SCKR cells in an additive fashion. Activation of EGFR connected to AKT and ERK signaling pathways may induce anti-apoptosis and promote cell proliferation, while L1CAM promoted cell proliferation by mainly activating ERK signaling. Inhibition of EGFR activation or L1ACM greatly sensitized the cells to cisplatin. EGFR and L1CAM may be important targets for ICC therapy. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581094</comments>
            <pubDate>Wed, 16 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581094</guid>        </item>
        <item>
            <title>Characterization of a cell culture model for clinically aggressive hepatocellular carcinoma induced by chronic hypoxia</title>
            <link>http://www.medworm.com/index.php?rid=5552122&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005994%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We demonstrated in an in vitro model (human HepG2 liver cells) that chronic hypoxia induced gene expression is associated with an aggressive phenotype in patients with hepatocellular carcinoma (HCC). The aim of this study was to characterize this model further using gene expression microarray, real-time PCR and immunocytochemistry. Subsequently, pathway analysis software was used to identify relevant processes. After examination, we selected 2% O2 during 72h as conditions to study chronic hypoxia. The most affected signaling is centered on TGF-β1 and PPARα/RXRα. Cells at 2% O2 showed a shift in expression of Epithelial-to-Mesenchymal-Transition (EMT) related genes. Furthermore, a downregulation of liver specific detoxification pathways including cytochrome P450’s and glutath...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552122</comments>
            <pubDate>Wed, 16 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552122</guid>        </item>
        <item>
            <title>Down-regulation of mitogen-inducible gene 6, a negative regulator of EGFR, enhances resistance to MEK inhibition in KRAS mutant cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5581095&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006409%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Previously, we found that KRAS mutant cancer cells showed variable response to AZD6244, a MEK inhibitor through differential activation of EGFR/AKT. To investigate its mechanism, we performed cDNA microarray using four KRAS mutant cancer cells. We found that treatment with AZD6244 reduced the expression of mitogen-inducible gene 6 (MIG6), a negative feedback regulator for EGFR, in AZD6244-resistant cells, while activity of EGFR and AKT was increased in these cells. Reconstitution or knockdown of MIG6 expression affected cancer cell responses to AZD6244. Treatment with a combination of EGFR inhibitor and AZD6244 inhibited cell proliferation synergistically without activation of AKT in AZD6244-resistant cells. Our study provides a mechanism of differential response to MEK inhibitio...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581095</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581095</guid>        </item>
        <item>
            <title>DNA demethylation by 5-aza-2-deoxycytidine treatment abrogates 17 beta-estradiol-induced cell growth and restores expression of DNA repair genes in human breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5581093&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006392%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Prolonged exposure to elevated levels of estrogen is a risk factor for breast cancer. Though increased cell growth and loss of DNA repair capacity is one of the proposed mechanisms for estrogen-induced cancers, the mechanism through which estrogen induces cell growth and decreases DNA repair capacity is not clear. DNA hypermethylation is known to inactivate DNA repair genes and apoptotic response in cancer cells. Therefore, the objective of this study was to determine the role of DNA hypermethylation in estrogen-induced cell growth and regulation of DNA repair genes expression in breast cancer cells. To achieve this objective, the estrogen-responsive MCF-7 cells either pretreated with 5-aza-2-deoxycytidine (5-aza-dC) or untreated (as control) were exposed to 17 beta-estradiol (E2...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581093</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581093</guid>        </item>
        <item>
            <title>Differential function of lysophosphatidic acid receptors in cell proliferation and migration of neuroblastoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5581097&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006471%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► LPA receptors have different biological functions in neuroblastoma cells. ► LPA2 and LPA3 stimulate cell proliferation and migration. ► LPA1 acts as a negative regulator of cell proliferation and migration. ► Mutated LPA1 enhances cell proliferation and migration activities.Abstract: Lysophosphatidic acid (LPA) is a bioactive lipid mediator that induces diverse cellular biological effects and interacts with G protein-coupled transmembrane LPA receptors. In the present study, to assess biological roles of LPA receptors in the pathogenesis of tumor cells, each LPA receptor (Lpar1, Lpar2 or Lpar3)-expressing rat neuroblastoma B103 cells (lpa1-1, lpa2-2 or lpa3-3-2 cells, respectively) were used. In cell motility and invasion assay, lpa2-2 and lpa3-3-2 cells showed signif...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5581097</comments>
            <pubDate>Mon, 14 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5581097</guid>        </item>
        <item>
            <title>CD133+ liver cancer stem cells modulate radioresistance in human hepatocellular carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5552116&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100629X%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► CD133+ cells activate cell-cycle-related proteins after irradiation. ► The activation of cell-cycle-related proteins regulate G2/M cell-cycle arrest. ► CD133+ cells show anti-apoptotic and proliferative activities after irradiation. ► The proliferation of CD133+ cells is enhanced via activation of ERK/MAPK pathway. ► Liver cancer cells expressing CD133 are associated with radioresistance.Abstract: CD133 is a cancer stem-cell (CSC) marker associated with radioresistance and chemoresistance in various cancers. In the present study, CD133-expressing liver cancer cells following radiation exposure showed higher activation of MAPK/PI3K signaling pathway and reduction in reactive oxygen species levels compared to CD133− cells. The in vivo study with a xenograft model sh...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552116</comments>
            <pubDate>Mon, 14 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552116</guid>        </item>
        <item>
            <title>CYR61 controls p53 and NF-κB expression through PI3K/Akt/mTOR pathways in carboplatin-induced ovarian cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5440385&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006331%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: CYR61 over-expression promotes cell proliferation by inhibiting carboplatin-induced apoptosis, decreasing Bax expression, and increasing Bcl-xL, Mcl-1, and Bcl-2. At the same time, down-regulating p53 expression, while up-regulated NF-κB expression. Additionally, p21 and p53 promoter activities were reduced, while NF-κB and Bcl-2 activities increased. In parallel, CYR61-expressing cells, during carboplatin-induced apoptosis, resulted in an increase of Akt phosphorylation, while rapamycin-treated cells were not affected. Carboplatin effectively inhibited the activation of mTOR signaling cascade, which includes mTOR, 4E-BP1, p70S6K, HIF-1α, and VEGF. These results provide evidence that CYR61 promotes cell proliferation and inhibits apoptosis. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440385</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440385</guid>        </item>
        <item>
            <title>Selenite induces apoptosis in colorectal cancer cells via AKT-mediated inhibition of β-catenin survival axis</title>
            <link>http://www.medworm.com/index.php?rid=5440384&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006318%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, with the aim to explore the detailed mechanisms how selenite induces apoptosis in colorectal cancer cells, we investigated the role of AKT/β-catenin signaling, a critical regulator of cell proliferation, survival and tumorigenesis, in selenite-induced apoptosis of colorectal cancer cells and xenograft tumors. We showed that selenite exerted a remarkable inhibitory effect on activation of AKT, leading to suppression of β-catenin activity and expression of its targets: cyclin D1 and survivin. Further experiments by transient expression of AKT and β-catenin revealed that inhibition of AKT/β-catenin was closely correlated with selenite-triggered apoptosis. Importantly, MnTMPyP pretreatment implied reactive oxygen species (ROS) was a crucial upstream signal for selenite-trigg...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440384</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440384</guid>        </item>
        <item>
            <title>Nanoliposome-mediated FL/TRAIL double-gene therapy for colon cancer: In vitro and in vivo evaluation</title>
            <link>http://www.medworm.com/index.php?rid=5440383&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006276%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Cationic nanoliposomes have the advantage of being gene carriers. The joint therapeutic effects of the two genes are superior to those of a single gene. Gene therapy combined with immunotherapy has significant implications for cancer treatment. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440383</comments>
            <pubDate>Wed, 09 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440383</guid>        </item>
        <item>
            <title>Histone H2A.Z prepares the prostate specific antigen (PSA) gene for androgen receptor-mediated transcription and is upregulated in a model of prostate cancer progression</title>
            <link>http://www.medworm.com/index.php?rid=5440380&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006161%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The histone variant H2A.Z is present at many eukaryotic gene regulatory regions and can affect rates of transcription. Here we show that total H2A.Z and an acetylated form of H2A.Z is mainly present at the prostate specific antigen (PSA) enhancer and promoter in prostate cancer cell lines where the gene is expressed, but the levels decrease during rapid cycles of transcription. Treatment of prostate cancer cells with androgen results in increased H2A.Z levels due to upregulation of the H2A.Z-1, but not the H2A.Z-2 gene. This upregulation is likely the result of increased MYC transcription factor binding that occurs in response to androgen at the H2A.Z-1 promoter. Furthermore, we show that in a LNCaP xenograft model of prostate cancer progression, there is a significant increase o...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440380</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440380</guid>        </item>
        <item>
            <title>Exosomes derived from human bone marrow mesenchymal stem cells promote tumor growth in vivo</title>
            <link>http://www.medworm.com/index.php?rid=5440379&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100615X%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we investigated the effects of bone marrow MSC-derived exosomes (MSC-exosomes) on tumor growth in vitro and in vivo. Our results showed that MSC-exosomes promoted tumor growth in vivo. MSC-exosomes enhanced vascular endothelial growth factor (VEGF) expression in tumor cells by activating extracellular signal-regulated kinase1/2 (ERK1/2) pathway. Inhibition of ERK1/2 activation reserved the increase of VEGF level by MSC-exosomes. Our findings demonstrate a new mechanism through which MSC-exosome-mediated cell–cell interactions may contribute to tumor progression. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440379</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440379</guid>        </item>
        <item>
            <title>Reactive oxygen species and p38 MAPK regulate Bax translocation and calcium redistribution in salubrinal-induced apoptosis of EBV-transformed B cells</title>
            <link>http://www.medworm.com/index.php?rid=5407320&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005532%2Fabstract%3Frss%3Dyes</link>
            <description>In this report, we found that salubrinal induced apoptosis of EBV-transformed B cells. Notably, salubrinal induced ROS generation and p38 MPAK activation, which then induced expression of FasL. Moreover, salubrinal subsequently led to activation of caspases, calcium redistribution, Bax translocation, cytochrome c release, and apoptosis. These findings suggest that salubrinal may be a novel therapeutic approach for EBV-associated malignant diseases. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407320</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407320</guid>        </item>
        <item>
            <title>TSC1/TSC2 inactivation inhibits AKT through mTORC1-dependent up-regulation of STAT3-PTEN cascade</title>
            <link>http://www.medworm.com/index.php?rid=5407317&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005362%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► PTEN is significantly up-regulated in Tsc1−/− or Tsc2−/− MEFs. ► Loss of TSC1/TSC2 up-regulates PTEN through activation of mTORC1-STAT3 pathway. ► STAT3 promotes the expression of PTEN at transcriptional level. ► Elevated PTEN suppresses Akt activity and inhibits the proliferation of Tsc1- or Tsc2-null MEFs.Abstract: Aberrant activation of mammalian target of rapamycin complex 1 (mTORC1), caused by loss or inactivation of TSC1/TSC2 protein complex, leads to negative feedback inhibition of Akt. The exact mechanisms of this process are still not fully understood. Here we present evidence for the involvement of STAT3, a known mTORC1 regulated transcription factor, in this process. We demonstrate that STAT3 promotes the transcription of PTEN by directly binding on...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407317</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407317</guid>        </item>
        <item>
            <title>Pegylated liposomal doxorubicin as first-line monotherapy in elderly women with locally advanced or metastatic breast cancer: Novel treatment predictive factors identified</title>
            <link>http://www.medworm.com/index.php?rid=5407311&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004319%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Elderly with breast cancer received pegylated-liposomal-doxorubicin (PLD) first line. ► Time to treatment failure was 5.5 months and overall survival 20.6 months. ► Tumor TOPO2α and MRN complex expression correlated to outcome. ► ABCB1 single nucleotide polymorphisms correlated to time to progression and toxicity. ► PLD is effective and potential predictive markers were identified.Abstract: We investigated the efficacy and safety of single-agent pegylated liposomal doxorubicin (PLD) as first-line treatment for elderly women with advanced breast cancer and evaluated predictive markers for response and toxicity.Twenty-five women ⩾65years received 40mg/m2 PLD every 28days. Time to treatment failure (TTF), response rate, time to progression (TTP) and overall survival...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407311</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407311</guid>        </item>
        <item>
            <title>PPARgamma-PGC-1alpha activity is determinant of alcohol related breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5440382&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006227%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Alcohol is a risk factor for postmenopausal breast cancer. One of several proposed mechanisms is that alcohol-related breast cancer is caused by increased sex hormone levels. PPARγ inhibits aromatase transcription in breast adipocytes. We reproduced previously found allele-specific effects of the wildtype Pro-allele of PPARG Pro12Ala in alcohol related breast cancer. In transiently transfected cells, transcriptional activation by PPARγ and the PPARγ-PGC-1α complex was inhibited by ethanol. PPARγ 12Ala-mediated transcription activation was not enhanced by PGC-1α, resulting in allele-specific transcription activation by the PPARγ 12Pro-PGC-1α complex.Our results suggest that PPARγ and PGC-1α activity is an important determinant of alcohol related breast cancer. (Source: C...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440382</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440382</guid>        </item>
        <item>
            <title>Nanoencapsulated anti-CK2 small molecule drug or siRNA specifically targets malignant cancer but not benign cells</title>
            <link>http://www.medworm.com/index.php?rid=5440381&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006203%2Fabstract%3Frss%3Dyes</link>
            <description>We present data on the TBG nanocapsule itself and on CK2 inhibition or downregulation in treated cells, including effects on Nuclear Factor-kappa B (NF-κB) p65. By direct comparison of two CK2-directed cargos, our data provide proof that the TBG encapsulation design for delivery of drugs specifically to cancer cells has strong potential for small molecule- and nucleic acid–based cancer therapy. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440381</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440381</guid>        </item>
        <item>
            <title>piR-823, a novel non-coding small RNA, demonstrates in vitro and in vivo tumor suppressive activity in human gastric cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5440377&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006173%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Piwi-interacting RNAs (piRNAs), new non-coding small RNAs, are association with chromatin organization, messenger RNA stability and genome structure. However, the roles of piRNA in carcinogenesis are not clearly defined. By using real-time reverse transcription-polymerase chain reaction technology, we found that the expression level of piR-823 in gastric cancer tissues was significant lower than that in non-cancerous tissues. After increase the level of piR-823 in gastric cancer cells, cell growth was inhibited. The results of xenograft nude mice model confirmed its tumor suppressive properties. All of the evidences indicated that piR-823 play a crucial role in the occult of gastric cancer. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440377</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440377</guid>        </item>
        <item>
            <title>HMGA-targeted phosphorothioate DNA aptamers increase sensitivity to gemcitabine chemotherapy in human pancreatic cancer cell lines</title>
            <link>http://www.medworm.com/index.php?rid=5440378&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006185%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Elevated high mobility group A (HMGA) protein expression in pancreatic cancer cells is correlated with resistance to the chemotherapy agent gemcitabine. Here, we demonstrate use of HMGA-targeted AT-rich phosphorothioate DNA (AT-sDNA) aptamers to suppress HMGA carcinogenic activity. Cell growth of human pancreatic cancer cells (AsPC-1 and Miapaca-2) transfected with AT-sDNA were monitored after treatment with gemcitabine. Significant increases in cell death in AT-sDNA transfected cells compared to non-AT-rich sDNA treated cells were observed in both cell lines. The data indicate the potential use of HMGA targeted DNA aptamers to enhance chemotherapy efficacy in pancreatic cancer treatment. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440378</comments>
            <pubDate>Mon, 31 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440378</guid>        </item>
        <item>
            <title>Protopine, a novel microtubule-stabilizing agent, causes mitotic arrest and apoptotic cell death in human hormone-refractory prostate cancer cell lines</title>
            <link>http://www.medworm.com/index.php?rid=5440376&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006021%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, the data suggest that protopine is a novel microtubule stabilizer with anticancer activity in HRPC cells through apoptotic pathway by modulating Cdk1 activity and Bcl-2 family of proteins. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440376</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440376</guid>        </item>
        <item>
            <title>Combination of salinomycin and gemcitabine eliminates pancreatic cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5407310&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003077%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Previous research has documented that a subpopulation of pancreatic cancer cells, named cancer stem cells (CSCs), harbor stem cell-like properties. Here, we examined the efficacy of combined treatments of salinomycin and gemcitabine in human pancreatic cancer cells. Salinomycin inhibited the growth of CSCs, while gemcitabine suppressed the viability of non-CSCs. Consistently, in vivo studies showed that salinomycin combined with gemcitabine could eliminate the engraftment of human pancreatic cancer more effectively than the individual agents. These data indicated that administration of salinomycin, which targets CSCs, may constitute a potential therapeutic strategy for improving the efficacy of gemcitabine to eradicate pancreatic cancer. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407310</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407310</guid>        </item>
        <item>
            <title>Identification of transaldolase as a novel serum biomarker for hepatocellular carcinoma metastasis using xenografted mouse model and clinic samples</title>
            <link>http://www.medworm.com/index.php?rid=5407312&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005283%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Serum proteome alterations associated with HCC metastasis were obtained from iTRAQ analysis. ► Tumor derived TALDO was identified in serum during HCC progression and metastasis. ► TALDO may serve as useful metastasis-associated biomarker in patients with HCC.Abstract: Hepatocellular carcinoma (HCC) is one of serious disorders with the highest morbidities and mortalities worldwide. Metastasis is the major concern that causes death in HCC. The goal of this study was to screen and identify potential serum proteins indicating HCC metastasis. Serum samples collected from control and HCCLM3-R metastatic HCC tumor model at specific stages of metastasis (1wk, 3wks and 6wks) were subjected to iTRAQ labeling followed by 2DLC-ESI-MS/MS analysis. A total of 554 proteins were identi...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407312</comments>
            <pubDate>Mon, 24 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407312</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5323753&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511006069%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323753</comments>
            <pubDate>Tue, 18 Oct 2011 01:03:23 +0100</pubDate>
            <guid isPermaLink="false">5323753</guid>        </item>
        <item>
            <title>Phosphorylation status of heat shock protein 27 plays a key role in gemcitabine-induced apoptosis of pancreatic cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5407318&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005386%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we investigated the relationship between the effect of gemcitabine and the phosphorylation status of HSP27 in pancreatic cancer cells, Panc1 and KP3. Gemcitabine suppressed pancreatic cancer cell growth and induced apoptosis. Gemcitabine caused activation of p38 mitogen-activated protein kinase (MAPK), MAPK-activated protein kinase 2 (MAPKAPK-2) and subsequently phosphorylation of HSP27 at Ser15, 78 and 82 without affecting total HSP27 levels. The inhibitions of p38 MAPK and MAPKAPK-2 reduced the phosphorylation of HSP27 and apoptosis in gemcitabine-treated cells. To further investigate the role of phosphorylated HSP27, we established Panc1 cell lines which were stably transfected with empty vector (empty cells), wild-type HSP27-encoding vector (WT cells) and 2 mutant HSP27-...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407318</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407318</guid>        </item>
        <item>
            <title>Hypoxia, stem cells and bone tumor</title>
            <link>http://www.medworm.com/index.php?rid=5407309&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005696%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Hypoxia plays an important role in normal development and growth of solid tumors. ► Hypoxia drives tumor bone metastases. ► Blockage of HIF pathway provides therapeutic advantage in bone tumor patients. ► HIF is highly expressed in cancer stem cells. ► Targeting hypoxia would be novel strategy to eliminate cancer stem cells and cure bone tumor.Abstract: Normal oxygen level is critical for niches that together with other components of the niche play vital role in regulating stem or tumor cells behavior. Hypoxia plays an important role in normal development and disease progression, including the growth of solid tumors. The hypoxia inducible factors (HIFs) are the key mediators of the cellular response to hypoxia. In this review, we focused on the role of HIFs on bone ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407309</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407309</guid>        </item>
        <item>
            <title>Involvement of reactive oxygen species in 2-methoxyestradiol-induced apoptosis in human neuroblastoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5407316&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005350%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► 2-ME inhibited the proliferation and induced apoptosis in human neuroblastoma cells. ► 2-ME treatment also resulted in the generation of ROS and mitochondrial injury. ► Co-treatment with antioxidants decreased 2-ME-induced ROS and mitochondrial injury. ► Treatment with antioxidants prevented 2-ME-induced apoptosis in neuroblastoma cells.Abstract: Neuroblastoma is the most common extra-cranial solid tumor in children. Despite advances in the treatment of childhood cancer, outcomes for children with advanced-stage neuroblastoma remain poor. Here we reported that 2-methoxyestradiol (2-ME) inhibited the proliferation and induced apoptosis in human neuroblastoma SK-N-SH and SH-SY5Y cells. 2-ME treatment also resulted in the generation of ROS and the loss of mitochondrial m...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407316</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407316</guid>        </item>
        <item>
            <title>Erratum to “A rearranged EP300 gene in the human B-cell lymphoma cell line RC-K8 encodes a disabled transcriptional co-activator that contributes to cell growth and oncogenicity” [Cancer Lett 302 (2011) 76–83]</title>
            <link>http://www.medworm.com/index.php?rid=5440386&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100560X%2Fabstract%3Frss%3Dyes</link>
            <description>The authors wish to correct two small errors in Fig. 2. In Fig. 2B, the DNA sequence at the end of exon 17 should read: CAGCTTTTAGGAATCCCT, i.e., there should be an additional C (italics) at the next to last position. In Fig. 2C, the p300ΔC protein should have 1087 (not 1047) p300-derived amino acids (aa), which are encoded by exons 1–17. Therefore, the p300ΔC protein consists of 1112 aa (1087 p300 aa plus 25 chromosome 6-encoded aa). These corrections to minor clerical errors do not affect experiments reported in the paper or conclusions of the paper. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440386</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440386</guid>        </item>
        <item>
            <title>Adjuvant effect of a natural TLR4 ligand on dendritic cell-based cancer immunotherapy</title>
            <link>http://www.medworm.com/index.php?rid=5407319&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005398%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► TLR4 ligand induces DC maturation through NF-κB pathway. ► TLR4 ligand enhances CCR7 expression through NF-κB and p38 pathway. ► TLR4 ligand enhances DC migration to CCL19 in vitro and DC homing into the lymph nodes in vivo. ► TLR4 ligand enhances antitumor activity of DCs in animal model.Abstract: The clinical efficacy of dendritic cell (DC) vaccine in cancer patients has been unsatisfactory due, at least in part, to the deficiency of maturation and impaired migration of ex vivo generated DCs to the draining lymph nodes. To solve this problem, we used angelan, a natural TLR4 ligand, to enhance the maturation and migration of DCs. Angelan increased the expression of MHC-I/II, CD80, and CD86, DC maturation markers, through the NF-κB pathway. This compound also incre...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407319</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407319</guid>        </item>
        <item>
            <title>Galectin-3 – A jack-of-all-trades in cancer</title>
            <link>http://www.medworm.com/index.php?rid=5407308&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005337%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Galectin-3 has multiple inter- and sub-cellular localizations. ► Alterations of galectin-3 expression and localization are common in cancer. ► Galectin-3 regulates cancer development, progression and metastasis. ► Galectin-3 interacts with different ligands at different localizations.Abstract: Galectin-3 is a mammalian β-galactoside-binding protein that is expressed by various types of human cells. Changes in galectin-3 expression and subcellular and intercellular localizations are commonly seen in cancer and pre-cancerous conditions. It is increasingly recognized that galectin-3 is an important regulator of a broad range of cancer cell activities and plays important roles in cancer cell growth, transformation, apoptosis, angiogenesis, adhesion, invasion and metastas...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407308</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407308</guid>        </item>
        <item>
            <title>A possible role of cIAP2 in Helicobacter pylori-associated gastric cancer</title>
            <link>http://www.medworm.com/index.php?rid=5407315&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005374%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we investigated the role cIAP2 in Helicobacter pylori (HP) related gastric carcinogenesis. We measured the expression of cIAP2 at mRNA and protein levels in a panel of gastric cancer cell lines and human gastric cancer tissues by semi-quantitative reverse transcriptase PCR (RT-PCR), quantitative real time PCR (qPCR), immunoblotting, and immunohistochemistry. The effects of cIAP2 down-regulation on gastric cell proliferation and apoptosis were detected by standard WST-1 assay and flow cytometry, respectively. Infection of gastric mucosa by HP enhances the expression of cIAP2 in mouse gastric tissues. Over 70% of human gastric cancer tissues express higher amount of cIAP2. Well-differentiated gastric cancer cells express more cIAP2 than moderately- and poorly-differentiated ga...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407315</comments>
            <pubDate>Mon, 03 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407315</guid>        </item>
        <item>
            <title>An RNA aptamer that specifically binds pancreatic adenocarcinoma up-regulated factor inhibits migration and growth of pancreatic cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5323761&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005155%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we generated and characterized a 2′-fluoropyrimidine modified RNA aptamer (P12FR2) directed against human PAUF. P12FR2 binds specifically to human PAUF with an estimated apparent KD of 77nM. P12FR2 aptamer inhibits PAUF-induced migration of PANC-1, human pancreatic cancer cells, in a wound healing assay. Moreover, intraperitoneal injection of P12FR2 decreased tumor growth by about 60% in an in vivo xenograft model with CFPAC-1 pancreatic cancer cells, without causing a loss of weight in the treated mice. Taken together, we propose here that PAUF-specific RNA aptamer, P12FR2, has the potential to be effective in the therapy of human pancreatic cancer. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323761</comments>
            <pubDate>Mon, 03 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323761</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5273328&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100543X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273328</comments>
            <pubDate>Mon, 03 Oct 2011 01:01:45 +0100</pubDate>
            <guid isPermaLink="false">5273328</guid>        </item>
        <item>
            <title>Lunasin potentiates the effect of oxaliplatin preventing outgrowth of colon cancer metastasis, binds to α5β1 integrin and suppresses FAK/ERK/NF-κB signaling</title>
            <link>http://www.medworm.com/index.php?rid=5407313&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005325%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► In vitro, lunasin inhibited metastasis by modulation of FAK/ERK/NF-κB signaling. ► In vitro, lunasin physically interacted with α5β1 integrin. ► Lunasin internalized into the cytoplasm and nucleus of KM12L4 colon cancer cells. ► In vivo lunasin inhibited metastasis of KM12L4 colon cancer cells. ► Lunasin potentiated the anti-metastatic effect of oxaliplatin in vivo.Abstract: The effect of lunasin on colon cancer metastasis was studied using three human colon cancer cell lines in vitro and a liver metastasis model of colon cancer in vivo. Lunasin bound with α5β1 integrin and internalized into the nucleus of KM12L4 human colon cancer cells. Lunasin (10μM) inhibited the activation of focal adhesion kinase (FAK) by 28%, 39% and 60% in RKO, HCT-116 and KM12L4 human...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407313</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407313</guid>        </item>
        <item>
            <title>Nitidine Chloride inhibits breast cancer cells migration and invasion by suppressing c-Src/FAK associated signaling pathway</title>
            <link>http://www.medworm.com/index.php?rid=5407314&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005313%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Nitidine Chloride inhibits breast cancer cells migration and invasion. ► NC reduces protrusion formation and proteolytic activity of MMP-9 and MMP-2. ► PDGF induced signaling and AP-1 transcriptional activity was decreased by NC. ► NC could have potential as a novel anti-metastasis drug to breast cancer.Abstract: Nitidine is a benzophenanthridine alkaloid, which has been shown to have anti-tumor properties. Here, we demonstrated that Nitidine Chloride (NC) could inhibit breast cancer cells migration and invasion both in vitro and in vivo. Meanwhile, the protrusion formation and partial proteolytic activity of MMP-9 and MMP-2 were attenuated by NC in a dose-dependent manner in MDA-MB-231 cells. Furthermore, addition NC to cells significantly decreases PDGF induced phos...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5407314</comments>
            <pubDate>Wed, 28 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5407314</guid>        </item>
        <item>
            <title>Toxicity and delivery methods for the linamarase/linamarin/glucose oxidase system, when used against human glioma tumors implanted in the brain of nude rats</title>
            <link>http://www.medworm.com/index.php?rid=5323764&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100526X%2Fabstract%3Frss%3Dyes</link>
            <description>In this study we evaluate a gene therapy suicide method against glioblastoma. ► Human gliomas are treated with linamarase, linamarin and glucose oxidase. ► Several delivery methods are evaluated with limited success. ► We conclude that the treatment is too toxic for the animal at curative concentrations.Abstract: Glioblastoma multiforme (GBM) is one of the deadliest forms of cancer, with an average survival time of approximately 1year despite aggressive surgery, radiotherapy and chemotherapy. Here, we report a preclinical study by which the two main energy pathways of the tumor cells, oxidative phosphorylation and aerobic glycolysis, are simultaneously disrupted. The therapy is based on a plant gene encoding a β-glucosidase, linamarase (lis), which react with the substrate linamarin...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323764</comments>
            <pubDate>Wed, 28 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323764</guid>        </item>
        <item>
            <title>Differential expression of microRNA expression in tamoxifen-sensitive MCF-7 versus tamoxifen-resistant LY2 human breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5323757&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005064%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► 97 miRNAs were differentially expressed in MCF-7 versus LY2 breast cancer cells. ► miRs-10a, 22, 29a, 125b, and 222 were higher in LY2 than MCF-7 cells. ► miRs-21, 200a, 200b, 200c, and 205 were higher in MCF-7 than LY2 cells. ► Identified control genes for miRNA QPCR for MCF-7 and LY2 cells treated with 4-OHT. ► Computationally identified miRNA target mRNA genes in 4-OHT-treated MCF-7 cells.Abstract: Microarrays identified miRNAs differentially expressed and 4-hydroxytamoxifen (4-OHT) regulated in MCF-7 endocrine-sensitive versus resistant LY2 human breast cancer cells. 97 miRNAs were differentially expressed in MCF-7 versus LY2 cells. Opposite expression of miRs-10a, 21, 22, 29a, 93, 125b, 181, 200a, 200b, 200c, 205, and 222 was confirmed. Bioinformatic analyses t...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323757</comments>
            <pubDate>Wed, 28 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323757</guid>        </item>
        <item>
            <title>Chemotherapy-induced neutropenia in lung cancer patients: The role of antibiotic prophylaxis</title>
            <link>http://www.medworm.com/index.php?rid=5323755&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100512X%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► We performed a PubMed literature search of manuscripts published until May 2011. ► Quinolones and trimethoprim/sulfamethoxazole were most frequently used. ► Episodes of febrile neutropenia and documented infections were fewer. ► Duration of hospitalisation was shorter. ► Prophylactic wide-spectrum antibiotics are an alternative preventive strategy.Abstract: Chemotherapy-induced neutropenia can cause fatal bacterial infections. Colony-stimulating factors (CSFs) are usually recommended as prophylaxis, while routine use of prophylactic antibiotics remains controversial. Based on our literature search in PubMed, quinolones and trimethoprim/sulfamethoxazole were the most frequently used prophylaxis, while CSFs were administered in 22.1% of patients. Lung cancer patients ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323755</comments>
            <pubDate>Wed, 28 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323755</guid>        </item>
        <item>
            <title>Hypoxia-inducible factors in OSCC</title>
            <link>http://www.medworm.com/index.php?rid=5323754&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005040%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► OSCCs are locally aggressive tumors showing high hypoxia levels. ► High hypoxia causes basic resistance to chemotherapy and other anticancer drugs. ► Tumor hypoxia depends directly on HIFs. ► Analyzing HIF expression in OSCC could determine its viability as therapeutic target.Abstract: Oral squamous cell carcinoma (OSCC) is a characteristic locally aggressive tumor in which hypoxia levels are very high, causing a low response to chemotherapy and providing basic resistance to anticancer drugs. Tumoral hypoxia directly depends on hypoxia-inducible factors (HIF). The goal of this paper is to describe HIF basic biology and tumor cells (HIF-1α, mainly), analyzing the effects of its expression in OSCC, study its relation with other molecules such as nitric oxide (NO), carb...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323754</comments>
            <pubDate>Wed, 28 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323754</guid>        </item>
        <item>
            <title>Human ovarian cancer cell morphology, motility, and proliferation are differentially influenced by autocrine TGFβ superfamily signalling</title>
            <link>http://www.medworm.com/index.php?rid=5323765&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005301%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Human ovarian cancer cells possess autocrine BMP4, BMP6, TGFβ, and activin signalling. ► Autocrine signalling regulates morphology, cell density, proliferation, and motility. ► BMP4-induced changes are Smad-dependent. ► Mean BMP4 levels in human ascites is 18pg/mL. ► Balance between BMP and TGFβ signalling may regulate epithelial–mesenchymal status.Abstract: TGFβ superfamily signalling participates in normal and pathophysiologic cellular processes. Despite several reports demonstrating active TGFβ superfamily signalling pathways in OvCa cell lines and primary cultures, few studies examine their functional outcome. Herein we show that primary human ovarian cancer cells possess intact autocrine BMP, TGFβ and activin signalling. Blocking autocrine signalling res...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323765</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323765</guid>        </item>
        <item>
            <title>Knockdown of RAGE expression inhibits colorectal cancer cell invasion and suppresses angiogenesis in vitro and in vivo</title>
            <link>http://www.medworm.com/index.php?rid=5323763&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005167%2Fabstract%3Frss%3Dyes</link>
            <description>This study aimed to investigate the effects of RAGE on the regulation of cell viability, invasion, and angiogenesis, as well as the underlying molecular mechanisms regulating these interactions in colorectal cancer cells.The RAGE mRNA and protein were evaluated in five colorectal cancer cell lines and in 45 cases of colorectal cancer tissue specimens (using immuohistochemistry). RAGE expression was then knockdown using RAGE shRNA for assessing cell viability and invasion assays as well as for tube formation and CAM assays in human umbilical vein endothelial cells and chick embryos, respectively.RAGE was highly expressed in colorectal cancer tissues, and was associated with increased microvessel density. Two of the four RAGE shRNA constructs were able to significantly knockdown RAGE express...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323763</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323763</guid>        </item>
        <item>
            <title>Chk2-mediated G2/M cell cycle arrest maintains radiation resistance in malignant meningioma cells</title>
            <link>http://www.medworm.com/index.php?rid=5323760&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005106%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, our data suggest that combination treatment with radiation and uPAR knock down or other inhibitors resulting in non-reversible G2/M arrest may be beneficial in the management of meningiomas. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323760</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323760</guid>        </item>
        <item>
            <title>Inactivation of Rac1 reduces Trastuzumab resistance in PTEN deficient and insulin-like growth factor I receptor overexpressing human breast cancer SKBR3 cells</title>
            <link>http://www.medworm.com/index.php?rid=5323759&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005118%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Rac1 activation promotes breast cancer cell proliferation and migration. ► Rac1 is highly activated in IGF-IR overexpression or PTEN deficient SKBR3 cells. ► Rac1 inhibition reduces Trastuzumab resistance in IGF-IR overexpression or PTEN deficient SKBR3 cells. ► Simultaneous inhibition of Rac1 and Akt causes a significant more decrease of Trastuzumab resistance in IGF-IR overexpression or PTEN deficient SKBR3 cells.Abstract: Drug resistance remains to be a big challenge in applying anti-HER2 monoclonal antibody Trastuzumab for treating breast cancer with HER2 overexpression. Amplification of insulin-like growth factor I receptor (IGF-IR) and deletion of tumor suppressor phosphatase and tensin homolog (PTEN) are implicated in Trastuzumab resistance, however, the underl...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323759</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323759</guid>        </item>
        <item>
            <title>Small molecular anticancer agent SKLB703 induces apoptosis in human hepatocellular carcinoma cells via the mitochondrial apoptotic pathway invitro and inhibits tumor growth invivo</title>
            <link>http://www.medworm.com/index.php?rid=5323758&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005131%2Fabstract%3Frss%3Dyes</link>
            <description>We reported that a novel synthesized compound SKLB703. ► 3-Amino-N-(4-chlorobenzyl)-6-(3-methoxyphenyl)thieno[2,3-b]pyridine-2-carboxamide. ► Exhibits antitumor activity both in vitro and in vivo. ► Induces tumor cell apoptosis via mitochondrial apoptotic pathway. ► Human hepatocellular carcinoma cell line HepG2 was the most sensitive to its treatment.Abstract: Inducing apoptosis is a promising therapeutic approach to overcome cancer. Here we described that a novel synthesized compound, 3-amino-N-(4-chlorobenzyl)-6-(3-methoxyphenyl)thieno[2,3-b]pyridine-2-carboxamide (SKLB703), exhibits antitumor activity via inducing apoptosis both in vitro and in vivo. Our results showed that SKLB703 inhibited the proliferation of a panel of human cancer cell lines, and human hepatocellular carci...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323758</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323758</guid>        </item>
        <item>
            <title>Preparation of camptothecin-loaded PCEC microspheres for the treatment of colorectal peritoneal carcinomatosis and tumor growth in mice</title>
            <link>http://www.medworm.com/index.php?rid=5313977&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004824%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► CPT–PCEC MSs inhibits the growth of colorectal cancer cells in vitro and in vivo. ► Microsphere system attenuates the hematologic toxicity of CPT. ► CPT–PCEC MSs inhibits the angiogenic growth of tumor. ► CPT–PCEC MSs may be a potent drug delivery system for abdominal chemotherapy.Abstract: The aim of this study was to prepare PCL–PEG–PCL (PCEC) microspheres to protect camptothecin from hydrolysis, to extend its release time and to enhance its treatment efficacy on colorectal peritoneal carcinomatosis and tumor growth in mice. Camptothecin (CPT)-loaded PCL–PEG–PCL (PCEC) microspheres were prepared by oil-in-water emulsion solvent evaporation method. The particle size, morphological characteristics, encapsulation efficiency, in vitro drug release studies ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313977</comments>
            <pubDate>Fri, 23 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313977</guid>        </item>
        <item>
            <title>Identification of the bleomycin hydrolase gene as a methylated tumor suppressor gene in hepatocellular carcinoma using a novel triple-combination array method</title>
            <link>http://www.medworm.com/index.php?rid=5313973&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004538%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Novel suppressor gene was identified using our designed triple-combination array. ► The bleomycin hydrolase gene was detected as a candidate suppressor gene. ► Its expression level was reduced in tumor tissues by promoter hypermethylation. ► The present study suggests that our new method can detect novel genes of interest.Abstract: In the present study, we sought to identify novel suppressor genes of hepatocellular carcinoma (HCC) using our newly designed triple-combination array. Using this method, the bleomycin hydrolase gene (BLMH) was detected as a candidate suppressor gene. We found that 28 of 48 (58.3%) tumor tissues showed BLMH promoter hypermethylation, and its expression level was significantly reduced in tumor tissues (P=0.001). The present study suggests th...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313973</comments>
            <pubDate>Fri, 23 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313973</guid>        </item>
        <item>
            <title>Preclinical assessment of JNJ-26854165 (Serdemetan1), a novel tryptamine compound with radiosensitizing activity in vitro and in tumor xenografts</title>
            <link>http://www.medworm.com/index.php?rid=5313979&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004861%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Serdemetan inhibits clonogenic survival synergistically with radiation in p53-WT tumor cells. ► Serdemetan inhibits proliferation, migration, and capillary formation of endothelial cells. ► Serdemetan enhances radiation-induced tumor growth delay in vivo. ► Serdemetan antitumor effects are associated with activation of p53 pathway and G2/M arrests. ► Lower effects in p53-null tumors suggest alternative molecular mechanisms of activity.Abstract: Serdemetan (JNJ-26854165) is a novel tryptamine compound with antiproliferative activity in various p53 wild-type (WT) tumor cell lines. We investigated its potential as radiosensitizer using four human cancer cell lines: H460, A549, p53-WT-HCT116, and p53-null-HCT116. Serdemetan inhibited clonogenic survival in all cell line...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313979</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313979</guid>        </item>
        <item>
            <title>The cdk1-cyclin B complex is involved in everolimus triggered resistance in the PC3 prostate cancer cell line</title>
            <link>http://www.medworm.com/index.php?rid=5323762&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005143%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Resistance to the mTOR-inhibitor everolimus was established in prostate cancer cells. ► Resistance led to accumulation of the cells in the G2/M-phase. ► Cdk1 and cyclin B were elevated in the resistant cells. ► Down-regulation of cyclin B restored the tumor cell sensitivity to everolimus.Abstract: The growth potential of PC3 prostate cancer cells, sensible (PC3par) or resistant (PC3res) to the mTOR inhibitor everolimus (RAD001) was investigated. Cell growth and proliferation of PC3res was similar to that of PC3par, and late apoptosis increased in PC3par but decreased in PC3res following treatment with low dosed everolimus. PC3res accumulated in the G2/M-phase, accompanied by cdk1, cdk2 and cyclin B elevation. Knocking down cdk1 or cyclin B distinctly blocked the growt...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323762</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323762</guid>        </item>
        <item>
            <title>Efficacy and safety of intraoperative radiotherapy in breast cancer: A systematic review</title>
            <link>http://www.medworm.com/index.php?rid=5323756&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005088%2Fabstract%3Frss%3Dyes</link>
            <description>The objective of this study is to assess the efficacy and safety of intraoperative radiotherapy (IORT) for early breast cancer through a systematic review. Fifteen studies met the inclusion criteria. Most studies assessed the combined treatment with IORT (10–24Gy) and external beam radiotherapy (EBRT) (45–50Gy) on early stage breast cancer (T0–2). Local control was over 95% for 1 and 4years of follow-up and the 5-year overall survival was 99%. The TARGIT-A study found a similar survival comparing IORT with standard treatment. The incidence of acute and chronic complications was scarce. IORT is well tolerated by patients and acute and late toxicities are low. There are no differences in survival for IORT treated patients versus standard treatment. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5323756</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5323756</guid>        </item>
        <item>
            <title>Noscapine inhibits tumor growth in TMZ-resistant gliomas</title>
            <link>http://www.medworm.com/index.php?rid=5313983&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005027%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Noscapine is a non-toxic agent used as a cough suppressant for decades. ► Noscapine increased survival of animals bearing temozolomide (TMZ)-resistant gliomas. ► Noscapine inhibited proliferation of TMZ-resistant glioma cells. ► Noscapine decreased the migration and invasion of TMZ-resistant glioma cells. ► Noscapine provides a potential alternative therapy for recurrent resistant gliomas.Abstract: Noscapine, a common oral antitussive agent, has been shown to have potent antitumor activity in a variety of cancers. Treatment of glioblastoma multiforme (GBM) with temozolomide (TMZ), its current standard of care, is problematic because the tumor generally recurs and is then resistant to this drug. We therefore investigated the effects of noscapine on human TMZ-resistan...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313983</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313983</guid>        </item>
        <item>
            <title>β-Caryophyllene oxide inhibits growth and induces apoptosis through the suppression of PI3K/AKT/mTOR/S6K1 pathways and ROS-mediated MAPKs activation</title>
            <link>http://www.medworm.com/index.php?rid=5313976&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004769%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► PI3K/AKT/mTOR/S6K1 and MAPK signaling cascades play a critical role in tumorigenesis. ► CPO inhibited the constitutive activation of PI3K/AKT/mTOR/S6K1 signaling cascade. ► CPO also caused the activation of ERK, JNK, and p38 MAPK in tumor cells. ► CPO can interfere with multiple signaling cascades involved in tumorigenesis.Abstract: Both PI3K/AKT/mTOR/S6K1 and mitogen activated protein kinase (MAPK) signaling cascades play an important role in cell proliferation, survival, angiogenesis, and metastasis of tumor cells. In the present report, we investigated the effects of β-caryophyllene oxide (CPO), a sesquiterpene isolated from essential oils of medicinal plants such as guava (Psidium guajava), oregano (Origanum vulgare L.), cinnamon (Cinnamomum spp.) clove (Eugenia ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313976</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313976</guid>        </item>
        <item>
            <title>Molecular targeting of malignant glioma cells with an EphA2-specific immunotoxin delivered by human bone marrow-derived mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5313975&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004605%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we used human bone marrow-derived mesenchymal stem cells (hMSCs) as a vehicle for the targeted delivery of EphrinA1-PE38, a very specific immunotoxin against the EphA2 receptor that is overexpressed in gliomas. hMSCs were transduced with adenovirus to express secretable EphrinA1-PE38. Our in vitro assays confirmed the expression, release and selective killing effect of the immunotoxin produced by hMSCs. Furthermore, the intratumoral injection of engineered hMSCs was effective at inhibiting tumor growth in a malignant glioma tumor model. These results indicate that gene therapy utilizing EphrinA1-PE38-secreting hMSCs may provide a novel approach for the local treatment of malignant gliomas. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313975</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313975</guid>        </item>
        <item>
            <title>A novel C-terminal HSP90 inhibitor KU135 induces apoptosis and cell cycle arrest in melanoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5313974&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004563%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Novel c-terminal Hsp90 inhibitor, KU135 is an effective drug against melanoma. ► It inhibited proliferation and induced G2/M cell cycle arrest, and apoptosis. ► KU135 reduced Hsp90 client proteins Akt, BRAF, RAF-1, cyclin B and cdc25 proteins.Abstract: Heat shock protein 90 (Hsp90) is differentially expressed in tumor cells including melanoma and involved in proper folding, stabilization and regulation of cellular proteins. We investigated a novobiocin-derived Hsp90 C-terminal inhibitor, KU135, for anti-proliferative effects in melanoma cells. The results indicate that KU135 reduced cell viability and cell proliferation in melanoma cells and IC50 values for A735(DRO), M14(NPA), B16F10 and SKMEL28 cells were 0.82, 0.92, 1.33 and 1.30μM respectively. KU135 induced a more...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313974</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313974</guid>        </item>
        <item>
            <title>DNA repair systems in malignant mesothelioma</title>
            <link>http://www.medworm.com/index.php?rid=5313972&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100509X%2Fabstract%3Frss%3Dyes</link>
            <description>This study presents the implications of DNA repair systems to malignant mesothelioma. ► Malignant mesothelioma is characterized by various alterations in DNA repair systems.Abstract: Malignant mesothelioma (MM) is an aggressive tumor of serosal surfaces with increasing incidence and poor prognosis. Asbestos exposure is the main cause of MM and asbestos-induced DNA damage is critical for MM pathogenesis. The present review summarizes the implications of DNA repair systems in MM development, focusing on gene expression alterations and single nucleotide polymorphisms of genes encoding for DNA repair enzymes. The involvement of DNA repair systems in MM improves understanding of MM pathogenesis and provides novel therapeutical targets. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313972</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313972</guid>        </item>
        <item>
            <title>Human DNAJ in cancer and stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5313971&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005076%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► DNAJ are a diverse family of co-chaperones of Hsp70 and Hsp90. ► DNAJ isoforms have both pro and anti-cancer activity. ► DNAJ represent a novel class of anti-cancer drug targets.Abstract: The heat shock protein 40kDa (HSP40/DNAJ) co-chaperones constitute the largest and most diverse sub-group of the heat shock protein (HSP) family. DNAJ are widely accepted as regulators of HSP70 function, but also have roles as co-chaperones for the HSP90 chaperone machine, and a growing number of biological functions that may be independent of either of these chaperones. The DNAJ proteins are differentially expressed in human tissues and demonstrate the capacity to function to both promote and suppress cancer development by acting as chaperones for tumour suppressors or oncoproteins. W...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313971</comments>
            <pubDate>Mon, 19 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313971</guid>        </item>
        <item>
            <title>Inhibition of tumor cell migration and metastasis by the proton-sensing GPR4 receptor</title>
            <link>http://www.medworm.com/index.php?rid=5313978&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004885%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Activation of GPR4 by acidosis inhibits tumor cell migration and invasion. ► GPR4 overexpression inhibits the lung metastasis of B16F10 melanoma cells in mice. ► Acidosis activation of GPR4 increases active Rho and actin stress fiber formation. ► Treatment with a Rho activator recapitulates the effects of GPR4 activation on cell motility.Abstract: GPR4 is a member of the proton-sensing G protein-coupled receptor family. Within tumor microenvironments, the interstitial acidic pH may activate GPR4 to regulate the behavior of tumor cells. Mouse B16F10 melanoma cells and TRAMP-C1 prostate cancer cells, genetically engineered to overexpress GPR4 or the control vector, were subject to a series of cell migration, invasion and metastasis assays. Upon GPR4 overexpression and a...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313978</comments>
            <pubDate>Wed, 14 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313978</guid>        </item>
        <item>
            <title>Neuromedin B receptor antagonist suppresses tumor angiogenesis and tumor growth in vitro and in vivo</title>
            <link>http://www.medworm.com/index.php?rid=5273342&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005015%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Neuromedin B (NMB) receptor antagonist PD168368 inhibits NMB-induced endothelial angiogenesis in vitro and in vivo. ► PD168368 reduces viability and xenograft tumor growth of human MDA-MB-231 breast cancer cells. ► PD168368 induces cell cycle arrest and apoptosis in MDA-MB-231 cells. ► PD168368 exerts antitumor activity through the inhibition of tumor growth and angiogenesis.Abstract: Neuromedin B (NMB), a member of the mammalian bombesin-like peptide family, and its receptor were aberrantly expressed in vascularized solid tumors. Here, the NMB receptor (NMB-R) antagonist PD168368 specifically inhibited both NMB-induced in vivo and in vitro angiogenesis. In addition, PD168368 showed growth inhibitory effects on MDA-MB-231 breast cancer cells by inducing cell cycle arr...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273342</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273342</guid>        </item>
        <item>
            <title>Low molecular weight heparin inhibits melanoma cell adhesion and migration through a PKCa/JNK signaling pathway inducing actin cytoskeleton changes</title>
            <link>http://www.medworm.com/index.php?rid=5313982&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511005039%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, LMWH through the downregulation of pPKCa and redistribution to nuclear region attenuates JNK activation, which in turn induces cytoskeleton changes correlated to M5 cell decreased adhesion/migration. This may provide clues for the pharmacological targeting of melanoma. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313982</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313982</guid>        </item>
        <item>
            <title>Cytotoxicity of troglitazone through PPARγ-independent pathway and p38 MAPK pathway in renal cell carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5313980&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100485X%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Troglitazone induced apoptosis in human renal cell carcinoma cell lines. ► It was not dependent on PPARγ. ► The p38 MAPK pathway was involved in the cytotoxicity. ► The G2/M cell cycle arrest was induced through activation of p38 MAPK.Abstract: Agonists of peroxisome proliferator-activated receptor gamma (PPARγ) have been examined as chemopreventive and chemotherapeutic agents. The aim was to investigate the cytotoxicity of troglitazone (TGZ) and its mechanisms in terms of PPARγ dependency and the p38 mitogen-activated protein kinase (MAPK) pathway in three human renal cell carcinoma (RCC) cell lines, 786-O, Caki-2 and ACHN cells. TGZ induced apoptosis and exerted cytotoxicity in a PPARγ-independent manner. We demonstrated that TGZ activated the p38 MAPK pathway a...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313980</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313980</guid>        </item>
        <item>
            <title>Growth inhibition of imatinib-resistant CML cells with the T315I mutation and hypoxia-adaptation by AV65 – a novel Wnt/β-catenin signaling inhibitor</title>
            <link>http://www.medworm.com/index.php?rid=5273339&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004770%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► AV65 is a novel Wnt/β-catenin signaling inhibitor. ► AV65 inhibited the proliferation of CML cell including T315I-mutated cells. ► AV65 also inhibited the proliferation of hypoxia-adapted primitive CML cells. ► AV65 inhibited the CML cell proliferation in combination with imatinib.Abstract: We investigated the effect of a novel Wnt/β-catenin signaling inhibitor, AV65 on imatinib mesylate (IM)-sensitive and -resistant human chronic myeloid leukemia (CML) cells in vitro. AV65 inhibited the proliferation of various CML cell lines including T315I mutation-harboring cells. AV65 reduced the expression of β-catenin in CML cells, resulting in the induction of apoptosis. Moreover, AV65 inhibited the proliferation of hypoxia-adapted primitive CML cells that overexpress β-ca...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273339</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273339</guid>        </item>
        <item>
            <title>Identification of tumoral glial precursor cells in neuroblastoma</title>
            <link>http://www.medworm.com/index.php?rid=5273337&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004794%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we describe, a neuroblastic-like subpopulation in neuroblastoma (NB) coexpressing GD2 and S100A6, neuroblastic and glial lineage markers respectively. The GD2+/S100A6+ neuroblastic subpopulation was found to be enriched in low risk NB, distributed around the perivascular niche. Some stromal bundles showed GD2+/S100A6 costaining. Metastatic bone marrow specimens also showed GD2+/S100A6+ cells. During in vitro retinoic acid induced differentiation of NB cell lines, rare GD2+/S100A6 neuroblatic cells appeared. We conclude that GD2+/S100A6+ neuroblasts may represent a tumoral glial precursor subpopulation in NBT. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273337</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273337</guid>        </item>
        <item>
            <title>Disruption of xCT inhibits cell growth via the ROS/autophagy pathway in hepatocellular carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5273335&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004496%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► xCT is upregulated in HCC and is associated with poor prognosis of HCC patients. ► The disruption of xCT inhibits HCC cell proliferation in vitro and in vivo. ► The xCT blockades induce autophagy by increasing the ROS levels in HCC cells.Abstract: xCT, the functional subunit of the system which plays an important role in maintaining intracellular glutathione (GSH) levels, is expressed in various malignant tumors. Here, we demonstrated that xCT expression is often elevated in HCC and is associated with poor prognosis in HCC patients; moreover, disruption of xCT suppressed HCC cell growth both in vitro and in vivo. xCT dysfunction has also been shown to increase intracellular reactive oxygen species (ROS) levels, thus in turn led to autophagic cell death of HCC cells. Tak...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273335</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273335</guid>        </item>
        <item>
            <title>Spectrum of KIT/PDGFRA/BRAF mutations and Phosphatidylinositol-3-Kinase pathway gene alterations in gastrointestinal stromal tumors (GIST)</title>
            <link>http://www.medworm.com/index.php?rid=5273334&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS030438351100454X%2Fabstract%3Frss%3Dyes</link>
            <description>We examined new pathogenetic pathways of GIST lacking mutations in KIT and PDGFRA. ► Three BRAF mutations (V600E) were found in tumors concomitantly were wild type for KIT and PDGFRA. ► One high risk GIST showed a coexistence of PIK3CA and KIT exon 11 mutations. ► We detected no mutations in KRAS, NRAS, and FGFR3.Abstract: Pathogenetic pathways of gastrointestinal stromal tumors (GIST) lacking mutations in KIT and PDGFRA (∼15%) are still poorly studied. Nearly nothing is known about PI3K alterations in GISTs and only a few GISTs with BRAF mutations have been reported. BRAF mutations (V600E) were found in 3/87 tumors (3.5%) concomitantly were wild type for KIT and PDGFRA. No mutations were detected in KRAS, NRAS, and FGFR3. For the first-time we demonstrated a PIK3CA mutation (H1047...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273334</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273334</guid>        </item>
        <item>
            <title>Nuclear receptor mRNA expression by HBV in human hepatoblastoma cell lines</title>
            <link>http://www.medworm.com/index.php?rid=5273333&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004502%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Nuclear receptor-signal pathways in HepG2.2.15 are different from those in HepG2. ► HBV affects nuclear receptors and their related signal transduction. ► We focused on androgen receptor and histone deacetylase among nuclear receptors. ► Nuclear receptors play important roles in viral replication and hepatocarcinogenesis.Abstract: Recent studies have implicated nuclear receptors (NRs) in the development of hepatocarcinogenesis. We assumed that hepatitis B virus (HBV) alters the expression of NRs and coregulators, and compared the gene expression profiling for 84 NRs and related genes between HpeG2.2.15, which secretes complete HBV virion, and HepG2 by real-time RT-PCR with SyBr green. Forty (47.6%) genes were upregulated 2-fold or greater, and only 5 (5.9%) were downr...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273333</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273333</guid>        </item>
        <item>
            <title>Mesenchymal stromal cells may enhance metastasis of neuroblastoma via SDF-1/CXCR4 and SDF-1/CXCR7 signaling</title>
            <link>http://www.medworm.com/index.php?rid=5273329&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003855%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Human mesenchymal stem cells (hMSCs) can enhance neuroblastoma cells migration and invasion in vitro. ► Such enhancement effect is likely to be in part contributed by the SDF-1 secreted by the hMSCs. ► SDF-1 activates the CXCR4/CXCR7 receptors of neuroblastoma cells and induces them to migrate and invade. ► Blocking of CXCR4/CXCR7 pathways can reduce the migration and invasion of neuroblastoma cells, even with MSCs support.Abstract: Bone marrow metastasis is frequently observed in patients with high-risk neuroblastoma. Mesenchymal stromal cells (MSCs) in bone marrow may enhance tumor metastasis through secreting stromal cell-derived factor-1 (SDF-1). Here we investigated neuroblastoma cell behaviors under the influence of MSCs and explored the function of SDF-1 signal...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273329</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273329</guid>        </item>
        <item>
            <title>Endostar enhances the antineoplastic effects of combretastatin A4 phosphate in an osteosarcoma xenograft</title>
            <link>http://www.medworm.com/index.php?rid=5273341&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004836%2Fabstract%3Frss%3Dyes</link>
            <description>This study evaluated the combination of vascular targeting (Endostar) and disrupting agents (CA4P) in osteosarcoma. ► This combination had a good anti-tumor activity with little toxicity. ► Their outcomes were comparable to adriamycin, the current gold standard of chemotherapy. ► This combination has synergy in the antitumor effect.Abstract: Vascular-targeting agents (VTAs) can be divided into two groups: anti-angiogenesis agents and vascular disrupting agents (VDAs). The purpose of this study was to evaluate the antineoplastic activity of a combination of the anti-angiogenesis agent, Endostar, and the VDA combretastatin, A4 phosphate (CA4P). This study is the first to evaluate the activity of this combination against tumors and the first to investigate the activity of the combinatio...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273341</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273341</guid>        </item>
        <item>
            <title>The anti-progestin RU-486 inhibits viability of MCF-7 breast cancer cells by suppressing WNT1</title>
            <link>http://www.medworm.com/index.php?rid=5273340&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004812%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, we identified WNT1 as a novel mediator of the anti-tumor effects of RU-486 in MCF-7 cells. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273340</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273340</guid>        </item>
        <item>
            <title>Establishment of a mammary carcinoma cell line from Syrian hamsters treated with N-methyl-N-nitrosourea</title>
            <link>http://www.medworm.com/index.php?rid=5273338&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004782%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Using N-methyl-N-nitrosourea, we induced mammary tumor formation in Syrian hamsters. ► One tumor was similar to a high-grade poorly differentiated human breast adenocarcinoma. ► Cell lines derived from the mammary tumor are likely from a luminal B subtype. ► The cell lines form tumors in vivo when implanted into syngeneic Syrian hamsters. ► These are the first mammary tumor cell lines available from the Syrian hamster.Abstract: Clearly new breast cancer models are necessary in developing novel therapies. To address this challenge, we examined mammary tumor formation in the Syrian hamster using the chemical carcinogen N-methyl-N-nitrosourea (MNU). A single 50mg/kg intraperitoneal dose of MNU resulted in a 60% incidence of premalignant mammary lesions, and a 20% incid...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273338</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273338</guid>        </item>
        <item>
            <title>Glycosylation-related gene expression is linked to differentiation status in glioblastomas undifferentiated cells</title>
            <link>http://www.medworm.com/index.php?rid=5273332&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004526%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Original glyco-gene signature in glioblastoma undifferentiated cells. ► Glyco-gene over-expression depends on differentiation status in cancer cell lines. ► Protein levels corresponding to selected genes increased in undifferentiated cells. ► Patient’s primary cultures from GBM showed over-expression of selected genes.Abstract: Glioblastoma Multiforme (GBM) is the most frequent malignant brain tumor with still poor prognosis. Tumor initiation, growth and recurrences might depend on Brain Tumor Stem Cells (BTSCs) which can promote tumor aggressiveness and potentially affords new therapeutic target. Recent works emphasized aberrant cell-surface glyco-conjugate expression in brain tumors suggesting that altered glycosylation is closely linked to cancer tumor metastasis...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273332</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273332</guid>        </item>
        <item>
            <title>Exploration of target genes of HOXA13 in esophageal squamous cell carcinoma cell line</title>
            <link>http://www.medworm.com/index.php?rid=5273331&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004368%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we examined the protein expression changes after HOXA13 knockdown by 2-dimentional electrophoresis. Forty-five spots were significantly different, among which 24 were down-regulated and 21 were up-regulated after HOXA13 knockdown. The proteins from 14 gel-spots were further characterized by MALDI-TOF MS, among which, AnnexinA2, MnSOD and ERAB, are validated by Western Blot analysis. Transcriptional target analysis revealed that HOXA13 regulated several cell signaling pathways that are critically involved in cell proliferation, survival and migration. These results provide an additional support to a hypothesis that HOXA13 might participate in the carcinogenesis of ESCC. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273331</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273331</guid>        </item>
        <item>
            <title>Nitroxoline (8-hydroxy-5-nitroquinoline) is more a potent anti-cancer agent than clioquinol (5-chloro-7-iodo-8-quinoline)</title>
            <link>http://www.medworm.com/index.php?rid=5273330&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003892%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► We compared the cytotoxicity of clioquinol analogues in human cancer cells. ► 8-Hydroxy-5-nitroquinoline (NQ) was the most toxic among six analogues tested. ► Unlike clioquinol, NQ is not a zinc ionophore. ► NQ increased generation of intracellular reactive oxygen species. ► NQ is another anti-microbial agent that may be useful in treating cancer.Abstract: Clioquinol has been shown to have anticancer activity both in vitro and in vivo. The present study compared the cytotoxicity of clioquinol with six analogues using human cancer cell lines. Of the analogues tested, 8-hydroxy-5-nitroquinoline (NQ) was the most toxic, with an IC50 that was five to ten fold lower than that of other congeners. Its activity was enhanced by copper, but not zinc, and the use of a zinc-sen...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273330</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273330</guid>        </item>
        <item>
            <title>Rapid automated detection of ABL kinase domain mutations in imatinib-resistant patients</title>
            <link>http://www.medworm.com/index.php?rid=5313981&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004848%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► We developed an automatic method to detect mutations observed in imatinib-resistance. ► The method utilizes guanine-quenching probes (QP). ► Seventeen mutations can be detected automatically. ► Detected mutations were almost identical between QP method and direct sequencing. ► We improved the sensitivity with mutation-biased PCR.Abstract: ABL tyrosine kinase inhibitor (TKI), imatinib is used for BCR–ABL+ leukemias. We developed an automatic method utilizing guanine-quenching probes (QP) to detect 17 kinds of mutations frequently observed in imatinib-resistance. Results were obtained from 100μL of whole blood within 90min by this method. Detected mutations were almost identical between QP method and direct sequencing. Furthermore, the mutation-biased PCR (MBP) was...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313981</comments>
            <pubDate>Mon, 05 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313981</guid>        </item>
        <item>
            <title>Pro-inflammatory and tumour proliferative properties of excess visceral adipose tissue</title>
            <link>http://www.medworm.com/index.php?rid=5273336&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004599%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Visceral fat has significantly higher VEGF, CD8+ and NKT cells than subcutaneous fat. ► VEGF levels in serum and vACM is significantly higher in viscerally obese patients. ► vACM from viscerally obese patients induces significant tumour cell proliferation. ► Neutralising VEGF but not IL-6 in vACM significantly reduces tumour cell proliferation. ► VEGF may represent a potential therapeutic target in obese cancer patients.Abstract: Obesity has been associated with increased incidence and mortality of oesophageal and colorectal adenocarcinoma. Excess central adiposity may drive this association through an altered inflammatory milieu. Utilising a unique adipose tissue bioresource we aimed to determine the pro-tumour properties of visceral adipose tissue. Comparing subcu...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273336</comments>
            <pubDate>Mon, 05 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273336</guid>        </item>
        <item>
            <title>5-Aza-2′-deoxycytidine enhances susceptibility of renal cell carcinoma to paclitaxel by decreasing LEF1/phospho-β-catenin expression</title>
            <link>http://www.medworm.com/index.php?rid=5260232&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004873%2Fabstract%3Frss%3Dyes</link>
            <description>This study suggests that LEF1 can enhance the proliferation of RCC cells and that the LEF1/β-catenin complex plays an important role in the synergy of DAC and PTX against RCC cells. Moreover, the synergy between DAC and PTX may be more effective in RCC cells expressing high levels of LEF1. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260232</comments>
            <pubDate>Wed, 31 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260232</guid>        </item>
        <item>
            <title>Reverse phase protein microarrays quantify and validate the bioenergetic signature as biomarker in colorectal cancer</title>
            <link>http://www.medworm.com/index.php?rid=5260230&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004381%2Fabstract%3Frss%3Dyes</link>
            <description>We report the quantity of proteins of energy metabolism in colon carcinomas. ► Colorectal carcinomas show a profound shift towards an enhanced glycolysis. ► The bioenergetic signature discriminates patients with bad or good prognosis. ► The bioenergetic signature is a relevant biomarker in colorectal cancer. ► The application of protein microarray technology is encouraged in cancer studies.Abstract: A reverse phase protein microarray approach has been applied to quantify proteins of energy metabolism in normal and tumor biopsies of colorectal cancer (CRC) patients. The metabolic proteome of CRC specimens revealed a profound shift towards and enhanced glycolytic phenotype and concurrent mitochondrial alteration. The metabolic signature discriminated CRC patients with highly signific...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260230</comments>
            <pubDate>Wed, 31 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260230</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5175516&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004927%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5175516</comments>
            <pubDate>Tue, 30 Aug 2011 12:58:03 +0100</pubDate>
            <guid isPermaLink="false">5175516</guid>        </item>
        <item>
            <title>Augmented therapeutic efficacy of irinotecan is associated with enhanced drug accumulation</title>
            <link>http://www.medworm.com/index.php?rid=5260231&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004484%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► The in vivo synergy between MSC and irinotecan is influenced by treatment schedule. ► Sequential combination has superior antitumor effect to concurrent combination. ► Intra-tumor highest drug concentration is at d14 post sequential combination; no impact on normal tissue concentrations. ► Intra-tumor microvessel maturation is enhanced at d14 after sequential combination. ► Sequential combination enhances apoptosis of tumor cells at d14 after treatment.Abstract: The goal of this study is to determine whether treatment with methylselenocysteine (MSC) results in differential uptake of irinotecan and its active metabolite (SN-38) between tumors of head and neck squamous cell carcinomas and normal tissue. The in vivo synergy between MSC and irinotecan is influenced by t...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260231</comments>
            <pubDate>Mon, 29 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260231</guid>        </item>
        <item>
            <title>The expression and function of miRNA-451 in non-small cell lung cancer</title>
            <link>http://www.medworm.com/index.php?rid=5260229&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004514%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► miRNA-451 expression was negatively associated with prognosis of NSCLC patients. ► Overexpression of miRNA-451 inhibited cell cycle progress of A549 cells. ► Increased miRNA-451 expression promoted the anoikis of A549 cells. ► Aberrantly expressed miRNA-451 may be associated with the development of NSCLC.Abstract: miRNAs are small, non-coding RNAs that negatively regulate gene expression at the post-transcriptional and translational levels. miRNA-451 was previously reported to be down-regulated in gastric and colorectal cancers. Here, we showed that miRNA-451 expression decreased in non-small cell lung cancer (NSCLC) tissues and that its expression was negatively associated with lymph node metastasis, the stage of TNM classification and poor prognosis of NSCLC patient...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260229</comments>
            <pubDate>Mon, 29 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260229</guid>        </item>
        <item>
            <title>Characterization and anti-tumor activity of chemical conjugation of doxorubicin in polymeric micelles (DOX-P) in vitro</title>
            <link>http://www.medworm.com/index.php?rid=5260227&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004277%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Chemical conjugation DOX-P had good loading efficiency and CMC value. ► DOX-P micelles maintained a sustained DOX release profile. ► DOX-P micelles could enhance DOX anti-tumor activity. ► DOX-P micelles could circumvent drug resistance of A549/DOX cells.Abstract: Characterization and anti-tumor activity of chemical conjugation of doxorubicin (DOX) in polymeric micelles were investigated. Polymeric micelles with chemical conjugation of doxorubicin (DOX-P) were prepared. Succinic anhydride activated pluronic F68 was first synthesized and the primary amine group in doxorubicin was conjugated to the terminal carboxyl of pluronic F68 via a amide. The resulting polymeric micelles in aqueous solution were characterized by measurement of size, ξ-potential, drug loading and ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260227</comments>
            <pubDate>Mon, 29 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260227</guid>        </item>
        <item>
            <title>Antitumor activities of recombinant human interferon (IFN)-λ1 in vitro and in xenograft models in vivo for colon cancer</title>
            <link>http://www.medworm.com/index.php?rid=5260222&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004009%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► rhIFN-λ1 inhibited the proliferation of colon cancer cells, HCT116 and HT29 in vitro. ► It prolonged the duration of activated STATs and induced apoptosis in both cells. ► rhIFN-λ1 suppressed tumor growth in a dose-dependent fashion in xenograft models. ► Its inhibition rate is 52% for HCT116 and 56% for HT29 in vivo. ► rhIFN-λ1 could be a new potential reagent for cancer therapy.Abstract: Interferon (IFN)-λ1, as a newly identified IFN, interacts with the structurally unique IFN-λ1 receptor complex and exhibits antiviral and antiproliferation effects. The major focus of our work was to study the antitumor activities of recombinant human IFN-λ1 (rhIFN-λ1) in vivo and in vitro. The MTT analysis showed that rhIFN-λ1 inhibited the proliferation of HCT116 cells i...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260222</comments>
            <pubDate>Mon, 29 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260222</guid>        </item>
        <item>
            <title>Overexpression of human papillomavirus (HPV) type 16 oncoproteins promotes angiogenesis via enhancing HIF-1α and VEGF expression in non-small cell lung cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5260224&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004083%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Overexpression of HPV-16 oncoproteins in NSCLC cells promoted angiogenesis. ► Overexpression of HPV-16 oncoproteins enhanced HIF-1α protein accumulation. ► Overexpression of HPV-16 oncoproteins increased VEGF protein and mRNA expression. ► HPV-16 oncoproteins-induced VEGF and IL-8 expression was HIF-1α-dependent.Abstract: HPV-16 infection may play an important role in the development of non-small cell lung cancer (NSCLC) among never-smokers. Due to the critical role of angiogenesis in NSCLC development, we describe here the effect of HPV-16 oncoproteins on angiogenesis in NSCLC and the underlying mechanisms. We found that overexpression of HPV-16 E6 and E7 oncoproteins in NSCLC cells significantly promoted angiogenesis both in vitro and in vivo, and correspondingly,...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260224</comments>
            <pubDate>Thu, 25 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260224</guid>        </item>
        <item>
            <title>Genetically engineered human neural stem cells with rabbit carboxyl esterase can target brain metastasis from breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5260223&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003971%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Human neural stem cells (NSCs) delivering therapeutic gene is used to treat brain metastasis of breast cancer. ► NSCs expressing a suicide gene carboxyl esterase migrated selectively into the brain tumor mass and killed tumor cells. ► The treatment significantly decreased tumor volume in brain metastasis of breast cancer, and prolonged animal survival. ► This stem cell-based suicide gene therapy could serve as an effective treatment for brain metastases of breast cancer.Abstract: Neural stem cells (NSCs) led to the development of a novel strategy for delivering therapeutic genes to tumors. NSCs expressing rabbit carboxyl esterase (F3.CE), which activates CPT-11, significantly inhibited the growth of MDA-MB-435 cells in the presence of CPT-11. F3.CE cells migrated sele...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260223</comments>
            <pubDate>Thu, 25 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260223</guid>        </item>
        <item>
            <title>Histone deacetylase inhibitor valproic acid suppresses the growth and increases the androgen responsiveness of prostate cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5260226&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004290%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► HDAC inhibitors up-regulate the expression of cPAcP, a negative growth regulator. ► Increased cPAcP expression is associated with ErbB-2 dephosphorylation. ► cPAcP is involved in growth suppression by HDAC inhibitors in PCa cells. ► Valporic acid treatment enhances the androgen-responsiveness of PCa cells. ► Intermit HDAC inhibitor treatments may prolong androgen ablation therapy.Abstract: We identified the molecular target by histone deacetylase (HDAC) inhibitors for exploring their potential prostate cancer (PCa) therapy. Upon HDAC inhibitors-treatment, LNCaP cell growth was suppressed, correlating with increased cellular prostatic acid phosphatase (cPAcP) expression, an authentic protein tyrosine phosphatase. In those cells, ErbB-2 was dephosphorylated, histone H...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260226</comments>
            <pubDate>Mon, 22 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260226</guid>        </item>
        <item>
            <title>Combined treatment with exogenous estradiol and progesterone increases the incidence of breast cancer in TA2 mice without ovaries</title>
            <link>http://www.medworm.com/index.php?rid=5260225&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004071%2Fabstract%3Frss%3Dyes</link>
            <description>This study found that the combination of exogenous estradiol and progesterone induced breast cancer formation in TA2 mice without ovaries. MMTV–LTR mRNA exhibited the highest expression in tumor tissue from the combination treatment group (CT). Mammary tissue from mice in the CT group had the highest Wnt1, Wnt5a, Wnt5b and Wnt10b mRNA expression levels. These results indicate that estradiol and progesterone act in a synergistic manner to upregulate MMTV, which subsequently induces breast cancer in TA2 mice. Various members of the Wnt gene family may play specific roles in different stages of carcinogenesis in TA2 mice. (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260225</comments>
            <pubDate>Fri, 19 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260225</guid>        </item>
        <item>
            <title>TLR4 signal transduction pathways neutralize the effect of Fas signals on glioblastoma cell proliferation and migration</title>
            <link>http://www.medworm.com/index.php?rid=5260228&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004320%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Fas or TLR4 (LPS receptor) pathway activation induces glioblastoma cell proliferation. ► Simultaneous cell treatment by Fas agonist antibody and LPS decreases proliferation. ► This anti-proliferative effect is caspase dependent. ► This treatment decreases cell migration and MMP-9 expression. ► Both TLR4 and MMP-9 are highly expressed in human glioblastomas.Abstract: The Fas pathway is described as an activator of the glioblastoma proliferation by increasing the pathogenicity of this tumour. The lipopolysaccharide (LPS) pathway depending on Toll-like receptor 4 (TLR4) could limit the glioblastoma spreading. Here, Fas and TLR4 pathways were activated in glioblastoma cell lines by an agonist antibody and/or LPS treatment. Activation of the Fas pathway or of the TLR4 pa...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260228</comments>
            <pubDate>Thu, 18 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260228</guid>        </item>
        <item>
            <title>Chitosan-coated triangular silver nanoparticles as a novel class of biocompatible, highly effective photothermal transducers for in vitro cancer cell therapy</title>
            <link>http://www.medworm.com/index.php?rid=5260221&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003673%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Chitosan-coated triangular silver nanoparticles (Chit-AgNTs) as novel class of plasmonic phototherapeutic agent. ► Chit-AgNTs act effectively as light-to-heat converters against human non-small lung cancer cells. ► Chit-AgNTs exhibit higher rate of cell destruction than common agents used as reference.Abstract: One of the relevant directions that nanotechnology is taking nowadays is connected with nanomedicine and specifically related to the use of light and nanoparticles in early diagnosis and effective therapeutics of cancer. Noble-metal nanoparticles can act under laser irradiation as effective photothermal transducers for triggering localized hyperthermia of tumors. In this work we report the performance of newly synthesized chitosan-coated silver nanotriangles (Chi...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260221</comments>
            <pubDate>Tue, 16 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260221</guid>        </item>
        <item>
            <title>Human leukocyte antigen-G in cancer: Are they clinically relevant?</title>
            <link>http://www.medworm.com/index.php?rid=5260220&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004332%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► HLA-G is an immunotolerant. ► Tumor cell restricted HLA-G expression was observed in various malignancies. ► Tumor cell or lesion HLA-G expression was associated with disease poor prognosis. ► Soluble HLA-G expression could be a potential diagnosis biomarker for malignancies.Abstract: The immunotolerant human leukocyte antigen (HLA)-G has direct inhibitory effects on natural killer cells (NK), dendritic cells (DC), T cells and can induce tolerant regulatory cells. The expression of HLA-G has been correlated with the tolerance of the fetus, the acceptance of organ transplants, and the immune escape of tumor cells and virus-infected cells. In the context of malignancies, aberrant induction of HLA-G expression has been extensively investigated and its clinical relevance ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260220</comments>
            <pubDate>Tue, 16 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260220</guid>        </item>
        <item>
            <title>Pituitary tumor transforming gene induces epithelial to mesenchymal transition by regulation of Twist, Snail, Slug, and E-cadherin</title>
            <link>http://www.medworm.com/index.php?rid=5175524&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003909%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► In the present study first time we showed the important role of PTTG in the regulation of TGF-β expression and secretion. ► Regulation of TGF-β expression by PTTG resulted in decrease in expression of E-cadherin by regulation of repressor genes Twist, Snail and Slug. ► PTTG induces EMT in human ovarian epithelial cancer cells through the regulation of TGF-β, Twist, Snail, Slug, E-cadherin and vimentin.Abstract: Pituitary tumor-transforming gene (PTTG) is an oncogene with its expression levels correlating with tumor development and metastasis. Epithelial to mesenchymal transition (EMT) is a crucial step in tumor progression and metastasis. Using ovarian epithelial tumor cell line (A2780) for loss-of-function or gain-of-function of PTTG in our experiments, we observed ...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5175524</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5175524</guid>        </item>
        <item>
            <title>Salinomycin inhibits osteosarcoma by targeting its tumor stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5175529&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004307%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► We have utilized three different methods to enrich TSCs in osteosarcoma. ► Salinomycin could selectively target TSCs in osteosarcoma both in vitro and in vivo. ► Wnt/β-catenin signaling pathway may be involved in this inhibition of salinomycin. ► Salinomycin is an effective inhibitor of osteosarcoma stem cells.Abstract: Osteosarcoma is the most common primary bone tumor in children and adolescents and is typically associated with a poor prognosis. Tumor stem cells (TSCs) are presumed to drive tumor initiation and tumor relapse or metastasis. Hence, the poor prognosis of osteosarcoma likely results from a failure to target the osteosarcoma stem cells. Here, we have utilized three different methods to enrich TSCs in osteosarcoma and further evaluated whether salinomyci...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5175529</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5175529</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5109034&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004423%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5109034</comments>
            <pubDate>Wed, 10 Aug 2011 16:00:29 +0100</pubDate>
            <guid isPermaLink="false">5109034</guid>        </item>
        <item>
            <title>Aberrant DNA methylation of cancer-associated genes in gastric cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC–EURGAST)</title>
            <link>http://www.medworm.com/index.php?rid=5175526&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003958%2Fabstract%3Frss%3Dyes</link>
            <description>This study identifies potential novel epigenetic biomarkers in gastric cancer.Abstract: Epigenetic events have emerged as key mechanisms in the regulation of critical biological processes and in the development of a wide variety of human malignancies, including gastric cancer (GC), however precise gene targets of aberrant DNA methylation in GC remain largely unknown. Here, we have combined pyrosequencing-based quantitative analysis of DNA methylation in 98 GC cases and 64 controls nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort and in cancer tissue and non-tumorigenic adjacent tissue of an independent series of GC samples. A panel of 10 cancer-associated genes (CHRNA3, DOK1, MGMT, RASSF1A, p14ARF, CDH1, MLH1, ALDH2, GNMT and MTHFR) and LINE-1 re...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5175526</comments>
            <pubDate>Tue, 09 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5175526</guid>        </item>
        <item>
            <title>Bystander cytotoxicity in human medullary thyroid carcinoma cells mediated by fusion yeast cytosine deaminase and 5-fluorocytosine</title>
            <link>http://www.medworm.com/index.php?rid=5175528&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004289%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Gene and cell therapy on medullary thyroid carcinoma model cell line TT. ► Fusion yeast cytosine deaminase and prodrug 5-fluorocytosine induced bystander effect. ► Strong tumor xenotransplant growth inhibition upon yCD-TT/5FC combination. ► Inhibition of TT xenotransplant tumor growth by mesenchymal stromal cells.Abstract: In our work, we have evaluated efficiency of gene-directed enzyme/prodrug therapy (GDEPT) based on combination of fusion yeast cytosine deaminase (yCD) and 5-fluorocytosine (5FC) on model human medullary thyroid carcinoma (MTC) cell line TT. We determined the efficiency of this GDEPT approach in suicide and bystander cytotoxicity induction. We have shown significant bystander effect in vitro and 5FC administration resulted in potent antitumor effect...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5175528</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5175528</guid>        </item>
        <item>
            <title>Detection of TFPI2 methylation in the serum of colorectal cancer patients</title>
            <link>http://www.medworm.com/index.php?rid=5175527&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004022%2Fabstract%3Frss%3Dyes</link>
            <description>We examined whether TFPI2 methylation can be used as a molecular marker for colorectal cancers by detecting TFPI2 methylation in colorectal cancer patients’ sera by using quantitative methylation-specific polymerase chain reaction (qMSP). The qMSP analysis showed that 39 of 215 (18%) patients exhibited TFPI2 methylation in their serum DNA, suggesting that TFPI2 methylation frequently existed in colorectal cancer patients’ sera. After completion of qMSP analysis, clinicopathological data were correlated with molecular data. TFPI2 methylation was significant in the sera of patients with large (p=0.0022), poorly differentiated carcinoma (p=0.0164), deep invasion (p=0.0002), lymph node metastasis (p=0.0147), or distant metastasis (p (Source: Cancer Letters)</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5175527</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5175527</guid>        </item>
        <item>
            <title>Suppression of carbonyl reductase expression enhances malignant behaviour in uterine cervical squamous cell carcinoma: Carbonyl reductase predicts prognosis and lymph node metastasis</title>
            <link>http://www.medworm.com/index.php?rid=5175525&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003934%2Fabstract%3Frss%3Dyes</link>
            <description>We examined how CR affects cancer cell behaviour in vitro. ► The reduced CR expression can be a useful predictor of metastasis and poor prognosis. ► Suppression of CR increased the activity of cancer cell invasion in vitro. ► Suppression of CR has a role in enhancing the metastatic potential of SCC cells.Abstract: Carbonyl reductase (CR) is an NADPH-dependent, mostly monomeric, cytosolic enzyme with broad substrate specificity for carbonyl compounds. CR appears to be involved in the regulation of tumour progression. However, molecular mechanisms of CR in tumour progression and clinical significance of CR status remain unclear in human uterine squamous cell carcinoma (SCC). Here, we investigated the clinical significance of CR using immunohistochemical analyses of human uterine cervic...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5175525</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5175525</guid>        </item>
        <item>
            <title>Hepatic oval cell lines generate hepatocellular carcinoma following transfection with HBx gene and treatment with aflatoxin B1 in vivo</title>
            <link>http://www.medworm.com/index.php?rid=5175517&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003375%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, partial transformation of rat HOC (LE/6) were accomplished by transfected HBV x gene (HBx), and then transfected cells were implanted both intra-hepatically and subcutaneously into nude mice treated with AFB1 in vivo. We found the oval cells produced tumors (4/24 of the animals) in liver following transfection with HBx gene and treatment with AFB1. These intrahepatic tumors included HCC cells (immunopositive for HepParl, ALB, CK8 and AFP) and mesenchymal cells (immunopositive for Vimentin and SMA). Whereas mesenchymal tumors were observed at the subcutaneous tissue with a similar rate in all controls treated with cell lines (10/24 in HBx-oval cells/AFB1 group, 8/20 in HBx-oval cells/non-AFB1 group, 10/20 in non-HBx/AFB1 group; 9/20 in non-HBx/non-AFB1 group). Conversely, non...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5175517</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5175517</guid>        </item>
        <item>
            <title>The antimitogenic effect of the cannabinoid receptor agonist WIN55212-2 on human melanoma cells is mediated by the membrane lipid raft</title>
            <link>http://www.medworm.com/index.php?rid=5143384&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004046%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► WIN induces apoptosis in melanoma cells which express both CB1 and CB2 receptors. ► Selective CB1 or CB2 agonists were unable to reproduce WIN effects. ► Selective CB1 and CB2 antagonists did not inhibit WIN-induced cell death. ► WIN activates caspases and pERK which were blunt in cells treated with MCD. ► WIN exerts antimitogenic effect upon melanoma cells via a mechanism involving lipid raft.Abstract: Here are reported the antiproliferative effects of the cannabinoid agonist WIN upon human melanoma cells expressing mRNA and protein for both CB1 and CB2 receptors. While WIN exerted antimitogenic effects, selective CB1 or CB2 agonists were unable to reproduce such effects and selective CB1 and CB2 antagonists did not inhibit WIN-induced cell death. Cells treated wit...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143384</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143384</guid>        </item>
        <item>
            <title>Combining an EGFR directed tyrosine kinase inhibitor with autophagy-inducing drugs: A beneficial strategy to combat non-small cell lung cancer</title>
            <link>http://www.medworm.com/index.php?rid=5143380&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003983%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Rapamycin rescues erlotinib resistance of p53 null H1299 NSCLC cells. ► Cytotoxicity by erlotinib/rapamycin is associated with increased autophagy. ► Erlotinib/rapamycin promote mitochondrial hyperpolarization.Abstract: The potential therapeutic value of combinatorial regimens based on an EGF receptor tyrosine kinase inhibitor (TKI) and autophagy inducing drugs was evaluated by comparing their molecular impacts on H1299 and A549 non-small cell lung cancer (NSCLC) cells, which overexpress wild type EGF receptor, but are either deficient or have wild type p53 alleles, respectively. We show that H1299 cells display a considerably lower sensitivity to erlotinib treatment, which can be restored by combining erlotinib with rapamycin or with imatinib, though to a lesser extent...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143380</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143380</guid>        </item>
        <item>
            <title>All-trans retinoic acid induces cellular senescence via upregulation of p16, p21, and p27</title>
            <link>http://www.medworm.com/index.php?rid=5143383&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004058%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► All-trans retinoic acid up-regulates levels of p16, p21, and p27. ► ATRA activates Rb and subsequently inactivates E2F1. ► ATRA inhibits tumor cell growth by inducing cellular senescence.Abstract: We here present a new anti-tumor mechanism of all-trans retinoic acid (ATRA). ATRA induced several biomarkers of cellular senescence including irreversible G1 arrest, morphological changes, senescence-associated β-galactosidase, and heterochromatin foci in HepG2 cells. ATRA also upregulated levels of p16, p21, and p27 which lead to activation of Rb and subsequent inactivation of E2F1. These effects were abolished by the RNA interference-mediated silencing of p16, p21, and p27. Moreover, ATRA failed to induce cellular senescence in Huh7 and HCT116, in which p16, p21, and p27 w...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143383</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143383</guid>        </item>
        <item>
            <title>Inhibition of the sonic hedgehog pathway by cyplopamine reduces the CD133+/CD15+ cell compartment and the in vitro tumorigenic capability of neuroblastoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5143382&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004010%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Sonic hedgehog inhibition by cyclopamine in neuroblastoma. ► Decrease of cell proliferation and tumorigenic potential. ► Decrease in percentage of CD15+ cell population. ► Increase of apoptosis.Abstract: Sonic hedgehog (Hh) developmental pathway deregulation has been proven to play an essential role in several malignancies as neuroblastoma. We found that Hh signaling is active in neuroblastoma, as most pathway components, including GLI1, were expressed in cell lines and tumor samples. Furthermore, SHH ligand expression was found in cell lines and tumors, and GLI1 up-regulation was achieved in response to SHH treatment, suggesting an autocrine mechanism of aberrant activation. A decrease of proliferation and tumorigenic potential, as well as increased apoptosis and a d...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143382</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143382</guid>        </item>
        <item>
            <title>Female hormonal and reproductive factors and head and neck squamous cell carcinoma risk</title>
            <link>http://www.medworm.com/index.php?rid=5143381&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511004034%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► This is a case-control study of head and neck squamous cell carcinoma (HNSCC) in women. ► We examine the association of HNSCC with hormonal and reproductive factors. ► We find a borderline protective effect of postmenopausal hormone use for HNSCC. ► The association between hormone use and HNSCC warrants further investigation.Abstract: Men are much more likely than women to develop head and neck squamous cell carcinoma (HNSCC), a discrepancy that is insufficiently explained by gender differences in smoking and alcohol consumption. It has been hypothesized that differential hormonal exposures may account for some of this risk but thus far the literature on female reproductive factors and HNSCC risk has been sparse. To address the association of HNSCC with female hormona...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143381</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143381</guid>        </item>
        <item>
            <title>MicroRNA-122 sensitizes HCC cancer cells to adriamycin and vincristine through modulating expression of MDR and inducing cell cycle arrest</title>
            <link>http://www.medworm.com/index.php?rid=5143375&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003843%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► Overexpression of miR-122 by adenovirus rendered HCC cell sensitive to chemotherapy. ► Treatment with miR122 and chemotherapy resulted in high accumulation of cells in G2/M. ► miR-122 downregulated expression of MDR related genes, Bcl-w and cyclin B1.Abstract: Hepatocellular carcinoma (HCC) is a hypervascular cancer characterized by rapid progression as well as resistance to conventional chemotherapy. It has been shown that microRNAs play critical roles in pathogenesis of HCC. MicroRNA-122 (miR-122) is a liver-specific microRNA and is frequently downregulated in HCC. In the present study, we investigated whether restoration of miR-122 in HCC cells could render cells sensitive to chemotherapeutic agents adriamycin (ADM) or vincristine (VCR). Our data showed that overexpr...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143375</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
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            <title>Therapeutic effect of neural stem cells expressing TRAIL and bortezomib in mice with glioma xenografts</title>
            <link>http://www.medworm.com/index.php?rid=5143374&amp;cid=s_34584_6_f&amp;fid=34584&amp;url=http%3A%2F%2Fwww.cancerletters.info%2Farticle%2FPIIS0304383511003867%2Fabstract%3Frss%3Dyes</link>
            <description>Highlights: ► NSCs engineered to express membrane-bound TRAIL induced apoptosis in glioma cells. ► Bortezomib enhanced response of glioma cells to NSCs expressing TRAIL. ► TRAIL expressed on the cell surface of NSCs is a more potent reagent than soluble TRAIL. ► Bortezomib upregulated expression of DR5 in glioma cells in vitro but not in vivo. ► Survival of animals with intracranial glioma was improved in combined treatment.Abstract: Treatment of glioblastoma remains a challenge in neuro-oncology. We investigated if treatment with neural stem cells engineered to express membrane-bound TRAIL (NSCs-mTRAIL) alone or in combination with proteasome inhibitors is a feasible therapeutic approach for experimental glioma. Glioma cells showed resistance to soluble TRAIL and proteasome inhi...</description>
            <author>Cancer Letters</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143374</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
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