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 'Molecular Cancer' source. Wed, 08 Feb 2012 08:41:50 +0100 http://www.medworm.com/index.php?rid=5646985&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F11%2F1%2F5 Conclusion: Loss of miR-31 expression in TNBC cell lines is attributed to hypermethylation of its promoter-associated CpG island. Together, our results provide the initial evidence for a mechanism by which miR-31, an important determinant of the invasion metastasis cascade, is regulated in breast cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5646985 Mon, 30 Jan 2012 05:00:00 +0100 5646985 http://www.medworm.com/index.php?rid=5580943&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F11%2F1%2F4 Conclusion: We conclude that chronic extrinsic lung inflammation induced by bacteria alone or in combination with NNK enhances lung tumorigenesis in Gprc5a-/- mice. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5580943 Thu, 12 Jan 2012 05:00:00 +0100 5580943 http://www.medworm.com/index.php?rid=5580944&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F11%2F1%2F3 CONCLUSION: These data suggest that the aberrant expression of CXCR3A and down-regulation of CXCR3B may switch a progression "stop" to a "go" signal to promote prostate tumor metastasis via stimulating cell migration and invasion. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5580944 Wed, 11 Jan 2012 05:00:00 +0100 5580944 http://www.medworm.com/index.php?rid=5571921&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F11%2F1%2F2 Conclusions: Ron receptor overexpression is associated with ERalpha-positive human and murine breast tumors. In addition, loss of ERalpha on a Ron overexpressing background in mice leads to the development of breast tumors which grow slower but which exhibit more metastasis and suggests that targeting of ERalpha, as in the case of tamoxifen therapy, may reduce the growth of Ron overexpressing breast cancers but may cause these tumors to be more metastatic. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5571921 Fri, 06 Jan 2012 05:00:00 +0100 5571921 http://www.medworm.com/index.php?rid=5559409&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F11%2F1%2F1 Conclusions: We have used unbiased RNAi based approaches to identify and characterize the function of CASP8AP2/FLASH, a protein not previously reported as required for the survival of colorectal cancer cells. This study further defines the role CASP8AP2/FLASH plays in regulating the expression of the replication-dependent histones and shows that its LOF results in broad and reproducible effects on the transcriptome of colorectal cancer cells, including the induction of expression of the recently described tumor suppressor gene NEFH. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5559409 Wed, 04 Jan 2012 05:00:00 +0100 5559409 http://www.medworm.com/index.php?rid=5537426&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F152 Bcl-3 is an established oncogene in hematologic malignancies, such as B-cell chronic lymphocytic leukemias. Nevertheless, recent research has shown that it also participates in progression of diverse solid tumors. The present review summarizes the current knowledge of Bcl3 role in solid tumors progression, including some new insights in its possible molecular mechanisms of action (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5537426 Fri, 23 Dec 2011 05:00:00 +0100 5537426 http://www.medworm.com/index.php?rid=5524064&cid=s_31130_6_f&fid=31130&url=%24%7Bitem.link%7D Conclusions: Matuzumab combined with chemoradiation did not induce cytotoxic effects on gynecological cancer cell lines in vitro, most likely due to impaired EGFR degradation. However, a combination of Matuzumab and PI3K inhibitor synergistically inhibited pAkt and cell survival, suggesting that the use of PI3K/Akt inhibitors could overcome intrinsic resistance to Matuzumab in vitro. Altogether, data presented here can pave the way to a rational design of clinical strategies in patients with resistant profile to anti-EGFR inhibitors based on combination therapy. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5524064 Tue, 20 Dec 2011 05:00:00 +0100 5524064 http://www.medworm.com/index.php?rid=5504304&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F149 Conclusion: Based on our findings we suggest that PGE2 act through PKA to promote beta-catenin nuclear translocation and tumor development in ApcMin/+ mice in vivo, indicating that the direct regulatory effect of PKA on beta-catenin nuclear translocation is operative in intestinal cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5504304 Thu, 15 Dec 2011 05:00:00 +0100 5504304 http://www.medworm.com/index.php?rid=5504303&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F150 Conclusions: IL-17 mediated tumor-promoting role involves a direct effect on HCC cells through IL-6/JAK2/STAT3 induction by activating the AKT pathway. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5504303 Thu, 15 Dec 2011 05:00:00 +0100 5504303 http://www.medworm.com/index.php?rid=5504306&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F147 Conclusions: This data highlights the potential to target cell surface associated enzymes, such as cathepsin S, as therapeutic targets using antibodies capable of eliciting ADCC in tumor cells. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5504306 Wed, 14 Dec 2011 05:00:00 +0100 5504306 http://www.medworm.com/index.php?rid=5504305&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F148 Conclusions: The study demonstrates that PAX2 activation by estradiol is selectively achieved in breast cancer cells of the luminal subtype, via ER, and identifies IGF-1 as a negative regulator of PAX2 activity in these cells. Further, it reveals a new role for PAX2 in the maintenance of a low invasive behavior in luminal breast cancer cells upon exposure to estradiol, and shows that overexpression and activation of PAX2 in these cells is sufficient to reduce their invasive ability. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5504305 Wed, 14 Dec 2011 05:00:00 +0100 5504305 http://www.medworm.com/index.php?rid=5449502&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F146 Conclusions: The blockage of beta2-adrenoceptor markedly induced PanCa cells to arrest at G1/S phase and consequently resulted in cell death, which is possibly due to that the blockage of beta2-adrenoceptor inhibited NFkappaB, extracellular signal-regulated kinase, and Akt pathways. Therefore, their upstream molecule Ras may be a key factor in the beta2-adrenoceptor antagonist induced G1/S phase arrest and apoptosis in PanCa cells. The new pathway discovered in this study may provide an effective therapeutic strategy for PanCa. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5449502 Sat, 26 Nov 2011 05:00:00 +0100 5449502 http://www.medworm.com/index.php?rid=5449503&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F145 Conclusion: These results suggest knocking down NONO or RALY significant counteracts oxaliplatin resistance in colorectal cancers overexpressing the YB-1 protein. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5449503 Fri, 25 Nov 2011 05:00:00 +0100 5449503 http://www.medworm.com/index.php?rid=5440293&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F143 Conclusion: Our findings suggest that gefitinib metabolism in lung cancer cells, elicited by CYP1A1 activity, might represent an early assessment of gefitinib responsiveness in NSCLC cells lacking activating mutations. On the other hand, in metabolizing cells, the inhibition of CYP1A1 might lead to increased local exposure to the active drug and thus increase gefitinib potency. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5440293 Wed, 23 Nov 2011 05:00:00 +0100 5440293 http://www.medworm.com/index.php?rid=5440292&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F144 Conclusions: FGF-BP is integrated in a complex network of cytoprotective effects, and represents a promising therapeutic target for RNAi-based knockdown approaches. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5440292 Wed, 23 Nov 2011 05:00:00 +0100 5440292 http://www.medworm.com/index.php?rid=5421560&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F142 Conclusion: This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5421560 Fri, 18 Nov 2011 05:00:00 +0100 5421560 http://www.medworm.com/index.php?rid=5407066&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F141 Conclusion: Our findings reveal sets of intronic lncRNAs expressed in pancreatic tissues whose abundance is correlated to PDAC or metastasis, thus pointing to the potential relevance of this class of transcripts in biological processes related to malignant transformation and metastasis in pancreatic cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5407066 Sun, 13 Nov 2011 05:00:00 +0100 5407066 http://www.medworm.com/index.php?rid=5400047&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F140 Papillomaviruses (PVs) are established agents of human and animal cancers. They infect cutaneous and mucous epithelia. High Risk (HR) Human PVs (HPVs) are consistently associated with cancer of the uterine cervix, but are also involved in the etiopathogenesis of other cancer types. The early oncoproteins of PVs: E5, E6 and E7 are known to contribute to tumour progression.While the oncogenic activities of E6 and E7 are well characterised, the role of E5 is still rather nebulous. The widespread causal association of PVs with cancer makes their study worthwhile not only in humans but also in animal model systems. The Bovine PV (BPV) system has been the most useful animal model in understanding the oncogenic potential of PVs due to the pivotal role of its E5 oncoprotein in cell transformation.... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5400047 Fri, 11 Nov 2011 05:00:00 +0100 5400047 http://www.medworm.com/index.php?rid=5400049&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F138 Conclusions: Notch pathway plays an important role in maintaining pancreas tumor phenotype. Targeting this pathway represents a reasonable strategy for the treatment of pancreas cancers. Notch modulates the Akt pathway through regulation of PTEN phosphorylation, an observation that has not been made previously. Furthermore, we discovered that this regulation is dependent on RhoA/Rock1 activation. Enhanced phospho-Akt suppression when GSI is combined with rapamycin suggests that targeting both pathways will lead to a greater efficacy in the treatment of patients with pancreas cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5400049 Thu, 10 Nov 2011 05:00:00 +0100 5400049 http://www.medworm.com/index.php?rid=5400048&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F139 Conclusion: We provide the first compelling evidence that upregulation of autocrine CXCL12 is a major mechanism underlying SLUG-mediated migration and invasion of prostate cancer cells. Our findings suggest that CXCL12 is a therapeutic target for prostate cancer metastasis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5400048 Thu, 10 Nov 2011 05:00:00 +0100 5400048 http://www.medworm.com/index.php?rid=5400050&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F137 Conclusion: Our findings suggest that SOX2 plays a role in the maintenance of a less differentiated glioma cell phenotype. In addition, the results indicate a critical role of SOX2 in adhesion and migration of malignant gliomas. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5400050 Wed, 09 Nov 2011 05:00:00 +0100 5400050 http://www.medworm.com/index.php?rid=5384462&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F136 Conclusions: Altered retinoic acid signaling has been validated especially in high risk Wilms tumors. In vitro testing of primary tumor cultures provided clear evidence of a potential utility of retinoids in Wilms tumor treatment based on the analysis of gene expression, proliferation, differentiation and apoptosis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5384462 Tue, 08 Nov 2011 05:00:00 +0100 5384462 http://www.medworm.com/index.php?rid=5384464&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F134 Conclusions: These results indicate that MSCs migrate to the tumor site in a time-dependent manner and could be an effective platform for the targeted delivery of CRAd and the amplification of tumor killing effects. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5384464 Thu, 03 Nov 2011 04:00:00 +0100 5384464 http://www.medworm.com/index.php?rid=5384463&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F135 Conclusion: These findings indicate that various genes and miRNAs orchestrate to temper the drug-resistance in cancer cells, and thus acquisition of drug-resistance is intricately controlled by genomic status, gene and miRNA expression changes. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5384463 Thu, 03 Nov 2011 04:00:00 +0100 5384463 http://www.medworm.com/index.php?rid=5384465&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F133 Conclusions: These results demonstrate that Ad.SPDD-HCCS1 was able to elicit reduced toxicity and enhanced efficacy both in vitro and in vivo compared to a previously constructed oncolytic adenovirus. Ad.SPDD-HCCS1 could be a promising candidate for liver cancer therapy. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5384465 Tue, 01 Nov 2011 04:00:00 +0100 5384465 http://www.medworm.com/index.php?rid=5384466&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F132 Conclusions: We conclude that the grade of genomic instability rather than the histopathological subtype correlates with specific gene and protein expression changes. The identified genes and proteins might be useful as molecular targets for improved diagnostic and therapeutic intervention and merit prospective validation. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5384466 Mon, 31 Oct 2011 04:00:00 +0100 5384466 http://www.medworm.com/index.php?rid=5335094&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F131 Conclusions: Our findings indicate that microtubule-generated forces are imbalanced in Aurora-A-defective cells and exert abnormal pressure at the level of spindle poles, ultimately causing their fragmentation. This study therefore highlights a novel role of the Aurora-A kinase in regulating the balance between microtubule forces during bipolar spindle assembly. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5335094 Wed, 19 Oct 2011 04:00:00 +0100 5335094 http://www.medworm.com/index.php?rid=5323639&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F130 Conclusions: Overall our results show that downregulation of uPA/uPAR, either singly or simultaneously, could be an effective approach to attenuate Notch 1 receptor cleavage, signaling and endosomal trafficking in U251MG cells and xenografts, and ultimately inhibiting GBM invasion. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5323639 Mon, 17 Oct 2011 04:00:00 +0100 5323639 http://www.medworm.com/index.php?rid=5313842&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F129 Conclusion: From these results, we propose that UCHL1 downregulation via promoter hypermethylation plays an important role in various molecular aspects of PCa biology, such as morphological diversification and regulation of proliferation. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5313842 Fri, 14 Oct 2011 04:00:00 +0100 5313842 http://www.medworm.com/index.php?rid=5304042&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F128 Glioblastomas (GBM) are a paradigm for the investigation of cancer stem cells (CSC) in solid malignancies. The susceptibility of GBM CSC to standard chemotherapeutic drugs is controversial as the existing literature presents conflicting experimental data. Here, we summarize the experimental evidence on the resistance of GBM CSC to alkylating chemotherapeutic agents, with a special focus on temozolomide (TMZ). The data suggests that CSC are neither resistant nor susceptible to chemotherapy per se. Detoxifying proteins such as O6-methylguanine-DNA-methyltransferase (MGMT) confer a strong intrinsic resistance to CSC in all studies. Extrinsic factors may also contribute to the resistance of CSC to TMZ. These may include TMZ concentrations in the brain parenchyma, TMZ dosing schemes, hypoxic mi... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5304042 Tue, 11 Oct 2011 04:00:00 +0100 5304042 http://www.medworm.com/index.php?rid=5304043&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F127 Background: The L1 cell adhesion molecule (L1CAM) is potentially involved in epithelial-mesenchymal transition (EMT). EMT marker expression is of prognostic significance in non-small cell lung cancer (NSCLC). The relevance of L1CAM for NSCLC is unclear. We investigated the protein expression of L1CAM in a cohort of NSCLC patients. L1CAM protein expression was correlated with clinico-pathological parameters including survival and markers of epithelial-mesenchymal transition. Results: L1CAM protein expression was found in 25% of squamous cell carcinomas and 24% of adenocarcinomas and correlated with blood vessel invasion and metastasis (p (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5304043 Mon, 10 Oct 2011 04:00:00 +0100 5304043 http://www.medworm.com/index.php?rid=5296572&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F126 Conclusion: This study confirms that multiple mechanisms contribute to Docetaxel resistance and the central transcription factor NF-kB plays an immensely important role in determining docetaxel-resistance which may represent an appropriate therapeutic target. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5296572 Fri, 07 Oct 2011 04:00:00 +0100 5296572 http://www.medworm.com/index.php?rid=5273162&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F124 Conclusion These comprehensive data may provide new insights into the epigenetic pathogenesis of human gliomas. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5273162 Fri, 30 Sep 2011 04:00:00 +0100 5273162 http://www.medworm.com/index.php?rid=5273161&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F125 Conclusion: These studies suggest that anti-multiple RTK strategy could be useful in the treatment of ovarian cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5273161 Fri, 30 Sep 2011 04:00:00 +0100 5273161 http://www.medworm.com/index.php?rid=5260095&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F122 In this study, we showed that CTGF was highly expressed in gastric cancer tissues compared with matched normal gastric tissues. The CTGF expression in tumor tissue was associated with histologic grade, lymph node metastasis and peritoneal dissemination (P (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5260095 Wed, 28 Sep 2011 04:00:00 +0100 5260095 http://www.medworm.com/index.php?rid=5260094&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F123 Conclusions: Overall, our data reveals that EEFEMP1 suppresses glioma growth in vivo, both by modulating the tumor extracellular microenvironment and by altering critical intracellular oncogenic signaling pathways. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5260094 Wed, 28 Sep 2011 04:00:00 +0100 5260094 http://www.medworm.com/index.php?rid=5250245&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F119 Conclusions: TGase 2 expression was significantly correlated with recurrence and shorter DFS in NSCLC, especially in the non-adenocarcinoma subtype including squamous cell carcinoma. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5250245 Sat, 24 Sep 2011 04:00:00 +0100 5250245 http://www.medworm.com/index.php?rid=5250244&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F120 There is growing evidence that interconnections among molecular pathways governing tissue differentiation are nodal points for malignant transformation. In this scenario, microRNAs appear as crucial players. This class of non-coding small regulatory RNA molecules controls developmental programs by modulating gene expression through post-transcriptional silencing of target mRNAs. During myogenesis, muscle-specific and ubiquitously-expressed microRNAs tightly control muscle tissue differentiation. In recent years, microRNAs have emerged as prominent players in cancer as well. Rhabdomyosarcoma is a pediatric skeletal muscle-derived soft-tissue sarcoma that originates from myogenic precursors arrested at different stages of differentiation and that continue to proliferate indefinitely. MicroRN... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5250244 Sat, 24 Sep 2011 04:00:00 +0100 5250244 http://www.medworm.com/index.php?rid=5250243&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F121 Conclusion: Our data demonstrate that GMME1 is a fusokine with a potent, CCR2 receptor-mediated pro-apoptotic effect on tumor cells and could be exploited as a novel biological therapy for CCR2+ malignancies including lymphoid and central nervous system malignancies. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5250243 Sat, 24 Sep 2011 04:00:00 +0100 5250243 http://www.medworm.com/index.php?rid=5250246&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F118 Conclusion: This study discriminates oncogene-specific cell migration and invasion pathways mediated by Rho GTPases in colon cancer cells and reveals potential new oncogene-specific characteristics for targeted therapeutics. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5250246 Fri, 23 Sep 2011 04:00:00 +0100 5250246 http://www.medworm.com/index.php?rid=5250248&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F116 Conclusion: Our results suggest for the first time that reduction of E-cad results in upregulation of EGFR transcriptionally. It also suggests that loss of E-cad may induce proliferation of SCCHN by activating EGFR and its downstream signaling pathways. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5250248 Thu, 22 Sep 2011 04:00:00 +0100 5250248 http://www.medworm.com/index.php?rid=5250247&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F117 Conclusions: We conclude that macrophages regulate the invasiveness of breast cancer cells through exosome-mediated delivery of oncogenic miRNAs. Our data provide insight into the mechanisms underlying the metastasis-promoting interactions between macrophages and breast cancer cells. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5250247 Thu, 22 Sep 2011 04:00:00 +0100 5250247 http://www.medworm.com/index.php?rid=5236736&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F115 Conclusions: Our data demonstrate a complex partnership between GSK-3beta and HDM2 in the regulation of p53 function in the nucleus and mitochondria. The data suggest that the ability of sorafenib to activate GSK-3beta and alter the intracellular distribution of p53 may be exploitable as an adjunct to agents that prevent the HDM2-dependent degradation of p53 in the treatment of melanoma. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5236736 Mon, 19 Sep 2011 04:00:00 +0100 5236736 http://www.medworm.com/index.php?rid=5224682&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F112 Background: Subpopulations of cancer cells with the capacity of generating solid tumors have been characterized. In various cancer types, including prostate cancer cells, a side population (SP) and CD133-expressing cells have been proposed as containing a population cancer cells with stem-like ability. Therefore the aim of this work was to determine, in prostate cancer cell lines, the frequency and tumorigenic potential of SP and CD133+ cells. Results: In vitro 2D colony-forming assay and sphere-forming assay, Flow cytometry analysis and magnetic cell sorting were utilized to sort CD133+, CD133- and Side population (SP) cells. Our findings indicate that CD44 and integrin alpha-6 are uniformly expressed in the hTERT cell lines; however, CD133 is expressed only in a small population ( (Sourc... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5224682 Wed, 14 Sep 2011 04:00:00 +0100 5224682 http://www.medworm.com/index.php?rid=5224681&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F113 Conclusions These results suggest that Dlx-2 may be implicated in tumor progression through regulating metabolic stress-induced necrosis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5224681 Wed, 14 Sep 2011 04:00:00 +0100 5224681 http://www.medworm.com/index.php?rid=5224680&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F114 Conclusion. These data reveal a novel switch in the requirement for RND3 and RHOA in coordinating the movement of residual WM793 cells that are initially refractive to BRAF inhibitor therapy. These results have important clinical implications because they suggest that combining BRAF inhibitors with therapies that target the invasion of drug-resistant cells could aid in controlling disease relapse. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5224680 Wed, 14 Sep 2011 04:00:00 +0100 5224680 http://www.medworm.com/index.php?rid=5207839&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F111 Conclusions: Our studies show that hMDMX has the essential properties of an oncogene. Its constitutive expression contributes to the oncogenic phenotype of transformed human cells. Its main function appears to be p53 inactivation. Therefore, developing new drugs targeting hMDMX is a valid approach to obtain new treatments for a subset of human tumors expressing wild-type p53. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5207839 Mon, 12 Sep 2011 04:00:00 +0100 5207839 http://www.medworm.com/index.php?rid=5207841&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F109 Conclusions: KV10.1 represents a novel therapeutic target for cancer. We could design a strategy that selectively kills tumor cells based on a KV10.1-specific antibody. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5207841 Wed, 07 Sep 2011 04:00:00 +0100 5207841 http://www.medworm.com/index.php?rid=5207840&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F110 Conclusions: This work establishes that, in HER2-overexpressing tumors, it is necessary, and maybe sufficient, to therapeutically impact on the Mcl-1/Bim balance for efficient induction of cancer cell death. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5207840 Wed, 07 Sep 2011 04:00:00 +0100 5207840 http://www.medworm.com/index.php?rid=5183284&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F107 Conclusions: Overall, our results indicate, for the first time, that plumbagin is a novel blocker of CXCR4 expression and thus has the potential to suppress metastasis of cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5183284 Wed, 31 Aug 2011 23:00:00 +0100 5183284 http://www.medworm.com/index.php?rid=5183283&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F108 Conclusions: These findings strongly indicate that miR-125b plays an important role in the development of pediatric APL at least partially mediated by repressing BAK1 protein expression and could be a potential therapeutic target for treating pediatric APL failure. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5183283 Wed, 31 Aug 2011 23:00:00 +0100 5183283 http://www.medworm.com/index.php?rid=5183286&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F105 In this study, we used a mouse model of tumor dormancy, DA1-3b leukemia cells. We previously showed that a minor population of DA1-3b cells persists in equilibrium with the immune system for long periods of time, and that the levels of surface expression of B7-H1 and B7.1 molecules correlates with the dormancy time. We found that leukemia cells DA1-3b/d365 cells, which derived from long-term dormant tumors and overexpressed B7-H1 and B7.1 molecules, were highly permissive to Ad5FB4, a human adenovirus serotype 5 (Ad5) vector pseudotyped with chimeric human-bovine fibers. Both B7-H1 and B7.1 were required for Ad5FB4-cell binding and entry, since (i) siRNA silencing of one or the other B7 gene transcript resulted in a net decrease in the cell binding and Ad5FB4-mediated transduction of DA1-3... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5183286 Tue, 30 Aug 2011 23:00:00 +0100 5183286 http://www.medworm.com/index.php?rid=5183285&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F106 Conclusions: Our study delineates a MSLN-Akt-NF-kappaB-IL-6-Mcl-1 survival axis that may be operative in PC cells, and might help cancer cells' survival in the highly inflammatory milieu evident in PC. Further, for the success of TNFerade + gemcitabine to be successful, we feel the simultaneous inhibition of components of this axis is also essential. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5183285 Tue, 30 Aug 2011 23:00:00 +0100 5183285 http://www.medworm.com/index.php?rid=5175438&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F103 Conclusions: These data highlight that ESE-1 contains NLS and NES signals that play a critical role in regulating its subcellular localization and function, and that an intact SAR domain mediates MEC transformation exclusively in the cytoplasm, via a novel nontranscriptional mechanism, whereby the SAR motif is accessible for ligand and/or protein interactions. These findings are significant, since they provide novel molecular insights into the functions of ETS transcription factors in mammary cell transformation. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5175438 Sat, 27 Aug 2011 23:00:00 +0100 5175438 http://www.medworm.com/index.php?rid=5160896&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F102 Conclusions: CypA is upregulated in majority of CCA patients' tissues and confers a significant growth advantage in CCA cells. Suppression of CypA expression decreases proliferation of CCA cell lines in vitro and reduces tumor growth in the nude mouse model. Inhibition of CypA activity also reduces CCA cell proliferation. The ERK1/2 pathway may be involved in the CypA-mediated CCA cell proliferation. Thus, CypA may represent an important new therapeutic target for liver fluke-associated CCA. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5160896 Thu, 25 Aug 2011 23:00:00 +0100 5160896 http://www.medworm.com/index.php?rid=5160897&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F101 Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene strongly predispose to development of gastro-intestinal tumors. Central to the tumorigenic events in APC mutant cells is the uncontrolled stabilization and transcriptional activation of the protein beta-catenin. Many questions remain as to how APC controls beta-catenin degradation. Remarkably, the large C-terminal region of APC, which spans over 2000 amino acids and includes critical regions in downregulating beta-catenin, is predicted to be natively unfolded. Here we discuss how this uncommonly large disordered region may help to coordinate the multiple cellular functions of APC. Recently, a significant number of germline and somatic missense mutations in the central region of APC were linked to tumorigenesis in the c... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5160897 Sun, 21 Aug 2011 23:00:00 +0100 5160897 http://www.medworm.com/index.php?rid=5143147&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F100 Conclusions: Taken together, our data demonstrate that IGF-1R signaling regulates LIP expression in an EGFR independent manner to increase the LIP/LAP ratio in mammary epithelial cells. C/EBPbeta expression and elevations in LIP play an important role in regulating cellular survival via suppression of anoikis, in an IGF-1R mediated context or in a manner independent of IGF-1R signaling. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5143147 Thu, 18 Aug 2011 23:00:00 +0100 5143147 http://www.medworm.com/index.php?rid=5143148&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F99 Conclusion: These findings demonstrate the novel mechanism for BMI-1 in contributing to EC cell invasion and that repression of BMI-1 by miR-194 could have a therapeutic potential to suppress EC metastasis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5143148 Wed, 17 Aug 2011 23:00:00 +0100 5143148 http://www.medworm.com/index.php?rid=5131662&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F98 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5131662 Mon, 15 Aug 2011 23:00:00 +0100 5131662 http://www.medworm.com/index.php?rid=5108910&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F96 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5108910 Mon, 08 Aug 2011 23:00:00 +0100 5108910 http://www.medworm.com/index.php?rid=5108909&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F97 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5108909 Mon, 08 Aug 2011 23:00:00 +0100 5108909 http://www.medworm.com/index.php?rid=5087176&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F95 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5087176 Sat, 30 Jul 2011 23:00:00 +0100 5087176 http://www.medworm.com/index.php?rid=5078597&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F94 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5078597 Thu, 28 Jul 2011 23:00:00 +0100 5078597 http://www.medworm.com/index.php?rid=5078599&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F92 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5078599 Wed, 27 Jul 2011 23:00:00 +0100 5078599 http://www.medworm.com/index.php?rid=5078598&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F93 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5078598 Wed, 27 Jul 2011 23:00:00 +0100 5078598 http://www.medworm.com/index.php?rid=5069983&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F91 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5069983 Tue, 26 Jul 2011 23:00:00 +0100 5069983 http://www.medworm.com/index.php?rid=5069984&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F90 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5069984 Mon, 25 Jul 2011 23:00:00 +0100 5069984 http://www.medworm.com/index.php?rid=5063273&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F89 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5063273 Mon, 25 Jul 2011 23:00:00 +0100 5063273 http://www.medworm.com/index.php?rid=5052341&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F88 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5052341 Thu, 21 Jul 2011 23:00:00 +0100 5052341 http://www.medworm.com/index.php?rid=5052344&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F85 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5052344 Wed, 20 Jul 2011 23:00:00 +0100 5052344 http://www.medworm.com/index.php?rid=5052343&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F86 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5052343 Wed, 20 Jul 2011 23:00:00 +0100 5052343 http://www.medworm.com/index.php?rid=5052342&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F87 ${item.shortDescription} (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5052342 Wed, 20 Jul 2011 23:00:00 +0100 5052342 http://www.medworm.com/index.php?rid=5030036&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F83 Conclusions: Collectively, these results indicate that RECQ1 has a unique and important role in the maintenance of genome integrity. Our results also suggest that RECQ1 might represent a new suitable target for anti cancer therapies aimed to arrest cell proliferation in brain gliomas. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5030036 Tue, 12 Jul 2011 23:00:00 +0100 5030036 http://www.medworm.com/index.php?rid=5030035&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F84 Conclusion: This study indicates that Integrin alpha5 subunit functions as a potential metastasis suppressor, while alpha6 subunit functions as a metastasis promoter. The modulation of integrins reduces cdc25 A, another possible mechanism for downregulation of CDK2. Taken together we demonstrate for a link between integrins and the chk1-cdc25-cyclin E/CDK2- Rb pathway. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5030035 Tue, 12 Jul 2011 23:00:00 +0100 5030035 http://www.medworm.com/index.php?rid=5020007&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F82 Conclusions: Zt/f2 is a potential therapeutic mAb capable of inhibiting RON-mediated oncogenesis by colon cancer cells in animal models. The inhibitory effect of Zt/f2 in vivo in combination with chemoagent 5-fluorouracil could represent a novel strategy for future colon cancer therapy. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5020007 Mon, 11 Jul 2011 23:00:00 +0100 5020007 http://www.medworm.com/index.php?rid=5009480&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F81 Conclusion: SNP rs12072037 modulates MFSD2A promoter activity and thus might affect MFSD2A levels in normal lung and in lung tumors, representing a candidate ethnically specific genetic factor underlying the association between the MYCL1 locus and lung cancer patients' survival. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5009480 Wed, 06 Jul 2011 23:00:00 +0100 5009480 http://www.medworm.com/index.php?rid=5009481&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F80 Conclusions: Altogether, these results suggest that the SXR pathway is involved in colon cancer irinotecan resistance in colon cancer cell line via the upregulation of select detoxification genes. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=5009481 Tue, 05 Jul 2011 23:00:00 +0100 5009481 http://www.medworm.com/index.php?rid=4993515&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F79 Conclusions: : While EGF first stimulates the activation of the EGFR and subsequently increases cancer cell proliferation, EGF concurrently induces the activation of ROCK, which then turns off the activated EGFR pathway via a negative feedback system.Key words: ROCK, EGFR, cell proliferation, pancreatic cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4993515 Sat, 02 Jul 2011 23:00:00 +0100 4993515 http://www.medworm.com/index.php?rid=4977277&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F78 Conclusion: Collectively, these data indicate that MiTMAB-induced apoptosis is dependent on both polyploidisation and specific intracellular signalling components. This suggests that dynamin and potentially other cytokinesis factors are novel targets for development of cancer therapeutics. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4977277 Mon, 27 Jun 2011 23:00:00 +0100 4977277 http://www.medworm.com/index.php?rid=4969836&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F76 Conclusions: Macrophages produce IGF-1 which directly stimulates neoplastic proliferation through Erk and Akt activation. This observation suggests that combining macrophage ablation therapy with IGF-1R, MEK and/or PI3K inhibition could improve therapeutic response in human lung cancer. Exploring macrophage-based intervention could be a fruitful avenue for future research. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4969836 Thu, 23 Jun 2011 23:00:00 +0100 4969836 http://www.medworm.com/index.php?rid=4969835&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F77 The aim of this study was to determine whether low prevalence human papillomavirus (HPV) 16 E6 variants differ from high prevalence types in their functional abilities. We evaluated functions relevant to carcinogenesis for the rarely-detected European variants R8Q, R10G and R48W as compared to the commonly detected L83V. Human immortalized keratinocytes (NIKS) stably transduced with the E6 variants were used in most functional assays. Low and high prevalence E6 variants displayed similar abilities in abrogation of growth arrest and inhibition of p53 elevation induced by actinomycin D. Differences were detected in the abilities to dysregulate stratification and differentiation of NIKS in organotypic raft cultures, modulate detachment induced apoptosis (anoikis) and hyperactivate Wnt signali... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4969835 Thu, 23 Jun 2011 23:00:00 +0100 4969835 http://www.medworm.com/index.php?rid=4936201&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F74 Conclusions: DNA-PK and FACT both play roles in DNA repair. Therefore both are putative targets for therapeutic inhibition. Since DNA-PK regulates apoptosis, silencing DNA-PKcs redirects cells treated with cisplatin toward necrosis. Silencing FACT however, allows both apoptosis and necrosis. Targeting DNA repair in cancer patients may have different therapeutic effects depending upon the roles played by factors targeted. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4936201 Wed, 15 Jun 2011 23:00:00 +0100 4936201 http://www.medworm.com/index.php?rid=4936202&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F73 In this study, we set out to assess the potential stimulation by CXCL12 of tumor cell TEM towards other chemokines and whether CXCR7 might be able to regulate such effects. Methods: The human Burkitt's lymphoma cell line NC-37, which expresses CXCR4, CXCR5, CXCR7 and CCR7, was selected as a model system. TEM of these cells through a human HUVEC endothelial cell monolayer was used as the main model system for these studies. Regulation of their TEM behavior by various concentrations of the various cognate chemokines for the above-mentioned receptors, placed in either the source or target wells of modified Boyden chamber migration plates, was assessed by quantifying the number of cells migrated under each experimental condition. Results: Exposure of CXCR4+CXCR7+ cancer cells to CXCL12 greatly... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4936202 Mon, 13 Jun 2011 23:00:00 +0100 4936202 http://www.medworm.com/index.php?rid=4936203&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F72 Conclusion: These findings suggest a potential new paradigm for the development of broad-spectrum cancer specific therapeutics with a companion diagnostic biomarker and a putative functional site for kinase-unrelated activities of Cdk4. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4936203 Sun, 12 Jun 2011 23:00:00 +0100 4936203 http://www.medworm.com/index.php?rid=4913197&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F71 Conclusion: The present data indicate that activation of the PI3-kinase/PKB/AKT pathway through PIK3CA regulates various transformed phenotypes as well as growth and differentiation of HPV-immortalized cells and may therefore play a pivotal role in HPV-induced carcinogenesis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4913197 Thu, 09 Jun 2011 23:00:00 +0100 4913197 http://www.medworm.com/index.php?rid=4903602&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F70 1-Oncogenes express proteins of "Tyrosine kinase receptor pathways", a receptor family including insulin or IGF- Growth Hormone receptors. Other oncogenes alter the PP2A phosphatase brake over these kinases.2- Experiments on pancreatectomized animals; treated with pure insulin or total pancreatic extracts, showed that choline in the extract, preserved them from hepatomas.Since choline is a methyle donor, and since methylation regulates PP2A, the choline protection may result from PP2A methylation, which then attenuates kinases.3- Moreover, kinases activated by the boosted signaling pathway inactivate pyruvate kinase and pyruvate dehydrogenase. In addition, demethylated PP2A would no longer deposphorylate these enzymes. A"bottleneck" between glycolysis and the oxidative-citrate cycle interr... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4903602 Mon, 06 Jun 2011 23:00:00 +0100 4903602 http://www.medworm.com/index.php?rid=4903603&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F69 Conclusions: MIPP might serve as a prototype for new drugs that could be used to induce non-apoptotic death in cancers that have become refractory to agents that work through DNA damage and apoptotic mechanisms. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4903603 Sun, 05 Jun 2011 23:00:00 +0100 4903603 http://www.medworm.com/index.php?rid=4877389&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F67 Conclusions: In malignant cells with a functional TGF-beta signalling pathway Rac1 antagonizes the TGF-beta1 growth inhibitory response and enhances cell migration by antagonistically regulating Smad2 and Smad3 activation. This study reveals that Rac1 is prooncogenic in that it can alter TGF-beta signalling at the R-Smad level from a tumour-suppressive towards a tumour-promoting outcome. Hence, Rac1 might represent a viable target for therapeutic intervention to inhibit PDAC progression. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4877389 Sun, 29 May 2011 23:00:00 +0100 4877389 http://www.medworm.com/index.php?rid=4873070&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F65 Conclusions: Since MCM7 expression was generally low in a number of normal tissues we examined, MCM7 has the characteristics of an ideal candidate for molecular targeted cancer therapy in various tumors and also as a good prognostic biomarker for NSCLC patients. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4873070 Fri, 27 May 2011 23:00:00 +0100 4873070 http://www.medworm.com/index.php?rid=4873071&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F64 Conclusions: These results indicate that the TOP1 mutations are involved in the development of SN38 resistance. We hypothesize that p.L617, p.R621 and p.E710 TOP1 residues are important for the functionality of the linker and that mutation of one of these residues is sufficient to alter or modulate its flexibility. Consequently, linker fluctuations could have an impact on SN38 binding by reducing the enzyme affinity for the drug. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4873071 Thu, 26 May 2011 23:00:00 +0100 4873071 http://www.medworm.com/index.php?rid=4863688&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F63 Conclusions: Both DNA methylation and histone methylation/acetylation play key roles in modulating Rhox5 expression in various cell types. The stem cell-like "bivalent domain", an epigenetic feature originally identified in key differentiation genes within stem cells, exists in the Rhox5 gene promoter in not only embryonic stem cells but also cancer cells, cancer stem cells, and differentiated Sertoli cells. As Ras signaling-dependent Rhox5 expression promotes tumor growth, Rhox5 may be an ideal target for therapeutic intervention in cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4863688 Mon, 23 May 2011 23:00:00 +0100 4863688 http://www.medworm.com/index.php?rid=4853933&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F61 Conclusions: These results highlight the critical role of PLK4 transcriptional deregulation in centriole multiplication in HPV-16 E7-expressing cells. Our findings encourage further experiments to test transcriptional inhibitors or small molecules targeting PLK4 to prevent centriole abnormalities, mitotic infidelity and malignant progression in HPV-associated neoplasms and other tumors in which PLK4 regulation is disrupted. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4853933 Mon, 23 May 2011 23:00:00 +0100 4853933 http://www.medworm.com/index.php?rid=4853934&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F60 Conclusions: Our results suggest that HOXD9 may be a novel marker of GCSCs and cell proliferation and/or survival factor in gliomas and glioma cancer stem-like cells, and a potential therapeutic target. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4853934 Sat, 21 May 2011 23:00:00 +0100 4853934 http://www.medworm.com/index.php?rid=4842585&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F59 Conclusion: These findings suggest an oncogenic role of miR-335 and shed new lights on the therapy of malignant astrocytomas by targeting miR-335. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4842585 Wed, 18 May 2011 23:00:00 +0100 4842585 http://www.medworm.com/index.php?rid=4842586&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F58 Conclusions: These data indicate that these two hormones combine to drive a differentiated phenotype, and reinforce the idea that the age dependent decline in both hormones results in the de-differentiation of prostate tumor cells, which results in increased proliferation, motility and invasion common to aggressive tumors. These studies also reinforce the potential importance of miRNAs in prostate cancer progression and therapeutic outcomes. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4842586 Tue, 17 May 2011 23:00:00 +0100 4842586 http://www.medworm.com/index.php?rid=4830668&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F56 Conclusions: Collectively, these results suggest that NPRA promotes PCa development in part by regulating MIF. Our findings also suggest that NPRA is a potential prognostic marker and a target for PCa therapy. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4830668 Mon, 16 May 2011 23:00:00 +0100 4830668 http://www.medworm.com/index.php?rid=4830667&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F57 Conclusions: The data presented here define POSH and Siah2 as important mediators of death receptor mediated apoptosis and suggest targeting the interaction of these two E3 ligases is a promising novel cancer therapeutic strategy. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4830667 Mon, 16 May 2011 23:00:00 +0100 4830667 http://www.medworm.com/index.php?rid=4830671&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F53 Conclusions: Our study indicates that IKKs tightly regulate Myc expression through prolonging protein stability, and suggests that IKKs are potentially therapeutic targets and that suppression of IKKs may be used following chemotherapy to reduce the risk of treatment-induced tumor progression. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4830671 Sun, 15 May 2011 23:00:00 +0100 4830671 http://www.medworm.com/index.php?rid=4830670&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F54 Conclusions: With our findings we can confirm and statistically validate the hypotheses for the gain-of-function and loss-of-function mechanisms of oncogenes and tumor suppressors, respectively. We show that the distinct mutational patterns can potentially be used to pre-classify newly identified cancer associated genes with yet unknown function. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4830670 Sun, 15 May 2011 23:00:00 +0100 4830670 http://www.medworm.com/index.php?rid=4830669&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F55 Conclusions: In concerted action miRNAs are able to potentiate their impact on G1-S progression. Thus the combination of miRNAs of the same network rather than individual miRNAs should be considered for assessing a biological response. Since miR-34a and miR-15a/16 are frequently down-regulated in the same tumour tissue, administrating a combination of both miRNAs may also potentiate their therapeutic impact. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4830669 Sun, 15 May 2011 23:00:00 +0100 4830669 http://www.medworm.com/index.php?rid=4830672&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F52 Conclusion: Examining almost all known human micro-RNA species confirmed the miR-371-373 cluster as a promising target for explaining cisplatin resistance, potentially by counteracting wild-type P53 induced senescence or linking it with the potency to differentiate. Moreover, we describe for the first time an association of the up-regulation of micro-RNA species such as hsa-miR-512-3p/-515/-517/-518/-525 and down-regulation of hsa-miR-99a/-100/-145 with a cisplatin resistant phenotype in human germ cell tumors. Further functional analyses are warranted to gain insight into their role in drug resistance. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4830672 Sat, 14 May 2011 23:00:00 +0100 4830672 http://www.medworm.com/index.php?rid=4805407&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F51 Conclusions: These results demonstrate for the first time an unexpected role of LPP3 in regulating glioblastoma progression by amplifying beta-catenin and CYCLIN-D1 activities. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4805407 Tue, 10 May 2011 23:00:00 +0100 4805407 http://www.medworm.com/index.php?rid=4795167&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F50 Conclusions: We demonstrate that PBX3 is up-regulated in prostate cancer and post- transcriptionally regulated by androgen through Let-7d. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4795167 Thu, 05 May 2011 23:00:00 +0100 4795167 http://www.medworm.com/index.php?rid=4754704&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F47 RNA polymerase (pol) III transcription is responsible for the transcription of small, untranslated RNAs involved in fundamental metabolic processes such mRNA processing (U6 snRNA) and translation (tRNAs). RNA pol III transcription contributes to the regulation of the biosynthetic capacity of a cell and a direct link exists between cancer cell proliferation and deregulation of RNA pol III transcription. Accurate transcription by RNA pol III requires TFIIIB, a known target of regulation by oncogenes and tumor suppressors. There have been significant advances in our understanding of how TFIIIB-mediated transcription is deregulated in a variety of cancers. Recently, BRF2, a component of TFIIIB required for gene external RNA pol III transcription, was identified as an oncogene in squamous cell ... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4754704 Sun, 24 Apr 2011 23:00:00 +0100 4754704 http://www.medworm.com/index.php?rid=4747985&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F46 Conclusion: This study showed the positive relationship between c-Myc expression in highly metastatic human prostate and colon cancer cells and susceptibility to TRAIL-induced apoptosis and therefore indicated that TRAIL might be used as an effective therapeutic modality for advanced metastatic cancers overexpressing c-Myc and combination of TRAIL therapy with agent that inhibits the DNA-PKcs/Akt signaling pathway might be clinically useful for the treatment of relatively TRAIL-insensitive human cancers. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4747985 Sun, 24 Apr 2011 23:00:00 +0100 4747985 http://www.medworm.com/index.php?rid=4735589&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F45 With cAMP signaling having a profound inhibitory effect on DNA damage-induced apoptosis in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells, understanding how this signaling pathway affects the survival capacity of the cell has important implications for cancer therapy. We have recently shown that p53 is critical for the inhibitory effect of cAMP on genotoxic agents-mediated apoptosis in BCP-ALLs. Here, we show that elevation of cAMP levels in cells exposed to DNA damage enhances the nuclear translocation and DNA binding of NF-kappaB by accelerating the phosphorylation of IKKbeta and thereby phosphorylation and degradation of IkappaBalpha. Furthermore, we show that the ability of cAMP to potentiate the ionizing radiation-induced activation of NF-kappaB requires the activity of... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4735589 Wed, 20 Apr 2011 23:00:00 +0100 4735589 http://www.medworm.com/index.php?rid=4735591&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F43 Conclusions: Our findings indicate that HBx exerts pro-apoptotic effect upon exposure to oxidative stress probably through accelerating the loss of Mcl-1 protein via caspase-3 cascade, which may shed a new light on the molecular mechanism of HBV-related hepatocarcinogenesis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4735591 Tue, 19 Apr 2011 23:00:00 +0100 4735591 http://www.medworm.com/index.php?rid=4735590&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F44 Conclusion: Our findings suggest that bile salt may function as a survival agonist and/or potential carcinogen in the development of HCC. Molecular approaches that inactivate Mcl-1 by blocking its T163 phosphorylation may represent new strategies for treatment of HCC. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4735590 Tue, 19 Apr 2011 23:00:00 +0100 4735590 http://www.medworm.com/index.php?rid=4725279&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F42 Conclusions: Altogether these data suggest that the combined use of two mAbs, such as anti-HLA-DR and anti-CD5, may significantly enhance their therapeutic potential. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4725279 Mon, 18 Apr 2011 23:00:00 +0100 4725279 http://www.medworm.com/index.php?rid=4725281&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F40 Conclusion: DZNeP is effective both in vitro and in vivo against PC cells. DZNeP antitumor activity is in part mediated by inhibition of CSC tumorigenic potential. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4725281 Sun, 17 Apr 2011 23:00:00 +0100 4725281 http://www.medworm.com/index.php?rid=4725280&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F41 Conclusions: This study uncovers microRNAs that are potentially involved in CML and the annotated functions of in silico filtered targets of selected miRNAs outline mechanisms whereby microRNAs may be involved in CML pathogenesis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4725280 Sun, 17 Apr 2011 23:00:00 +0100 4725280 http://www.medworm.com/index.php?rid=4715201&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F39 Conclusion: These results indicate that berberine can effectively target both the host and viral factors responsible for development of cervical cancer through inhibition of AP-1 and blocking viral oncoproteins E6 and E7 expression. Inhibition of AP-1 activity by berberine may be one of the mechanisms responsible for the anti-HPV effect of berberine. We propose that berberine is a potentially promising compound for the treatment of cervical cancer infected with HPV. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4715201 Thu, 14 Apr 2011 23:00:00 +0100 4715201 http://www.medworm.com/index.php?rid=4709808&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F38 Long non-coding RNAs (lncRNAs) are emerging as new players in the cancer paradigm demonstrating potential roles in both oncogenic and tumor suppressive pathways. These novel genes are frequently aberrantly expressed in a variety of human cancers, however the biological functions of the vast majority remain unknown. Recently, evidence has begun to accumulate describing the molecular mechanisms by which these RNA species function, providing insight into the functional roles they may play in tumorigenesis. In this review, we highlight the emerging functional role of lncRNAs in human cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4709808 Tue, 12 Apr 2011 23:00:00 +0100 4709808 http://www.medworm.com/index.php?rid=4705300&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F37 Background Nrf2 is a key transcriptional regulator of a battery of genes that facilitate phase II/III drug metabolism and defence against oxidative stress. Nrf2 is largely regulated by Keap1, which directs Nrf2 for proteasomal degradation. The Nrf2/Keap1 system is dysregulated in lung, head and neck, and breast cancers and this affects cellular proliferation and response to therapy. Here, we have investigated the integrity of the Nrf2/Keap1 system in pancreatic cancer.Results Keap1, Nrf2 and the Nrf2 target genes AKR1c1 and GCLC were detected in a panel of five pancreatic cancer cell lines. Mutation analysis of NRF2 exon 2 and KEAP1 exons 2-6 in these cell lines identified no mutations in NRF2 and only synonomous mutations in KEAP1. RNAi depletion of Nrf2 caused a decrease in the prolifera... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4705300 Tue, 12 Apr 2011 23:00:00 +0100 4705300 http://www.medworm.com/index.php?rid=4698008&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F36 Conclusions: VEGF-C/D are the main factors of lymphangiogenesis and lymphatic metastasis in bladder cancer. Moreover, TAMs play an important role in these processes by producing VEGF-C/D. The therapeutic inhibition of lymphangiogenesis could provide another therapeutic target to inhibit lymphatic metastasis and recurrence in patients with invasive bladder cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4698008 Sun, 10 Apr 2011 23:00:00 +0100 4698008 http://www.medworm.com/index.php?rid=4685747&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F35 Survivin (BIRC5), a member of the inhibitor of apoptosis protein (IAP) family that inhibits caspases and blocks cell death is highly expressed in cancer and is associated with a poorer clinical outcome. Functioning simultaneously during cell division and apoptosis inhibition, survivin plays a pivotal role in determining cell survival. Survivin has consistently been identified by molecular profiling analysis to be associated with higher tumor grade, more advanced disease, abbreviated survival, accelerated rates of recurrence, and chemotherapy and radiation resistance. Survivin's differential expression in cancer compared to normal tissue and its role as a nodal protein in a number of cellular pathways make it a highly flexible therapeutic target, suitable for small-molecule inhibitiors, mol... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4685747 Tue, 05 Apr 2011 23:00:00 +0100 4685747 http://www.medworm.com/index.php?rid=4659069&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F33 Small-cell lung cancer (SCLC) is the most aggressive lung cancer subtype and lacks effective early detection methods and therapies. A number of rare paraneoplastic neurologic autoimmune diseases are strongly associated with SCLC. Most patients with such paraneoplastic syndromes harbor high titers of antibodies against neuronal proteins that are abnormally expressed in SCLC tumors. These autoantibodies may cross-react with the nervous system, possibly contributing to autoimmune disease development. Importantly, similar antibodies are present in many SCLC patients without autoimmune disease, albeit at lower titers. The timing of autoantibody development relative to cancer and the nature of the immune trigger remain to be elucidated. Here we review what is currently known about SCLC-associate... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4659069 Tue, 29 Mar 2011 23:00:00 +0100 4659069 http://www.medworm.com/index.php?rid=4654144&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F32 Conclusions: Our findings demonstrate, for the first time, that t-DARPP regulates beta-catenin/TCF activity, thereby implicating a novel oncogenic signaling in upper gastrointestinal cancers. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4654144 Mon, 28 Mar 2011 23:00:00 +0100 4654144 http://www.medworm.com/index.php?rid=4643808&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F31 Conclusions: We report here that the CCND1/CDKN2A mRNA expression ratio predicts the RB1 status of cell lines in vitro and xenograft tumors and clinical tumor samples in vivo. Given the high predictive accuracy and quantitative nature of the CCND1/CDKN2A expression assay, the assay could be utilized to stratify patients for anti-tumor agents with preferential effects on either RB1-positive or -negative tumors. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4643808 Mon, 28 Mar 2011 23:00:00 +0100 4643808 http://www.medworm.com/index.php?rid=4627483&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F30 Conclusions: Systemic inhibition of HA-synthesis and knockdown of tumour cell HAS3 cause decreased ESCC progression accompanied by tumour stroma remodelling and may therefore be used in novel approaches to ESCC therapy. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4627483 Wed, 23 Mar 2011 00:00:00 +0100 4627483 http://www.medworm.com/index.php?rid=4606650&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F29 Conclusions: In this study, we document a diminished expression of miR-449 in Gastrin KO mice and further confirmed its loss in human gastric tumours. We investigated the function of miR-449 by identifying its direct targets. Furthermore we show that miR-449 induces senescence and apoptosis by activating the p53 pathway. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4606650 Fri, 18 Mar 2011 00:00:00 +0100 4606650 http://www.medworm.com/index.php?rid=4593747&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F28 Conclusion: Our studies describe that an increase of Aurora-A expression levels on its own has a tumor suppressing function, but in combination with the appropriate altered intracellular setting it might exert its oncogenic potential. The presented data indicate that deactivation of the tumor suppressor RB is one of the requirements for overriding a cell cycle checkpoint triggered by increased Aurora-A levels. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4593747 Wed, 16 Mar 2011 00:00:00 +0100 4593747 http://www.medworm.com/index.php?rid=4593748&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F27 Conclusion: NRP-1 is inversely associated with levels of butyrate and other SCFA in vivo and is expressed in a subset of CgA expressing cells. EEC number is related to butyrate level in the same way. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4593748 Mon, 14 Mar 2011 00:00:00 +0100 4593748 http://www.medworm.com/index.php?rid=4561362&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F25 Background: Thromboxane synthase (TXS) metabolizes prostaglandin H2 into thromboxanes, which are biologically active on cancer cells. TXS over-expression has been reported in a range of cancers, and associated with a poor prognosis. TXS inhibition induces cell death in-vitro, providing a rationale for therapeutic intervention. We aimed to determine the expression profile of TXS in NSCLC and if it is prognostic and/or a survival factor in the disease. Methods: TXS expression was examined in human NSCLC and matched controls by western analysis and IHC. TXS metabolite (TXB2) levels were measured by EIA. A 204-patient NSCLC TMA was stained for COX-2 and downstream TXS expression. TXS tissue expression was correlated with clinical parameters, including overall survival. Cell proliferation/survi... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4561362 Wed, 09 Mar 2011 00:00:00 +0100 4561362 http://www.medworm.com/index.php?rid=4561361&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F26 Conclusions: These findings indicate that apoptosis inducers and EGFR-targeted inhibitors enhance mitochondrial translocalization of both EGFR and EGFRvIII and that mitochondrial accumulation of these receptors contributes to tumor drug resistance. The findings also provide evidence for a potential link between the mitochondrial EGFR pathway and apoptosis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4561361 Wed, 09 Mar 2011 00:00:00 +0100 4561361 http://www.medworm.com/index.php?rid=4561363&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F24 Conclusion: Our studies indicate that the level of NER factors in ovarian cancer cell lines is neither a determinant of their NER capacity nor of the sensitivity to cisplatin, and suggest that manipulation of the HRR but not the NER factor expression provides an effective strategy for sensitizing cisplatin-resistant tumors to platinating agents. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4561363 Tue, 08 Mar 2011 00:00:00 +0100 4561363 http://www.medworm.com/index.php?rid=4528136&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F23 Conclusion: This study confirms the importance of previously characterized genes and identifies novel candidate genes that could be activated for aneuploidy to occur. Further functional analyses are required to clearly confirm the role of these new identified genes in the molecular mechanisms involved in breast cancer aneuploidy. The novel genes identified here, and/or the two-gene expression signature, might serve as diagnostic or prognostic markers and form the basis for novel therapeutic strategies. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4528136 Sun, 27 Feb 2011 00:00:00 +0100 4528136 http://www.medworm.com/index.php?rid=4502479&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F22 Many hypotheses have been postulated to explain the intricate nature of the metastatic process, but none of them completely accounted for the actual biological and clinical observations. Consequently, metastasis still remains an open issue with only few metastasis-inducing proteins experimentally validated so far. Recently proposed novel metastatic model, where serial and parallel metastatic processes are adequately integrated, might help to bridge the current gap between experimental results and clinical observations. In addition, the identification, isolation and molecular characterization of cancer stem cells, a population of the cells within the tumour mass able to proliferate, self-renew and induce tumorigenesis, will shed new light on the complex molecular events mediating metastasis... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4502479 Tue, 22 Feb 2011 00:00:00 +0100 4502479 http://www.medworm.com/index.php?rid=4502481&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F20 Conclusions: These data demonstrate that the PKR- and NF-kappaB-dependent induction of pro-inflammatory molecules that accompanies reovirus-mediated killing can recruit and activate innate and adaptive effector cells, thus potentially altering the tumour microenvironment to support bystander immune-mediated therapy as well as direct viral oncolysis. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4502481 Mon, 21 Feb 2011 00:00:00 +0100 4502481 http://www.medworm.com/index.php?rid=4502480&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F21 Conclusions: We conclude that PIAS1 is a common partner for two cancer-related nuclear factors, c-Myb and FLASH. Our results point to a functional cooperation between FLASH and PIAS1 in the enhancement of c-Myb activity in active nuclear foci. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4502480 Mon, 21 Feb 2011 00:00:00 +0100 4502480 http://www.medworm.com/index.php?rid=4473432&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F19 Conclusions: Estimates of eIF4E activity predict sensitivity to mTOR inhibition in cell lines but breast tumours with high estimated eIF4E activity gain changes in eIF4E regulation in order to enhance resistance. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4473432 Mon, 14 Feb 2011 00:00:00 +0100 4473432 http://www.medworm.com/index.php?rid=4465125&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F15 Conclusions: By comparing murine markers for the ductal carcinoma in situ (DCIS) of the mammary gland with genes up-regulated in human DCIS-samples we were able to identify a set of genes which might allow early detection of DCIS and invasive carcinomas. The similarities between gene expression in DCIS and invasive carcinomas suggest that the early detection and treatment of DCIS is of utmost relevance for the survival of patients who are at high risk of developing breast carcinomas. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4465125 Fri, 11 Feb 2011 00:00:00 +0100 4465125 http://www.medworm.com/index.php?rid=4465124&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F16 Conclusions: We propose that sFZD7 is a feasible therapeutic agent with specific activity, which can potentially be combined with other chemotherapeutic agents for the improved management of HCC. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4465124 Fri, 11 Feb 2011 00:00:00 +0100 4465124 http://www.medworm.com/index.php?rid=4465123&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F17 Conclusions: These pilot studies of GBM patients with sodium channel mutations indicate an association with a more aggressive disease and significantly shorter survival. Moreover, inhibition of GBM cells by ion channel inhibitors such as cardiac glycosides suggest a therapeutic strategy with relatively safe drugs for targeting GBM ion channel mutations. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4465123 Fri, 11 Feb 2011 00:00:00 +0100 4465123 http://www.medworm.com/index.php?rid=4455989&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F13 Conclusions: IFNgamma is equally effective in DSL-6A/C1 tumors with and without stellate cells. While its action in the presence of PSC may be explained by inhibition of fibrogenesis, its efficiency in PSC-free tumors is unlikely to be caused by direct effects on the tumor cells alone but may involve inhibitory effects on local stroma cells as well. To gain further insights, we also plan to apply computer simulations to the analysis of tumor growth in vivo. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4455989 Thu, 10 Feb 2011 00:00:00 +0100 4455989 http://www.medworm.com/index.php?rid=4446559&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F12 Curcumin (diferuloylmethane) is a polyphenol derived from the Curcuma longa plant, commonly known as turmeric. Curcumin has been used extensively in Ayurvedic medicine for centuries, as it is nontoxic and has a variety of therapeutic properties including anti-oxidant, analgesic, anti-inflammatory and antiseptic activity. More recently curcumin has been found to possess anti-cancer activities via its effect on a variety of biological pathways involved in mutagenesis, oncogene expression, cell cycle regulation, apoptosis, tumorigenesis and metastasis. Curcumin has shown anti-proliferative effect in multiple cancers, and is an inhibitor of the transcription factor NF-kB and downstream gene products (including c-myc, Bcl-2, COX-2, NOS, Cyclin D1, TNF-alpha, interleukins and MMP-9). In addition... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4446559 Mon, 07 Feb 2011 00:00:00 +0100 4446559 http://www.medworm.com/index.php?rid=4433462&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F11 Conclusions: LMP1 can lead to the activation of several key factors mediating proliferation, angiogenesis and inflammation in vivo. With the initiation of an inflammatory programme, leukocyte recruitment follows which then itself contributes to the progressing pathology in these transgenic mice, with a pivotal role for B-and/or T-cells in the process. The model suggests a basis for the leukocyte infiltrate observed in EBV-associated cancer and its supporting role, as well as potential points for therapeutic intervention. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4433462 Thu, 03 Feb 2011 00:00:00 +0100 4433462 http://www.medworm.com/index.php?rid=4406537&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F10 Conclusions: This study demonstrates that Bmi-1 promotes the invasion and metastasis of human breast cancer and predicts poor survival. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4406537 Fri, 28 Jan 2011 00:00:00 +0100 4406537 http://www.medworm.com/index.php?rid=4400532&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F9 Conclusions: AND CLINICAL RELEVANCE: PLZ4 can specifically bind to canine bladder cancer cells. This suggests that the preclinical studies of PLZ4 as a potential diagnostic and therapeutic agent can be performed in dogs with naturally occurring bladder cancer, and that PLZ4 can possibly be developed in the management of canine bladder cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4400532 Thu, 27 Jan 2011 00:00:00 +0100 4400532 http://www.medworm.com/index.php?rid=4344036&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F8 Conclusions: In conclusion, the discovery of the involvement of Cyr61/CCN1 in pancreatic carcinogenesis may represent an important marker for PDAC and suggests Cyr61/CCN1 can be a potential cancer therapeutic target. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4344036 Thu, 13 Jan 2011 00:00:00 +0100 4344036 http://www.medworm.com/index.php?rid=4338909&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F7 Conclusions: This study presents a new method to investigate tumour reversion by epigenetic reprogramming. After testing extracts from different sources, we found that axolotl oocyte extracts possess superior reprogramming ability, which reverses epigenetic silencing of tumour suppressor genes and tumorigenicity of breast cancer cells in a mouse xenograft model. Therefore this system can be extremely valuable for dissecting the mechanisms involved in tumour suppressor gene silencing and identifying molecular activities capable of arresting tumour growth. These applications can ultimately shed light on the contribution of epigenetic alterations in breast cancer and advance the development of epigenetic therapies. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4338909 Thu, 13 Jan 2011 00:00:00 +0100 4338909 http://www.medworm.com/index.php?rid=4327197&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F5 Conclusion: NEK1 is required for the maintenance of genome stability by acting at multiple junctures, including control of chromosome stability. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4327197 Mon, 10 Jan 2011 00:00:00 +0100 4327197 http://www.medworm.com/index.php?rid=4325038&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F4 Conclusions: Treatment with acyclic retinoid produces a dual activation of caspase 3 and TG2 induced apoptosis of hepatocellular carcinoma cells via modification and inactivation of Sp1, resulting in reduced expression of epidermal growth factor receptor. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4325038 Sun, 09 Jan 2011 00:00:00 +0100 4325038 http://www.medworm.com/index.php?rid=4319155&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F3 Cancer vaccines are the promising tools in the hands of the clinical oncologist. Many tumor-associated antigens are excellent targets for immune therapy and vaccine design. Optimally designed cancer vaccines should combine the best tumor antigens with the most effective immunotherapy agents and/or delivery strategies to achieve positive clinical results. Various vaccine delivery systems such as different routes of immunization and physical/ chemical delivery methods have been used in cancer therapy with the goal to induce immunity against tumor-associated antigens. Two basic delivery approaches including physical delivery to achieve higher levels of antigen production and formulation with microparticles to target antigen-presenting cells (APCs) have demonstrated to be effective in animal m... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4319155 Fri, 07 Jan 2011 00:00:00 +0100 4319155 http://www.medworm.com/index.php?rid=4319156&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F2 Conclusions: Despite high expression in melanoma cells, the role of SKI in melanoma remains elusive: SKI does not efficiently interfere with the pro-oncogenic activities of TGF-beta, unless stabilized by proteasome blockade. Its highly labile nature makes it an unlikely target for therapeutic intervention. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4319156 Thu, 06 Jan 2011 00:00:00 +0100 4319156 http://www.medworm.com/index.php?rid=4310209&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F10%2F1%2F1 Conclusions: These findings provide important evidence that miR-148b targets CCKBR and is significant in suppressing gastric cancer cell growth. Maybe miR-148b would become a potential biomarker and therapeutic target against gastric cancer. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4310209 Tue, 04 Jan 2011 00:00:00 +0100 4310209 http://www.medworm.com/index.php?rid=4300879&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F9%2F1%2F320 Background: Different isoforms of VEGF-A (mainly VEGF121, VEGF165 and VEGF189) have been shown to display particular angiogenic properties in the generation of a functional tumor vasculature. Recently, a novel class of VEGF-A isoforms, designated as VEGFxxxb, generated through alternative splicing, have been described. Previous studies have suggested that these isoforms may inhibit angiogenesis. In the present work we have produced recombinant VEGF121/165b proteins in the yeast Pichia pastoris and constructed vectors to overexpress these isoforms and assess their angiogenic potential. Results: Recombinant VEGF121/165b proteins generated either in yeasts or mammalian cells activated VEGFR2 and its downstream effector ERK1/2, although to a lesser extent than VEGF165. Furthermore, treatment o... Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4300879 Fri, 31 Dec 2010 00:00:00 +0100 4300879 http://www.medworm.com/index.php?rid=4295255&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F9%2F1%2F319 Conclusions: These findings support the proposal that PC3 tumors are sustained by a small number of tumor-initiating cells with stem-like characteristics, including strong self-renewal and pro-angiogenic capability and marked by the expression pattern FAM65B(high)/MFI2(low)/LEF1(low). These markers may serve as targets for therapies designed to eliminate cancer stem cell populations associated with aggressive, androgen-independent prostate tumors such as PC3. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4295255 Wed, 29 Dec 2010 00:00:00 +0100 4295255 http://www.medworm.com/index.php?rid=4278172&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F9%2F1%2F318 Conclusions: Our results suggested an important role of FBI-1 in ovarian cancer cell proliferation, cell mobility, and invasiveness, and that FBI-1 can be a potential target of chemotherapy. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4278172 Tue, 21 Dec 2010 00:00:00 +0100 4278172 http://www.medworm.com/index.php?rid=4272711&cid=s_31130_6_f&fid=31130&url=http%3A%2F%2Fwww.molecular-cancer.com%2Fcontent%2F9%2F1%2F315 Conclusions: DR5 induction plays a critical role in mediating perifosine/TRAIL-induced apoptosis. Perifosine induces DR5 expression through a JNK-dependent mechanism independent of reactive oxygen species. (Source: Molecular Cancer) Molecular Cancer journals http://www.medworm.com/rss/comments.php?id=4272711 Mon, 20 Dec 2010 00:00:00 +0100 4272711