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        <title>Breast Cancer Research via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Breast Cancer Research' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Breast+Cancer+Research&t=Breast+Cancer+Research&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 08:41:16 +0100</lastBuildDate>
        <item>
            <title>The role and function of cadherins in the mammary gland</title>
            <link>http://www.medworm.com/index.php?rid=5666646&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F203</link>
            <description>Cadherins are transmembrane receptors that function through calcium-dependent homophilic and heterophilic interactions that provide cell-cell contact and communication in many different organ systems.  In the mammary gland only a few of the cadherins that make up this large superfamily of proteins have been characterized. Frequently in metastatic breast cancer, the genes for cadherins are epigenetically silenced, mutated, or regulated differently. During epithelial mesenchymal transition, cadherins that are expressed normally in the epithelial cells are down regulated, while cadherins expressed in the mesenchyme are up regulated. This process is known as cadherin switching, and its regulation can sometime facilitates the increase motility, invasiveness and proliferation that occurs in meta...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5666646</comments>
            <pubDate>Wed, 08 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5666646</guid>        </item>
        <item>
            <title>Key signaling nodes in mammary gland development and cancer: Smad signal integration in epithelial cell plasticity</title>
            <link>http://www.medworm.com/index.php?rid=5666645&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F204</link>
            <description>Smad proteins are the key intermediates of TGF-beta-signaling during development and in tissue homeostasis. Pertubations in TGF-beta/Smad signaling have been implicated in cancer, and other diseases. In the cell nucleus Smad complexes trigger cell type- and context-specific transcriptional programs, thereby transmitting and integrating signals from a variety of ligands of the TGF-beta-superfamily and other stimuli in the cell micro-environment. The actual transcriptional and biological outcome of Smad activation critically depends on the genomic integrity and the modification state of genome and chromatin of the cell. The cytoplasmic and nuclear Smads can also modulate the activity of other signal transducers and enzymes such as microRNA processing factors. In the case of breast cancer the...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5666645</comments>
            <pubDate>Wed, 08 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5666645</guid>        </item>
        <item>
            <title>Contribution of CXCL12 secretion to invasion of breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5666650&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR23</link>
            <description>Conclusions:
Expression of CXCL12 by tumor cells results in increased macrophage and microvessel density and in vivo invasiveness. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5666650</comments>
            <pubDate>Tue, 07 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5666650</guid>        </item>
        <item>
            <title>Germline DNA copy number variation in familial and early-onset breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5666649&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR24</link>
            <description>Conclusions:
This is the first study to explore the contribution of germline CNVs to BRCA1/2 negative familial and early-onset breast cancer. The data suggest that rare CNVs may contribute to cancer predisposition in this small cohort of patients, and this trend needs to be confirmed in larger samples. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5666649</comments>
            <pubDate>Tue, 07 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5666649</guid>        </item>
        <item>
            <title>Breast cancer risk prediction and individualised screening based on common genetic variation and breast density measurement</title>
            <link>http://www.medworm.com/index.php?rid=5666648&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR25</link>
            <description>Conclusions:
Taken together, genetic risk factors and mammographic density offer moderate improvements to clinical risk factor models for predicting breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5666648</comments>
            <pubDate>Tue, 07 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Initiating breast cancer by PIK3CA mutation</title>
            <link>http://www.medworm.com/index.php?rid=5666647&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F301</link>
            <description>PIK3CA mutations confer constitutive activation of PI3K, which initiates intracellular kinase signaling cascades that promote cell proliferation and survival. Recent studies by Meyer et al. and Liu et al. demonstrate that expression of the H1047R exon 20 mutant of PIK3CA in luminal mammary epithelial cells induces tumorigenesis, implying that PIK3CA mutations are an early event in breast cancer. PIK3CA-H1047R-initiated tumors exhibit variable dependence on the oncogene, and variable sensitivity to PI3K inhibition. Amplification of the oncogenes MYC and MET was observed in tumors which recurred following silencing of PIK3CA-H1047R, suggesting that these pathways represent mechanisms of escape from PI3K inhibition. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5666647</comments>
            <pubDate>Tue, 07 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5666647</guid>        </item>
        <item>
            <title>Small interfering RNA library screen identified polo-like kinase-1 (PLK1) as a potential therapeutic target for breast cancer that uniquely eliminates tumour-initiating cells</title>
            <link>http://www.medworm.com/index.php?rid=5666651&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR22</link>
            <description>Conclusion:
Inhibiting PLK1 with siRNA or BI 2536 blocked growth of TNBCs including the CD44high/CD24-/low TIC subpopulation and mammosphere formation. Thus, PLK1 could be a potential therapeutic target for the treatment of TNBC as well as other subtypes of breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5666651</comments>
            <pubDate>Mon, 06 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5666651</guid>        </item>
        <item>
            <title>Use of glucocorticoids and risk of breast cancer: a Danish population-based case-control study</title>
            <link>http://www.medworm.com/index.php?rid=5659309&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR21</link>
            <description>IntroductionGlucocorticoids are widely prescribed drugs. In the human body, glucocorticoid is the main stress hormone, and controls a variety of physiological and cellular processes, including metabolism and immune response. It belongs to the same steroid superfamily as estrogens, which are known to play a role in breast cancer. However, the effect of glucocorticoid use on the risk of breast cancer is not clear.
Methods:
We conducted a case-control study using population-based medical databases from Northern Denmark (1.8 million inhabitants) to investigate the association between glucocorticoid prescriptions and breast cancer risk. The study included 9,488 incident breast cancer cases diagnosed between 1994 and 2008 and 94,876 population controls. We estimated the odds ratios (ORs) and 95%...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659309</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5659309</guid>        </item>
        <item>
            <title>Phospho-ibuprofen (MDC-917) suppresses breast cancer growth: an effect controlled by the thioredoxin system</title>
            <link>http://www.medworm.com/index.php?rid=5646911&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR20</link>
            <description>Conclusions:
P-I is safe and effective against breast cancer. Liposomal formulation enhances its efficacy; its effect is heavily dependent on the induction of oxidative stress and the suppression of the thioredoxin system. P-I merits further evaluation as an agent for the treatment of breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5646911</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5646911</guid>        </item>
        <item>
            <title>Do we need biomarkers to predict the benefit of adding adjuvant taxanes for treatment of breast cancer?</title>
            <link>http://www.medworm.com/index.php?rid=5646910&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F104</link>
            <description>The current understanding of the molecular biology of breast cancer presents an extremely complex portrait of the disease. Based on this knowledge, considerable efforts are being made to identify biomarkers that will predict the response to a specific treatment while minimizing the risk of unnecessary side effects. In breast cancer, the Ki67 index has been associated with poor prognosis and might play a relevant role in predicting benefit from adjuvant docetaxel, as observed in the article accompanying this editorial. Taxanes are one of the most active cytotoxic agents for breast cancer. However, the role of taxane-based chemotherapy as adjuvant treatment of early breast cancer remains controversial in some subsets of patients. For this reason, the Ki67 index might help to better define th...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5646910</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5646910</guid>        </item>
        <item>
            <title>Validation of the Gail model for predicting individual breast cancer risk in a prospective nationwide study of 28,104 Singapore women</title>
            <link>http://www.medworm.com/index.php?rid=5646912&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR19</link>
            <description>Conclusions:
The GM over-predicts the risk of invasive breast cancer in an Asian developed-country setting as demonstrated in a large prospective trial, with the largest difference seen in older women aged between 60 and 64 years old. The reason for the discrepancy is likely to be multifactorial, including a true reduction of breast cancer, as well as lower mammographic screening prevalence locally. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5646912</comments>
            <pubDate>Mon, 30 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5646912</guid>        </item>
        <item>
            <title>The dynamic Yin-Yang  interaction of CXCR4 and CXCR7 in breast cancer metastasis</title>
            <link>http://www.medworm.com/index.php?rid=5637953&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F103</link>
            <description>The contribution of CXCR7 to the tumor microenvironment has introduced a new level of complexity to CXCL12 signaling in breast cancer. In the previous issue of Breast Cancer Research, Hernandez and colleagues delineate the roles of CXCR4 and CXCR7 in tumor invasion and metastasis. The authors demonstrate that co-expression of CXCR7 and CXCR4 results in inhibition of CXCL12-mediated invasion, reduced intravasation of tumor cells into the vasculature, and fewer lung metastases compared with parental tumors. The results of this study suggest the combination of small molecule inhibitors of CXCR4 and CXCR7 could dramatically reduce invasion, intravasation, and metastasis and could be highly beneficial for the treatment of invasive breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5637953</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5637953</guid>        </item>
        <item>
            <title>Metastasis is an early event in mouse mammary carcinomas and is associated with cells bearing stem cell markers</title>
            <link>http://www.medworm.com/index.php?rid=5637955&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR18</link>
            <description>Conclusions:
The tumorigenic and metastatic potential of a subpopulation of mammary epithelial/tumor cells in MMT mice is endowed relatively early in mammary neoplasms and suggests a potential role for cancer stem cell sub-populations in metastasis. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5637955</comments>
            <pubDate>Wed, 25 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5637955</guid>        </item>
        <item>
            <title>Fatty breasts increase or decrease breast cancer risk?</title>
            <link>http://www.medworm.com/index.php?rid=5637954&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F102</link>
            <description>Few studies have investigated the association of non-dense area or fatty breasts in conjunction with breast density and breast cancer risk. Two articles in a recent issue of Breast Cancer Research investigate the role of absolute non-dense breast area measured on mammograms and find conflicting results: one article finds that non-dense breast area has a modest positive association with breast cancer risk, whereas the other finds that non-dense breast area has a strong protective effect to reduce breast cancer risk. Understanding the interplay of body mass index, menopause status, and measurement of non-dense breast area would help to clarify the contribution of non-dense breast area to breast cancer risk. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5637954</comments>
            <pubDate>Wed, 25 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5637954</guid>        </item>
        <item>
            <title>Breast cancer risk assessment with five independent genetic variants and two risk factors in chinese women</title>
            <link>http://www.medworm.com/index.php?rid=5637956&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR17</link>
            <description>IntroductionRecently, several genome-wide association studies (GWAS) have identified novel single nucleotide polymorphisms (SNPs) associated with breast cancer risk. However, most of the studies were conducted among Caucasians and only one from Chinese.
Methods:
In the current study, we first tested whether 15 SNPs identified by previous GWAS were also breast cancer marker SNPs in this Chinese population. Then, we grouped the marker SNPs, and modeled them with clinical risk factors, to see the usage of these factors in breast cancer risk assessment. Two methods (risk factors counting and OR weighted risk scoring) were used to evaluate the cumulative effects of the 5 significant SNPs and two clinical risk factors (age at menarche and age at first live birth).
Results:
Five SNPs located at 2...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5637956</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5637956</guid>        </item>
        <item>
            <title>STAT1-deficient mice spontaneously develop estrogen receptor alpha-positive luminal mammary carcinomas</title>
            <link>http://www.medworm.com/index.php?rid=5619613&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR16</link>
            <description>Conclusions:
Our findings demonstrate that STAT1 suppresses mammary tumor formation and its expression is frequently lost during breast cancer progression. Spontaneous mammary tumors that develop in STAT1-/- mice closely recapitulate the progression, ovarian hormone responsiveness, and molecular characteristics of human luminal breast cancer, the most common subtype of human breast neoplasms, and thus represent a valuable platform for testing novel treatments and detection modalities. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619613</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619613</guid>        </item>
        <item>
            <title>Expression of stem cell and epithelial-mesenchymal transition markers in primary breast cancer patients with circulating tumor cells.</title>
            <link>http://www.medworm.com/index.php?rid=5607956&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR15</link>
            <description>Conclusion:
Our data indicate that (1) a subset of primary breast cancer patients shows EMT and stem cell characteristics and (2) the currently used detection methods for CTC are not efficient to identify a subtype of CTC which underwent EMT. (3) The clinical relevance on prognosis and therapy response has to be further evaluated in a prospective trial. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607956</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607956</guid>        </item>
        <item>
            <title>Understanding the mechanisms of AI resistance</title>
            <link>http://www.medworm.com/index.php?rid=5607958&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F201</link>
            <description>Aromatase inhibitors (AIs) have a central role in the treatment of breast cancer. However, resistance is a major obstacle to optimal management. Evidence from i) endocrine, molecular and pathological measurements in clinical material taken before and after therapy with AIs and ii) data from clinical trials in which AIs have been given as treatment either alone or in combination with other targeted agents suggest diverse causes for resistance. These include inherent tumour insensitivity to oestrogen, ineffective inhibition of aromatase, sources of oestrogenic hormones independent of aromatase, activation of signalling by non-endocrine pathways, enhanced cell survival and selection of hormone-insensitive cellular clones during treatment. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607958</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607958</guid>        </item>
        <item>
            <title>Epithelial-mesenchymal transition, cancer stem cells and treatment resistance</title>
            <link>http://www.medworm.com/index.php?rid=5607957&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F202</link>
            <description>Mortality from breast cancer has steadily been declining over the last decade, primarily due to earlier detection, adjuvant therapies and the advent of targeted therapies for ER positive and HER2 positive cancers [1, 2]. Despite these advances, a large number of patients relapse after an initial response to standard of care therapy. Novel therapies that prevent breast cancer relapse and metastasis are needed. An emerging hypothesis is that tumors contain a subpopulation of cells, called cancer stem cells (CSCs), which have the ability to self renew and regenerate the tumor. Increasingly, clinical evidence points to an intrinsic resistance to endocrine therapy and chemotherapy of this subpopulation of cancer stem cells [3]. The residual tumors after chemotherapy are enriched for CSCs and ha...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607957</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607957</guid>        </item>
        <item>
            <title>MicroRNA let-7a suppresses breast cancer cell migration and invasion through down-regulation of C-C chemokine receptor type 7</title>
            <link>http://www.medworm.com/index.php?rid=5607959&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR14</link>
            <description>MicroRNA let-7a binds directly to the 3'UTR of C-C chemokine receptor type 7 (CCR7), blocking its protein expression and suppressing migration and invasion of breast cancer cells. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607959</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607959</guid>        </item>
        <item>
            <title>Tibolone increases bone mineral density but also relapse in breast cancer survivors: LIBERATE Trial Bone Sub-study</title>
            <link>http://www.medworm.com/index.php?rid=5607960&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR13</link>
            <description>IntroductionLivial Intervention Following Breast Cancer; Efficacy, Recurrence and Tolerability Endpoints (LIBERATE - ClinicalTrials.gov number NCT00408863), a randomized, placebo controlled, double-blind trial which demonstrated that tibolone (Livial), a tissue selective hormone replacement therapy (HRT) increased breast cancer (BC) recurrence HR 1.40 (95% CI 1.14-1.70; p=0.001) entered a subgroup of women into a study of Bone Mineral Density (BMD).
Methods:
Women with surgically excised primary BC (T1-3, N0-2, M0) within the last 5 years complaining of vasomotor symptoms, were assigned to tibolone 2.5mg daily or placebo treatment for a maximum of 5 years. The BMD sub-study enrolled 763 patients utilizing dual-energy X-ray absorptiometry (DXA) scanning at baseline and at 2 years.
Results:
...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607960</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607960</guid>        </item>
        <item>
            <title>MIBE acts as antagonist ligand of both estrogen receptor alpha and GPER in breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5596844&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR12</link>
            <description>Conclusions:
Our findings provide novel insights on the functional cross-talk between GPER and EGFR signaling. Furthermore, the exclusive antagonistic activity exerted by MIBE on ERalpha and GPER could represent an innovative pharmacological approach targeting breast carcinomas which express one or both receptors at the beginning and/or during tumor progression. Hence, the simultaneous inhibition of both ERalpha and GPER may guarantee major therapeutic benefits respect to the use of a selective estrogen receptor antagonist. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5596844</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5596844</guid>        </item>
        <item>
            <title>Molecular profiling of patient-derived breast cancer xenografts</title>
            <link>http://www.medworm.com/index.php?rid=5596845&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR11</link>
            <description>Conclusions:
This panel of human BC xenografts maintains the overall genomic and gene expression profile of the corresponding patient tumors and remains stable throughout sequential in vivo generations. The observed genomic profile and gene expression differences appear to be due to the loss of human stromal genes. These xenografts therefore represent a validated model for preclinical investigation of new therapeutic agents. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5596845</comments>
            <pubDate>Mon, 16 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5596845</guid>        </item>
        <item>
            <title>Balancing harms and benefits of service mammography screening programs: a cohort study.</title>
            <link>http://www.medworm.com/index.php?rid=5580851&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR9</link>
            <description>Conclusions:
Comparing the breast cancer mortality and breast cancer incidence between attenders and non-attenders, we have evaluated that the overall cost to save one life corresponds to no more than one overdiagnosed tumour (from 0.6 to 1 depending on the selection criteria of the cohort), even if a residual self-selection bias cannot be excluded. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580851</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580851</guid>        </item>
        <item>
            <title>Trends in incidence and detection of advanced breast cancer at biennial screening mammography in The Netherlands: a population based study</title>
            <link>http://www.medworm.com/index.php?rid=5580850&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR10</link>
            <description>Conclusion:
We observed no decline in the risk of advanced breast cancer during 12 years of biennial screening mammography. The majority of these cancers could not have been prevented through earlier detection at screening. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580850</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580850</guid>        </item>
        <item>
            <title>Steps solidifying a role for SEPT9 in breast cancer suggest that greater strides are needed</title>
            <link>http://www.medworm.com/index.php?rid=5580849&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2F101</link>
            <description>Septins comprise a conserved family of GTPase proteins. Of these, human SEPT9 has been widely implicated in cancers of epithelial origin, including breast cancer, as well as leukemia. In a previous issue of Breast Cancer Research, Connolly and colleagues present compelling data further supporting a role for SEPT9 isoforms in early breast cancer development as well as evidence suggesting that cellular localization patterns of SEPT9 isoforms may contribute to oncogenesis. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580849</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580849</guid>        </item>
        <item>
            <title>Hypoxia inducible factor-1alpha promotes primary tumor growth and tumor-initiating cell activity in breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5571845&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR6</link>
            <description>Conclusion:
These results demonstrate that HIF-1alpha plays a key role in promoting primary mammary tumor growth and metastasis, in part through regulation of TICs. HIF-1 regulates expression of several members of the Notch pathway, CD133 and markers of the basal lineage in mammary tumors. Our results suggest that CD133, which has not been profiled extensively in breast cancer, may be a useful marker of TICs in the PyMT model. These data reveal for the first time that HIF-1 directly regulates breast TIC activity in vivo. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571845</comments>
            <pubDate>Sat, 07 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5571845</guid>        </item>
        <item>
            <title>No evidence for association of inherited variation in genes involved in mitosis and percent mammographic density</title>
            <link>http://www.medworm.com/index.php?rid=5571844&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR7</link>
            <description>We examined the association of inherited variation in genes from pathways that mediate cell division with percent mammographic density (PMD) adjusted for age, body mass index (BMI) and postmenopausal hormones, in two studies of healthy postmenopausal women.
Methods:
We investigated 2058 single nucleotide polymorphisms (SNPs) in 378 genes involved in regulation of mitosis for associations with adjusted PMD among 484 unaffected postmenopausal controls (without breast cancer) from the Mayo Clinic Breast Cancer Study (MCBCS) and replicated the findings in postmenopausal controls (n=726) from the Singapore and Sweden Breast Cancer Study (SASBAC) study. PMD was assessed in both studies by a computer-thresholding method (Cumulus) and linear regression approaches were used to assess the associatio...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571844</comments>
            <pubDate>Sat, 07 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5571844</guid>        </item>
        <item>
            <title>Hyperinsulinemia enhances c-Myc-mediated mammary tumor development and advances metastatic progression to the lung in a mouse model of Type 2 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5571843&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR8</link>
            <description>Conclusions:
Hyperinsulinemia in a mouse model promotes breast cancer metastasis to lung. Therapies to reduce insulin levels in hyperinsulinemic patients suffering from breast cancer could lessen the likelihood of metastatic progression. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571843</comments>
            <pubDate>Sat, 07 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5571843</guid>        </item>
        <item>
            <title>Effect of dietary patterns differing in carbohydrate and fat content on blood lipid and glucose profiles based on weight loss success of breast cancer survivors</title>
            <link>http://www.medworm.com/index.php?rid=5571850&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR1</link>
            <description>Conclusions:
Since an individual's dietary preferences can impact dietary adherence and weight loss success, the lack of evidence of a negative effect of dietary pattern on biomarkers associated with cardiovascular risk is an important consideration in the development of breast cancer practice guidelines for physicians who recommend that their patients lose weight. Whether dietary pattern affects biomarkers that predict long term survival is a primary question in this ongoing clinical trial. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571850</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5571850</guid>        </item>
        <item>
            <title>Alterations in tumor necrosis factor signaling pathways are associated with cytotoxicity and resistance to taxanes:  a study in isogenic resistant tumor cells</title>
            <link>http://www.medworm.com/index.php?rid=5571849&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR2</link>
            <description>Conclusions:
We report for the first time that taxanes can promote dose-dependent sTNFalpha production in tumour cells at clinically relevant concentrations, which can contribute to their cytotoxicity. Defects in the TNF cytotoxicity pathway or activation of TNF-dependent NF-kappaB survival genes may, in contrast, contribute to taxane resistance in tumour cells. These findings may be of strong clinical significance. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571849</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5571849</guid>        </item>
        <item>
            <title>Prognostic value of proliferation assay in the luminal, HER2 positive and triple negative biological classes of breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5571848&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR3</link>
            <description>Conclusions:
Assessment of proliferation using Ki67LI and MS can distinguish subgroups of patients within luminal/hormone receptor positive breast cancer significantly different in clinical outcomes. Overall, both Ki67LI and mitotic count scores showed comparable results. The methodology described could provide a cost effective method for prognostic sub-classification of luminal/hormone receptor positive breast cancer in routine clinical practice. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571848</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5571848</guid>        </item>
        <item>
            <title>Evidence that GTP-binding domain but not catalytic domain of transglutaminase 2 is essential for epithelial-to-mesenchymal transition in mammary epithelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5571847&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR4</link>
            <description>Conclusions:
Our results suggest that transamidation activity of TG2 is not essential for promoting its oncogenic functions and provide strong rationale for developing small molecule inhibitors to block GTP-binding pockets of TG2. Such inhibitors may have great potential for inhibiting the TG2-regulated pathways and for reversing drug resistance and inhibiting metastasis of cancer cells. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571847</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5571847</guid>        </item>
        <item>
            <title>Breast cancer incidence and case fatality among 4.7 million women in relation to social and ethnic background: a population-based cohort study</title>
            <link>http://www.medworm.com/index.php?rid=5571846&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F14%2F1%2FR5</link>
            <description>Conclusions:
Disparities found in case fatality among immigrants by age, duration of residence, age at immigration and country of birth emphasize the importance of targeting interventions on women that are not likely to attend screening or are not likely to adhere to the therapy suggested by physicians. The lower risk of breast cancer amongst immigrant women calls for more knowledge about how the lifestyle factors in these women differ from those with high risk, so that preventative measures may be implemented. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571846</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5571846</guid>        </item>
        <item>
            <title>Long-term prognosis of breast cancer detected by mammography
screening or other methods</title>
            <link>http://www.medworm.com/index.php?rid=5551876&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR134</link>
            <description>Patients with breast cancer detected in mammography screening have a more favorable prognosis than those diagnosed outside a screening program and this should be taken into account in order to avoid over-treatment of screen-detected patients. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5551876</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5551876</guid>        </item>
        <item>
            <title>Lack of EGFR activating mutations in European patients with triple negative breast cancer could emphasize geographic and ethnic variations in breast cancer mutation profiles</title>
            <link>http://www.medworm.com/index.php?rid=5537373&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR133</link>
            <description>Potential geographic and ethnic variations in the prevalence of EGFR mutations in triple negative breast cancer have implications for clinical trial design for anti-estrogen growth factor receptor (EGFR) therapies. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537373</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537373</guid>        </item>
        <item>
            <title>A genome-wide linkage study of mammographic density, a risk factor for breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5523979&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR132</link>
            <description>Conclusions:
The suggestive peaks and the larger linkage signal seen in the subset of pedigrees with younger participants highlight regions of interest for further study to identify genes that determine MD with the goal to understand mammographic density and its involvement in susceptibility to breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5523979</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5523979</guid>        </item>
        <item>
            <title>A novel inhibitor of fatty acid synthase shows activity against HER2+ breast cancer xenografts and is active in anti-HER2 drug-resistant cell lines</title>
            <link>http://www.medworm.com/index.php?rid=5514964&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR131</link>
            <description>Conclusions:
G28UCM inhibits FASN activity and the growth of breast carcinoma xenografts in vivo, and is active in cells with acquired resistance to anti-HER2 drugs, which make it a candidate for further pre-clinical development. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514964</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514964</guid>        </item>
        <item>
            <title>Variants on the promoter region of PTEN affect breast cancer progression and patient survival</title>
            <link>http://www.medworm.com/index.php?rid=5504235&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR130</link>
            <description>Conclusions:
Inherited variation in the PTEN promoter region affects the tumor progression and gene expression profile in breast cancer. Further studies are warranted to establish PTEN promoter variants as clinical markers for prognosis in breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5504235</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5504235</guid>        </item>
        <item>
            <title>Landscape of somatic allelic imbalances and copy number alterations in HER2-amplified breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5504236&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR129</link>
            <description>IntroductionHER2-amplified breast cancer represents a clinically well-defined subgroup due to availability of targeted treatment. However, HER2-amplified tumors have been shown to be heterogeneous at the genomic level by genome-wide microarray analyses, pointing towards a need of further investigations for identification of recurrent copy number alterations and delineation of patterns of allelic imbalance.
Methods:
High-density whole genome array-based comparative genomic hybridisation (aCGH) and SNP array data from 260 HER2-amplified breast tumors or cell lines, and 346 HER2-negative breast cancers with molecular subtype information were assembled from different repositories. Copy number alteration (CNA), loss-of-heterozygosity (LOH), copy number neutral allelic imbalance (CNN-AI), subclo...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5504236</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5504236</guid>        </item>
        <item>
            <title>Regulation of Breast Cancer Metastasis by Runx2 and Estrogen Signaling: Role of SNAI2.</title>
            <link>http://www.medworm.com/index.php?rid=5486272&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR127</link>
            <description>Conclusions:
E2 antagonizes Runx2-induced EMT and invasiveness of BCa cells, partly through attenuating expression of SNAI2, a Runx2 target required for mediating its pro-metastatic property. That ERalpha loss promotes non-osseous metastasis by unleashing Runx2/SNAI2 is supported by negative correlation observed in corresponding tumors. Unknown mechanisms in bone-seeking BCa allow high Runx2/SNAI2 expression despite high ERalpha levels. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486272</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5486272</guid>        </item>
        <item>
            <title>Opposing roles of CXCR4 and CXCR7 in breast cancer metastasis</title>
            <link>http://www.medworm.com/index.php?rid=5486271&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR128</link>
            <description>Conclusions:
We find that CXCR4 and CXCR7 play different roles in metastasis, with CXCR4 mediating breast cancer invasion and CXCR7 impairing invasion but enhancing primary tumor growth through angiogenesis. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486271</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5486271</guid>        </item>
        <item>
            <title>Tumor infiltrating lymphocytes predict response to anthracycline-based chemotherapy in estrogen receptor-negative breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5486275&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR126</link>
            <description>IntroductionInfiltration of breast tumors by lymphocytes (TIL) has been linked to sensitivity to anthracycline-based chemotherapy. However, it is unclear if this is true within the estrogen receptor alpha negative (ER-) subset of breast tumors that manifest relatively high inherent TIL levels.
Methods:
The association of TIL with short-term and long-term clinical response to anthracycline-based therapy was assessed in two independent ER- breast cancer cohorts in which patients were categorized as TIL-high or TIL-low. We defined an 8-gene lymphocyte mRNA expression signature (including CD19, CD3D, CD48, GZMB, LCK, MS4A1, PRF1, and SELL) and used unsupervised hierarchical clustering to examine the association between TIL and short-term response to neoadjuvant chemotherapy in a previously pub...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486275</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5486275</guid>        </item>
        <item>
            <title>'Omic approaches to preventing or managing metastatic breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5486274&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F230</link>
            <description>Early detection of metastasis prone breast cancers and characterization of residual metastatic cancers are important in efforts to improve management of breast cancer. Applications of genome scale molecular analysis technologies are making these complementary approaches possible by revealing molecular features uniquely associated with metastatic disease. Assays that reveal these molecular features will facilitate development of anatomic, histological and blood based strategies that may enable detection prior to metastatic spread. Knowledge of these features also will guide development of therapeutic strategies that can be applied when metastatic disease burden is low thereby increasing the probability of a curative response. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486274</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5486274</guid>        </item>
        <item>
            <title>New insights into the role of AR and ER in molecular apocrine breast tumours</title>
            <link>http://www.medworm.com/index.php?rid=5486273&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F318</link>
            <description>Two recent studies on a rare androgen-dependent form of breast cancer have shed light on the biology of luminal tumours and reinforced the view that interfering with androgen signalling may have a place in the therapy of some forms of breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486273</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5486273</guid>        </item>
        <item>
            <title>Activator protein 1 (AP-1) contributes to EpCAM-dependent breast cancer invasion</title>
            <link>http://www.medworm.com/index.php?rid=5468331&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR124</link>
            <description>Conclusion:
These data demonstrate for the first time that EpCAM expression can influence the JNK/AP-1 signal transduction pathway, and suggest that modulation of AP-1 transcription factor activity contributes to EpCAM-dependent breast cancer invasion. These data have important implications for the design and application of molecular therapies targeting EpCAM. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5468331</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5468331</guid>        </item>
        <item>
            <title>Phosphatidylinositol 3-kinase (PI3K) pathway activation in breast cancer brain metastases</title>
            <link>http://www.medworm.com/index.php?rid=5468330&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR125</link>
            <description>Conclusions:
The PI3K pathway is active in most BCBM regardless of subtype. Inhibition of this pathway represents a promising therapeutic strategy for patients with BCBM, a group of patients with poor prognosis and limited systemic therapeutic options. While expression of the PI3K pathway did not correlate with OS and survival following BCBM, PTEN- association with time to recurrence and OS (among patients with TNBC) is worthy of further study. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5468330</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5468330</guid>        </item>
        <item>
            <title>Advantages of adjuvant chemotherapy for patients with triple-negative breast cancer at stage II: usefulness of prognostic markers E-cadherin and Ki67</title>
            <link>http://www.medworm.com/index.php?rid=5468335&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR122</link>
            <description>IntroductionTriple-negative breast cancer (TNBC), which is characterized by negativity for estrogen receptor, progesterone receptor, and HER2, is a high risk breast cancer that lacks specific targets for treatment selection. Chemotherapy is therefore the primary systemic modality used in the treatment of this disease, but reliable parameters to predict the chemosensitivity of TNBC have not been clinically available.
Methods:
A total of 190 TNBC patients who had undergone a curative resection of a primary breast cancer were enrolled. The adjuvant chemotherapy was performed for 138 (73%) of 190 TNBC cases; 60 cases had an anthracyclin-based regimen and 78 a 5-fluorouracil-based regimen. The prognostic value of E-cadherin, Ki67, and p53 expression in the outcome of TNBC patients with adjuvant...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5468335</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5468335</guid>        </item>
        <item>
            <title>Anti-tumor activity and toxicokinetics analysis of MGAH22, an anti-HER2 monoclonal antibody with enhanced Fc-gamma receptor binding properties</title>
            <link>http://www.medworm.com/index.php?rid=5468334&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR123</link>
            <description>Conclusions:
The data support the clinical development of MGAH22, which may have utility in patients with low HER2 expressing tumors or carrying the CD16A low-binding allele. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5468334</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5468334</guid>        </item>
        <item>
            <title>Luminal B breast cancer and novel therapeutic targets</title>
            <link>http://www.medworm.com/index.php?rid=5468333&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F221</link>
            <description>Gene expression profiling has led to a new molecular classification of breast cancer characterized by four intrinsic subtypes: basal-like; erbB2/HER2-positive; luminal-A; and luminal-B. Despite expressing estrogen receptor, the luminal-B subtype confers increased risk of early relapse with endocrine therapy compared to luminal-A. Although luminal-B definitions vary, the hallmark appears to be increased expression of proliferation-related genes. Several biological pathways are identified as possible contributors to the poor outcomes and novel agents targeting these pathways are being developed with aims to improve survival.  We review the definition of luminal-B breast cancer, its pathological and clinical features and potential targets for treatment. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5468333</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5468333</guid>        </item>
        <item>
            <title>beta1 integrins signaling and mammary tumor progression in transgenic mouse models: implications for human breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5468332&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F229</link>
            <description>Consistent with their essential role in cell adhesion to the extracellular matrix, integrins and their associated signaling pathways have been shown to be involved in cell proliferation, migration, invasion and survival, processes required in both tumorigenesis and metastasis. beta1 integrins represent the predominantly expressed integrins in mammary epithelial cells and have been proven to be crucial for mammary gland development and differentiation. Here we provide an overview of the studies that have used transgenic mouse models of mammary tumorigenesis to establish beta1 integrin as a critical mediator of breast cancer progression and thereby as a potential therapeutic target for the development of new anticancer strategies (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5468332</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5468332</guid>        </item>
        <item>
            <title>Different mechanisms for resistance to trastuzumab versus lapatinib in HER2-positive breast cancers - role of estrogen receptor and HER2 reactivation</title>
            <link>http://www.medworm.com/index.php?rid=5468337&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR121</link>
            <description>Combined lapatinib and trastuzumab therapy may improve outcomes in patients with human epidermal growth factor 2 (HER2)-positive breast cancer; adding estrogen receptor inhibition may be optimal in some patients. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5468337</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5468337</guid>        </item>
        <item>
            <title>Cancer's sweet tooth for serine</title>
            <link>http://www.medworm.com/index.php?rid=5468336&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F317</link>
            <description>Exemplified by the cancer cell's preference for glycolysis (the Warburg effect), altered metabolism has taken center stage as an emerging hallmark of cancer. Charting the landscape of cancer metabolic addictions should reveal new avenues for therapeutic attack. Two recent studies found subsets of human melanoma and breast cancers to have high levels of phopsoglycerate dehydrogenase (PHGDH), a key enzyme for serine biosynthesis, and these cancer cells are dependent on PHGDH for their growth and survival. Thus tumors may harbor distinct metabolic alterations to support their malignancy and targeting enzymes such as PHGDH might prove a viable therapeutic strategy in this scenario. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5468336</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5468336</guid>        </item>
        <item>
            <title>CHEK2 germline mutation contribution to hereditary breast cancer in non-BRCA-mutated families</title>
            <link>http://www.medworm.com/index.php?rid=5440242&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR119</link>
            <description>Conclusion:
Our work indicates that a variety of deleterious CHEK2 alleles make an appreciable contribution to breast cancer susceptibility, and their identification could help the clinical management of patients carrying a CHEK2 mutation. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440242</comments>
            <pubDate>Thu, 24 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440242</guid>        </item>
        <item>
            <title>Targeting cholesterol-rich microdomains to circumvent tamoxifen-resistant breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5440241&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR120</link>
            <description>Conclusions:
Data for the first time document that targeting cholesterol rich lipid microdomains is a potential strategy to circumvent TAMR and combination of alpha-TEA + TAM can circumvent TAMR by suppression of pro-survival signaling via disruption of cholesterol rich lipid microdomains and activation of apoptotic pathways via induction of endoplasmic reticulum stress. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440241</comments>
            <pubDate>Thu, 24 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440241</guid>        </item>
        <item>
            <title>MicroRNA 34b as a tumor suppressor in estrogen-dependent growth of breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5440245&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR116</link>
            <description>Conclusions:
These findings reveal miR-34b as an onco-suppressor microRNA requiring both ER-positive and wild-type p53 phenotypes in breast cancer cells. These results improve our knowledge for developing new therapeutic strategies to target the complex estrogenic pathway in human breast cancer progression through microRNA regulation. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440245</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440245</guid>        </item>
        <item>
            <title>A different immunologic profile characterizes patients with HER-2-overexpressing  and  HER-2-negative locally advanced breast cancer: implications for immune-based therapies</title>
            <link>http://www.medworm.com/index.php?rid=5440244&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR117</link>
            <description>Conclusions:
Compared to HER2- cases, patients with HER2-overexpressing locally advanced breast cancer show a more limited tumor-related immune suppression. This may account for the clinical benefit achieved in this subset of patients with the use of drugs acting through, but also promoting, immune-mediated effects. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440244</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440244</guid>        </item>
        <item>
            <title>Cancer stem cell markers in breast cancer: pathological, clinical and prognostic significance</title>
            <link>http://www.medworm.com/index.php?rid=5440243&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR118</link>
            <description>Conclusion:
Breast CSC markers do not identify identical subpopulations in primary tumours. Both ITGA6 and a composite Total CSC score show independent prognostic significance in ER- disease. The use of multiple markers to identify tumours enriched for CSCs has greatest prognostic value. In the absence of more specific markers, we propose that the effective translation of the CSC hypothesis into patient benefit will necessitate the use of a panel of markers to robustly identify tumours enriched for CSCs. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5440243</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5440243</guid>        </item>
        <item>
            <title>Single nucleotide polymorphisms associated with risk for contralateral breast cancer in the Women's Environment, Cancer and Radiation Epidemiology (WECARE) study</title>
            <link>http://www.medworm.com/index.php?rid=5421454&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR114</link>
            <description>Conclusion:
Our results indicate that some common risk variants associated with primary breast cancer also increase risk for contralateral breast cancer, and that these risks vary with the ER status of the first tumor. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421454</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421454</guid>        </item>
        <item>
            <title>Inhibition of cathepsin B activity attenuates extracellular matrix degradation and inflammatory breast cancer invasion</title>
            <link>http://www.medworm.com/index.php?rid=5421453&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR115</link>
            <description>Conclusion:
Our study is the first to show that the proteolytic activity of cathepsin B and its co-expression with caveolin-1 contributes to the aggressiveness of IBC. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421453</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421453</guid>        </item>
        <item>
            <title>Sensitization of epithelial growth factor receptors by nicotine exposure to promote breast cancer cell growth</title>
            <link>http://www.medworm.com/index.php?rid=5406996&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR113</link>
            <description>Conclusion:
Our study reveals the existence of a potential, regulatory network governed by the interaction of nicotine and nAChR that integrates the conventional, mitogenic Src and EGFR signals for breast cancer development. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5406996</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5406996</guid>        </item>
        <item>
            <title>ARTEMIN synergizes with TWIST1 to promote metastasis and poor survival outcome in patients with ER negative mammary carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5384308&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR112</link>
            <description>Conclusions:
ARTN and TWIST1 synergize to produce a worse outcome in ER-MC and combined inhibition of ARTN and Phosphatidylinositol 3-kinase/ protein kinase B (PI3K/AKT) may therefore provide a novel therapeutic strategy in this subtype of mammary carcinoma. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5384308</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5384308</guid>        </item>
        <item>
            <title>Loss of interferon regulatory factor 5 (IRF5) expression in human ductal carcinoma correlates with disease stage and contributes to metastasis</title>
            <link>http://www.medworm.com/index.php?rid=5384309&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR111</link>
            <description>Conclusions:
IRF5 is an important tumor suppressor that regulates multiple cellular processes (i.e. growth, response to DNA damage, and invasion/metastasis) involved in the conversion of normal mammary epithelial cells to tumor epithelial cells with metastatic potential. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5384309</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5384309</guid>        </item>
        <item>
            <title>Common breast cancer susceptibility alleles are associated with tumor subtypes in BRCA1 and BRCA2 mutation carriers: results from the Consortium of Investigators of Modifiers of BRCA1/2.</title>
            <link>http://www.medworm.com/index.php?rid=5384310&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2FR110</link>
            <description>Conclusions:
The associations of the twelve SNPs with risk for BRCA1 and BRCA2 carriers differ by ER-positive or ER-negative breast cancer status. The apparent differences in SNP associations between BRCA1 and BRCA2 carriers, and non-carriers, may be explicable by differences in the prevalence of tumor subtypes. As more risk modifying variants are identified, incorporating these associations into breast cancer subtype-specific risk models may improve clinical management for mutation carriers. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5384310</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5384310</guid>        </item>
        <item>
            <title>The microenvironment in breast cancer progression: biology and implications for treatment</title>
            <link>http://www.medworm.com/index.php?rid=5399994&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F227</link>
            <description>Breast cancer comprises a heterogeneous group of malignancies derived from the ductal epithelium. The microenvironment of these cancers is now recognized as a critical participant in tumor progression and therapeutic responses. Recent data demonstrate significant gene expression and epigenetic alterations in cells composing the microenvironment during disease progression, which can be explored as biomarkers and targets for therapy. Indeed, gene expression signatures derived from tumor stroma have been linked to clinical outcomes. There is increasing interest in translating our current understanding of the tumor microenvironment to the development of novel therapies. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5399994</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5399994</guid>        </item>
        <item>
            <title>Breast cancer: current state and future promise</title>
            <link>http://www.medworm.com/index.php?rid=5384315&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F113</link>
            <description>Over the past 50 years, deaths from cardiovascular disease, stroke and pneumonia have plummeted as a result of new therapies and preventive strategies based upon a detailed understanding of the causes and pathogenesis of these diseases. Over this same period, deaths from cancer have changed relatively little. Consequently, we have now reached a tipping point in history at which deaths from cancer will soon surpass those from cardiovascular disease. In this regard, breast cancer holds the dubious honor of having become the leading cause of cancer mortality among women worldwide. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5384315</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5384315</guid>        </item>
        <item>
            <title>Mammographic density and breast cancer risk: 
current understanding and future prospects</title>
            <link>http://www.medworm.com/index.php?rid=5384314&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F223</link>
            <description>Variations in percent mammographic density (PMD) reflect variations in the amounts of collagen and number of epithelial and non-epithelial cells in the breast. Extensive PMD is associated with a marked increased risk of invasive breast cancer. The PMD phenotype is important in the context of breast cancer prevention because extensive PMD is common in the population, is strongly associated with risk of the disease, and unlike most breast cancer risk factors, can be changed.Work now in progress makes it likely that measurement of PMD will be improved in the near future, and that understanding of the genetics and biological basis of the association of PMD with breast cancer risk will also improve. Future prospects for the application of PMD include mammographic screening, risk prediction in i...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5384314</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5384314</guid>        </item>
        <item>
            <title>Mutations in the PI3K pathway: role in tumor progression and therapeutic implications in breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5384313&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F224</link>
            <description>Mutations in genes that constitute the phosphatidylinositol 3-kinase (PI3K) pathway occur in &gt;70% of breast cancers. Clinical and experimental evidence suggest that PI3K pathway activation promotes resistance to some of the current breast cancer therapies. PI3K is a major signaling hub downstream of HER2 and other receptor tyrosine kinases. PI3K activates AKT, SGK, PDK1, mTOR, and several other molecules involved in cell cycle progression and survival. In ER+ breast cancer cells, PI3K activation promotes estrogen-dependent and -independent ER transcriptional activity which, in turn, may contribute to antiestrogen resistance. Activation of this pathway also confers resistance to HER2-targeted therapies. In experimental models of resistance to antiestrogens and HER2 inhibitors, pharmacologic...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5384313</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5384313</guid>        </item>
        <item>
            <title>Epigenetics in breast cancer - what's new?</title>
            <link>http://www.medworm.com/index.php?rid=5384312&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F225</link>
            <description>Epigenetic changes are critical for development and progression of cancers, including breast cancer. Significant progress has been made in the basic understanding of how various epigenetic changes such as DNA methylation, histone modification, miRNA expression, and higher order chromatin structure affect gene expression. In this review we will focus on methylation and demethylation of histones. While the acetylation of histones has been at the forefront of well-characterized posttranslational modifications of histones, including the development of inhibitors targeting de-acetylating enzymes, the last few years have witnessed a dramatic increase in knowledge of the role of histone methylation/demethylation. This is an exciting and rapidly evolving area of research, with much promise for pot...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5384312</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5384312</guid>        </item>
        <item>
            <title>Breast cancer epithelial-to-mesenchymal transition: examining the functional consequences of plasticity</title>
            <link>http://www.medworm.com/index.php?rid=5384311&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F6%2F226</link>
            <description>The epithelial-to-mesenchymal transition (EMT) is a critical developmental process that has recently come to the forefront of cancer biology. In breast carcinomas, acquisition of a mesenchymal-like phenotype that is reminiscent of an EMT, termed oncogenic EMT, is associated with pro-metastatic properties including increased motility, invasion, anoikis resistance, immunosuppression and cancer stem cell characteristics. This oncogenic EMT is a consequence of cellular plasticity, which allows for interconversion between epithelial and mesenchymal-like states, and is thought to enable tumor cells not only to escape from the primary tumor, but also to colonize a secondary site. Indeed, the plasticity of cancer cells may explain the range of pro-metastatic traits conferred by oncogenic EMT, such...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5384311</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5384311</guid>        </item>
        <item>
            <title>Detection of breast cancer cells using targeted
magnetic nanoparticles and ultra-sensitive magnetic field sensors</title>
            <link>http://www.medworm.com/index.php?rid=5359765&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR108</link>
            <description>Antibody-conjugated magnetic nanoparticles and superconducting quantum interference device sensors may provide a useful, viable and highly-sensitive alternative to mammographic screening in breast tumor cell detection. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359765</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359765</guid>        </item>
        <item>
            <title>MMP-13 stimulates osteoclast differentiation and activation in tumour breast bone metastases.</title>
            <link>http://www.medworm.com/index.php?rid=5359768&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR105</link>
            <description>Conclusions:
These results indicate that within the inflammatory bone microenvironment MMP-13 production was up-regulated in breast tumor cells leading to increased pre-osteoclast differentiation and their subsequent activation. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359768</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359768</guid>        </item>
        <item>
            <title>Metastatic breast cancer cells inhibit osteoblast differentiation through the Runx2/CBFbeta-dependent expression of the Wnt antagonist, Sclerostin.</title>
            <link>http://www.medworm.com/index.php?rid=5359767&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR106</link>
            <description>Conclusion:
This study demonstrates that Runx2 and CBFbeta are required for the expression of genes that mediate the ability of metastatic breast cancer cells to directly modulate both osteoclast and osteoblast function. We also show that Runx2-dependent inhibition of osteoblast differentiation by breast cancer cells is mediated through the Wnt antagonist, sclerostin. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359767</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359767</guid>        </item>
        <item>
            <title>Quantitative copy number analysis by Multiplex Ligation-dependent Probe Amplification (MLPA) of BRCA1-associated breast cancer regions identifies BRCAness</title>
            <link>http://www.medworm.com/index.php?rid=5359766&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR107</link>
            <description>Conclusions:
Since the MLPA assay can identify BRCA1-deficient breast cancer patients, this method could be applied both for clinical genetic testing and as a predictor of treatment benefit. BRCA1-like tumors are highly sensitive to chemotherapy with DNA damaging agents, and most likely to poly ADP ribose polymerase (PARP)-inhibitors. The MLPA assay is rapid and robust, can easily be multiplexed, and works well with DNA derived from paraffin-embedded tissues. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359766</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359766</guid>        </item>
        <item>
            <title>Mammographic density and breast cancer risk: the role of the fat surrounding the fibroglandular tissue</title>
            <link>http://www.medworm.com/index.php?rid=5359770&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR103</link>
            <description>When studying the relationship between breast dense area and breast cancer risk, adjustments for non-dense tissue may give more valid results than adjustment for BMI. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359770</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359770</guid>        </item>
        <item>
            <title>Replacement of E-cadherin by N-cadherin in the mammary gland leads to fibrocystic changes and tumor formation</title>
            <link>http://www.medworm.com/index.php?rid=5359769&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR104</link>
            <description>Conclusions:
Our results demonstrate a possible role for N-cad in the formation of fibrosis and cysts in the mammary gland. Moreover, we show that these lesions precede the development of malignant tumors. Thus, we provide a new mouse model to investigate the molecular mechanisms of fibrocystic mastopathy and the transition from benign to malignant tumors. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359769</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359769</guid>        </item>
        <item>
            <title>Three interrelated themes in current breast cancer research: 
gene addiction, phenotypic plasticity, and cancer stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5346776&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2F216</link>
            <description>Recent efforts to understand breast cancer biology involve three interrelated themes that are founded on a combination of clinical and experimental observations. The central concept is &quot;gene addiction.&quot; The clinical dilemma is the &quot;escape&quot; from gene addiction which is mediated, in part, by phenotypic plasticity as exemplified by epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET). Finally, cancer stem cells (CSC) are now recognized as the basis for minimal residual disease and malignant progression over time. These themes cooperate in breast cancer, as induction of EMT enhances CSC self-renewal, and expression of CSC and EMT markers facilitates tumor cell resistance. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346776</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346776</guid>        </item>
        <item>
            <title>Minimal residual disease and circulating tumor cells in breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5346775&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F%2F</link>
            <description>Tumor cell dissemination in bone marrow or other organs is thought to represent an important step in the metastatic process. The detection of bone marrow disseminated tumor cells is associated with worse outcome in early breast cancer. Moreover, the detection of peripheral blood circulating tumor cells is an adverse prognostic factor in metastatic breast cancer and emerging data suggest that this is also true for early disease. Beyond enumeration, the characterization of these cells has the potential to improve risk assessment, treatment selection/monitoring, the development of novel therapeutic agents and advance our understanding of the biology of metastasis. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346775</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346775</guid>        </item>
        <item>
            <title>Hsp27 participates in the maintenance of breast cancer stem cells through regulation of epithelial-mesenchymal transition and nuclear factor-kappa B</title>
            <link>http://www.medworm.com/index.php?rid=5346778&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR101</link>
            <description>Conclusions:
Our data suggest that Hsp27 regulates EMT process and NF-kappa B activity to contribute the maintenance of BCSCs. Targeting Hsp27 may be considered as a novel strategy in breast cancer therapy. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346778</comments>
            <pubDate>Mon, 24 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346778</guid>        </item>
        <item>
            <title>Pleurocidin-family cationic antimicrobial peptides are cytolytic for breast carcinoma cells and prevent growth of tumor xenografts</title>
            <link>http://www.medworm.com/index.php?rid=5346777&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR102</link>
            <description>Pleurocidin-family cationic antimicrobial peptides are cytotoxic for multiple breast cancer cell lines and prevent growth of tumour xenografts, suggesting the possible use of NRC-03 and NRC-07 as novel anticancer agents. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346777</comments>
            <pubDate>Mon, 24 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346777</guid>        </item>
        <item>
            <title>The combined influence of multiple sex and growth hormones on risk of postmenopausal breast cancer: a nested case-control study</title>
            <link>http://www.medworm.com/index.php?rid=5334964&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR99</link>
            <description>The presence of several sex and growth hormones at high levels increases breast cancer risk particularly for ER+ disease, and this observation should be considered when improving existing risk prediction models. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5334964</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5334964</guid>        </item>
        <item>
            <title>Non-dense mammographic area and risk of breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5334963&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR100</link>
            <description>Higher absolute non-dense area on a mammogram is associated with a decreased risk of breast cancer, suggesting adipose breast tissue may have a protective role against breast carcinogenesis. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5334963</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5334963</guid>        </item>
        <item>
            <title>Prognostic utility of the breast cancer index and comparison to Adjuvant! Online in a clinical case series of early breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5313787&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR98</link>
            <description>Breast Cancer Index is a significant predictor of distant recurrence and breast-cancer specific mortality; Adjuvant! Online was significantly associated with risk of recurrence; and both are significantly predictive of outcome. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313787</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313787</guid>        </item>
        <item>
            <title>The devil is in the methods: lineage tracing, functional screens and sequencing, hormones, tumour-stroma interactions, and expansion of human breast tumours as xenografts</title>
            <link>http://www.medworm.com/index.php?rid=5313786&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2F316</link>
            <description>The meeting of the European Network for Breast Development and Cancer (ENBDC) on &quot;Methods in Mammary Gland Development and Cancer&quot; has become an annual international rendezvous for scientists with interests in the normal and neoplastic breast. The third meeting in this series, held in April-May 2011 in Weggis, Switzerland, focussed on functional screens and sequencing, hormones, lineage tracing, tumor-stroma interactions and the expansion of human breast tumours as xenografts. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313786</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313786</guid>        </item>
        <item>
            <title>The amplifier effect: How Pin1 empowers mutant p53</title>
            <link>http://www.medworm.com/index.php?rid=5313788&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2F315</link>
            <description>P53 mutations occur in 15-20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certainp53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolyl isomerization, a regulatory mechanism intended by evolutionto support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313788</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313788</guid>        </item>
        <item>
            <title>Rats: gnawing through the barriers to understanding genetic susceptibility and breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5303996&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2F112</link>
            <description>Advances in genotyping technology have provided us with a large number of genetic loci associated with cancer susceptibility, however our ability to understand the functional effects of the genetic variants of these loci remains limited. In this issue, Smits and colleagues demonstrate the use of congenic rat strains to discover that the Mcs5a breast cancer susceptibility locus is most likely acting through the immune system, via novel transcriptional regulatory mechanisms. This challenges our conventional thinking of cancer susceptibility and gene regulation pathways, and illustrates the potential for rodent models to help us functionally characterize polymorphisms of cancer associated loci. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5303996</comments>
            <pubDate>Wed, 12 Oct 2011 00:19:17 +0100</pubDate>
            <guid isPermaLink="false">5303996</guid>        </item>
        <item>
            <title>Signal transducer and activator of transcription 5 as a key signalling pathway in normal mammary gland developmental biology and breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5303995&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2F220</link>
            <description>STAT5 consists of two proteins STAT5a/b. In normal mammary gland development STAT5 expression and activity are regulated by a prolactin signalling node including JAK2/Elf5 and EGF signalling networks with contributions from growth hormone, estrogen, progesterone and glucocorticoid signalling pathways. In mammary cancer c-Src and erythropoietin signalling can be added. STAT5 activation levels are impacted by AKT, Caveolin, PIKE-A, Pak1, c-Myb, Stap2, Brk, beta-integrin, Dystroglycan, other STATs and STAT pathway molecules JAK1, Shp-2, and SOCs. TGF-beta can down-regulate prolactin and PTPN9 can down-regulate EGF mediated STAT5 activation. IGF signalling, AKT, RANKL, Cyclin D1, BCL6, HSP90A and HOXA1 lie downstream of STAT5. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5303995</comments>
            <pubDate>Wed, 12 Oct 2011 00:19:17 +0100</pubDate>
            <guid isPermaLink="false">5303995</guid>        </item>
        <item>
            <title>A clinically relevant gene signature in triple negative and basal-like breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5296498&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR97</link>
            <description>IntroductionCurrent prognostic gene expression profiles for breast cancer mainly reflect proliferation status and are most useful in ER-positive cancers. Triple negative breast cancers (TNBC) are clinically heterogeneous and prognostic markers and biology-based therapies are needed to better treat this disease.
Methods:
We assembled Affymetrix gene expression data for 579 TNBC and performed unsupervised analysis to define metagenes that distinguish molecular subsets within TNBC. We used n=394 cases for discovery and n=185 cases for validation. Sixteen metagenes emerged that identified basal-like, apocrine and claudin-low molecular subtypes, or reflected various non-neoplastic cell populations including immune cells, blood, adipocytes, stroma, angiogenesis and inflammation within the cancer...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5296498</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5296498</guid>        </item>
        <item>
            <title>Transglutaminase 2 facilitates the distant hematogenous metastasis of breast cancer by modulating interleukin-6 in cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5285052&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR96</link>
            <description>Conclusions:
We provide evidences that TG2 is an important link in IL-6-mediated tumor aggressiveness, and that TG2 could be an important mediator of distant metastasis, both in a xenograft animal model and in patients with advanced breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5285052</comments>
            <pubDate>Mon, 03 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5285052</guid>        </item>
        <item>
            <title>Genomic and phenotypic analysis of BRCA2 mutated breast cancers reveals co-occurring changes linked to progression</title>
            <link>http://www.medworm.com/index.php?rid=5273091&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR95</link>
            <description>Conclusions:
The results presented here demonstrate divergent paths of tumor evolution in BRCA2 carriers and that deletion of the wild-type BRCA2 allele together with co-occurring changes at 6q, 11q, and 17q, are important events in progression towards advanced disease. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5273091</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5273091</guid>        </item>
        <item>
            <title>Generation of tumor initiating cells by exogenous delivery of OCT4 Transcription Factor</title>
            <link>http://www.medworm.com/index.php?rid=5260024&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR94</link>
            <description>Conclusions:
Transduction of OCT4 in normal breast preparations lead to the generation of cell lines possessing tumor initiating and colonization capabilities. These cells developed high-grade, poorly differentiated breast carcinomas in nude mice. Genome-wide analysis of OTBCs outlined an embryonic TF circuitry that could be operative in TICs, resulting in up-regulation of oncogenes and loss of tumor suppressive functions. These OTBCs represent a patient-specific model system for the discovery of novel oncogenic targets in claudin-low tumors. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260024</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260024</guid>        </item>
        <item>
            <title>A new gene expression signature, the ClinicoMolecular Triad Classification, may improve prediction and prognostication of breast cancer at the time of diagnosis</title>
            <link>http://www.medworm.com/index.php?rid=5250131&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR92</link>
            <description>Conclusions:
CMTC correlates well with current clinical classification of BCs and has the potential to be easily integrated into routine clinical practice readily. Using FNABs, CMTC can be determined at the time of diagnostic needle biopsies for tumors of all sizes. Using the public databases as the validation cohort in our analyses, CMTC appeared to be able to provide treatment guidance more accurately, could be available in preoperative settings and applicable to all BC types independent of size, receptor and nodal status. The unique oncogenic signaling pathway pattern of each CMTC group may provide guidance to new treatment strategies. Further validation of CMTC will required prospective randomized controlled trials. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5250131</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5250131</guid>        </item>
        <item>
            <title>Breast tumors from CHEK2 1100delC mutation carriers: genomic landscape and clinical implications</title>
            <link>http://www.medworm.com/index.php?rid=5236665&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR90</link>
            <description>Conclusions:
We have shown that copy number aberrations of certain genomic regions are associated with CHEK2 mutation 1100delC. On these regions we have identified potential drivers of CHEK2 1100delC associated tumorigenesis, whose role in cancer progression is worth investigating. Furthermore, poorer survival related to the CHEK2 1100delC gene expression signature highlights pathways that are likely to have a role in the development of metastatic disease in carriers of CHEK2 1100delC mutation. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5236665</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5236665</guid>        </item>
        <item>
            <title>The chemokine receptor CX3CR1 is directly involved in the arrest of breast cancer cells to the skeleton</title>
            <link>http://www.medworm.com/index.php?rid=5236664&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR91</link>
            <description>Conclusions:
We provide compelling evidence that the functional interactions between fractalkine produced by both the endothelial and stromal cells of bone marrow and the CX3CR1 receptor on breast cancer cells are determinant in the arrest and initial lodging needed for skeletal dissemination. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5236664</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5236664</guid>        </item>
        <item>
            <title>Mammary gland specific expression of Brk/PTK6 promotes delayed involution and tumor formation associated with activation of p38 MAPK</title>
            <link>http://www.medworm.com/index.php?rid=5224572&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR89</link>
            <description>Conclusions:
These studies illustrate that forced expression of Brk/PTK6 in non-transformed mammary epithelial cells mediates p38 MAPK phosphorylation and promotes increased cellular survival, delayed involution, and latent tumor formation. Brk expression in human breast tumors may contribute to progression by inducing p38-driven pro-survival signaling pathways. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224572</comments>
            <pubDate>Sat, 17 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224572</guid>        </item>
        <item>
            <title>Suppression of apoptosis inhibitor c-FLIP selectively eliminates breast cancer stem cell activity in response to the anti-cancer agent, TRAIL</title>
            <link>http://www.medworm.com/index.php?rid=5224573&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR88</link>
            <description>Conclusions:
We describe an apoptotic mechanism that selectively and repeatedly removes bCSC activity from breast cancer cell lines and suggest that a combined TRAIL/FLIPi therapy could prevent metastatic disease progression in a broad range of breast cancer subtypes. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224573</comments>
            <pubDate>Wed, 14 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224573</guid>        </item>
        <item>
            <title>Persistent upregulation of U6:SNORD44 small RNA ratio in the serum of breast cancer patients</title>
            <link>http://www.medworm.com/index.php?rid=5224575&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR86</link>
            <description>Conclusions:
Elevated serum U6 levels in breast cancer patients irrespective of disease activity at the time of serum collection suggest a new paradigm in cancer; persistent systemic changes during cancer progression, which result in elevated activity of RNAP-III and/or the stability/release pathways of U6 in non-cancer tissues. Additionally, these results highlight the need for developing standards for normalization between samples in microRNA-related studies for healthy versus cancer and for inter-laboratory reproducibility. Our studies rule out the utility of miR-16, U6 and 5S RNAs for this purpose. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224575</comments>
            <pubDate>Tue, 13 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224575</guid>        </item>
        <item>
            <title>Breast cancer biological subtypes and protein expression predict for the preferential distant metastasis sites: a nationwide cohort study</title>
            <link>http://www.medworm.com/index.php?rid=5224574&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR87</link>
            <description>Conclusions:
Breast tumor biological subtypes have a tendency to give rise to first distant metastases at certain body sites. Several primary tumor proteins were associated with homing of breast cancer cells. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224574</comments>
            <pubDate>Tue, 13 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224574</guid>        </item>
        <item>
            <title>A protective role for BRCA2 at stalled replication forks</title>
            <link>http://www.medworm.com/index.php?rid=5207727&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2F314</link>
            <description>The hereditary breast and ovarian cancer predisposition genes, BRCA1 and BRCA2 account for the lion's share of heritable breast cancer risk in the human population. Loss of function of either gene results in defective homologous recombination (HR) and triggers genomic instability, accelerating breast tumorigenesis. A long-standing hypothesis proposes that BRCA1 and BRCA2 mediate HR following attempted replication across damaged DNA, ensuring error-free processing of the stalled replication fork. A recent paper describes a new replication fork protective function of BRCA2, which appears to collaborate with its HR function to suppress genomic instability. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5207727</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5207727</guid>        </item>
        <item>
            <title>Evaluation of prognostic and predictive value of microtubule associated protein tau in two independent cohorts</title>
            <link>http://www.medworm.com/index.php?rid=5183160&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F5%2FR85</link>
            <description>Conclusions:
Quantitative measurement of MAP-tau expression has prognostic value in both cohorts, with high expression associated with longer TTP and OS. Differences by treatment arm or response rate in low versus high MAP-tau groups were not observed indicating that MAP-tau is not associated with response to taxanes and is not a useful predictive marker for taxane-based chemotherapy. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5183160</comments>
            <pubDate>Thu, 01 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5183160</guid>        </item>
        <item>
            <title>NF-kappaB activation within macrophages leads to an anti-tumor phenotype in a mammary tumor lung metastasis model</title>
            <link>http://www.medworm.com/index.php?rid=5183162&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR83</link>
            <description>Conclusions:
Our results have identified a brief, defined window in which activation of NF-kappaB has significant anti-metastatic effects and inhibition of NF-kappaB results in a worse outcome. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5183162</comments>
            <pubDate>Tue, 30 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5183162</guid>        </item>
        <item>
            <title>beta1 Integrin mediates an alternative survival pathway in breast cancer cells resistant to lapatinib</title>
            <link>http://www.medworm.com/index.php?rid=5183161&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR84</link>
            <description>Conclusions:
Our data suggest that HER2 activity, which is suppressed in resistance involving L but not T alone, dictates whether beta1 mediates an alternative pathway driving resistance. Our findings justify clinical studies investigating the inhibition of beta1 or its downstream signaling moieties as strategies to overcome acquired L and LT resistance. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5183161</comments>
            <pubDate>Tue, 30 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5183161</guid>        </item>
        <item>
            <title>Tribbles homolog 3 denotes a poor prognosis in breast cancer and is involved in hypoxia response</title>
            <link>http://www.medworm.com/index.php?rid=5160833&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR82</link>
            <description>Conclusions:
TRIB3 is independently associated with poor prognosis of breast cancer patients, possibly through its association with tumor cell hypoxia. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5160833</comments>
            <pubDate>Tue, 23 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5160833</guid>        </item>
        <item>
            <title>Targeting bone metastases starting from the preneoplastic niche: home, sweet home</title>
            <link>http://www.medworm.com/index.php?rid=5143003&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2F111</link>
            <description>Metastatic process is multistep coordinated event with an high degree of efficiency. A specific sub-populations of cancer stem cells with tumor-initiating and migratory capacity can selectively migrate towards sites that are able to promote survival, and/or proliferation of metastatic tumor cells through a microenvironment modification. Cross-talking between bone microenvironment and cancers cells can facilitate bone tropism of cancers cells.Understanding deeply this complexity represent a major challenge in anti-cancer research and a mandatory step towards the development of new drugs potentially able not only to reduce the consequences of bone lesions but also to target metastatic process in visceral sites. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143003</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143003</guid>        </item>
        <item>
            <title>Vitamin D and breast cancer: interpreting current evidence</title>
            <link>http://www.medworm.com/index.php?rid=5143002&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2F217</link>
            <description>Preclinical investigations and selected clinical observational studies support an association between higher vitamin D intake and 25-hydroxyvitamin D levels with lower breast cancer risk. However, the recently updated report from the Institute of Medicine concluded that, for cancer and vitamin D, the evidence was &quot;inconsistent and insufficient to inform nutritional requirements&quot;. Against this background, reports examining vitamin D intake, 25-hydroxyvitamin D levels and breast cancer incidence and outcome were reviewed. Current evidence supports pursuit of several research questions but not routine 25-hydroxyvitamin D monitoring and vitamin D supplementation to reduce breast cancer incidence or improve breast cancer outcome. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143002</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143002</guid>        </item>
        <item>
            <title>Poly(ADP-ribose) polymerase inhibition: a new direction for BRCA and triple-negative breast cancer?</title>
            <link>http://www.medworm.com/index.php?rid=5143001&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2F218</link>
            <description>Inhibitors of poly(ADP-ribose) polymerase mediated DNA repair have shown promise in early clinical studies in the treatment of specific subgroups of breast cancer. Notably, phase II trials indicate that olaparib, an oral PARP inhibitor, has activity as a single agent in BRCA-related tumours, and that a combination of iniparib, an intravenous PARP inhibitor, and chemotherapy offers a survival advantage, compared with chemotherapy alone, in triple-negative breast cancer. Phase III data on the latter indication are expected in 2011. Intriguingly, iniparib does not increase toxicity when used as a chemo-potentiating agent, suggesting that it differs in its mechanism of action from other agents in this class. Overall PARP inhibitors represent a potentially important new class of anti-cancer age...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143001</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143001</guid>        </item>
        <item>
            <title>The 'alternative' EMT switch</title>
            <link>http://www.medworm.com/index.php?rid=5143000&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2F313</link>
            <description>Epithelial to mesenchymal transition (EMT) is an essential process in embryonic development and is aberrantly induced in many disease settings. Work carried out by Chonghui Cheng's lab addressed the involvement of alternative RNA splicing in EMT and its link to tumour progression. They describe a switch in CD44 expression from variant isoform(s) to the standard isoform and showed, for the first time, that this is required for normal epithelial cells to undergo EMT. In addition, they link expression of the CD44 standard isoform to activation of the PI3K/Akt pathway and apoptosis resistance in a mouse model of recurrent disease and with high grade human breast cancer samples. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143000</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5143000</guid>        </item>
        <item>
            <title>Estrogen receptor degradation: a CUE for endocrine resistance?</title>
            <link>http://www.medworm.com/index.php?rid=5142999&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2F312</link>
            <description>Despite the undoubted success of adjuvant endocrine therapies that target the estrogen receptor pathway, not all women with estrogen receptor-positive breast cancer respond to these therapies, and many who initially respond will subsequently relapse. Deregulation of various aspects of estrogen receptor signaling has been highlighted as a mechanism of resistance and as a basis for alternative therapeutic approaches. However, a recent publication refocuses attention on the estrogen receptor itself by showing that the ubiquitin-binding CUE domain-containing protein 2 is a regulator of estrogen receptor protein degradation and a marker of endocrine resistance in breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142999</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142999</guid>        </item>
        <item>
            <title>The non-protein coding breast cancer susceptibility locus Mcs5a acts in a non-mammary cell-autonomous fashion through the immune system and modulates T-cell homeostasis and functions</title>
            <link>http://www.medworm.com/index.php?rid=5131613&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR81</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5131613</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5131613</guid>        </item>
        <item>
            <title>Identification of germline alterations of the mad homology 2 domain of SMAD3 and SMAD4 from the Ontario site of the breast cancer family registry (CFR)</title>
            <link>http://www.medworm.com/index.php?rid=5119588&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR77</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119588</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119588</guid>        </item>
        <item>
            <title>Dietary fat increases solid tumor growth and metastasis of 4T1 murine mammary carcinoma cells, and mortality in obesity-resistant BALB/c mice</title>
            <link>http://www.medworm.com/index.php?rid=5119587&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR78</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119587</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119587</guid>        </item>
        <item>
            <title>Transcriptome analysis of embryonic mammary cells reveals insights into mammary lineage establishment</title>
            <link>http://www.medworm.com/index.php?rid=5119586&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR79</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119586</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119586</guid>        </item>
        <item>
            <title>Roscovitine confers tumor suppressive effect on therapy-resistant breast tumor cells</title>
            <link>http://www.medworm.com/index.php?rid=5119585&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR80</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119585</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119585</guid>        </item>
        <item>
            <title>Analysis of EpCAM positive cells isolated from sentinel lymph nodes of breast cancer patients identifies subpopulations of cells with distinct transcription profiles</title>
            <link>http://www.medworm.com/index.php?rid=5096419&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR75</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5096419</comments>
            <pubDate>Wed, 03 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5096419</guid>        </item>
        <item>
            <title>Serum 25-hydroxyvitamin D and postmenopausal breast cancer survival: a prospective patient cohort study</title>
            <link>http://www.medworm.com/index.php?rid=5069946&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR74</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5069946</comments>
            <pubDate>Mon, 25 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5069946</guid>        </item>
        <item>
            <title>NF-kappa B, stem cells and breast cancer: the links get stronger</title>
            <link>http://www.medworm.com/index.php?rid=5063224&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2F214</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5063224</comments>
            <pubDate>Mon, 25 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5063224</guid>        </item>
        <item>
            <title>Rare variants in the ATM gene and risk of breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5063225&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR73</link>
            <description>${item.shortDescription} (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5063225</comments>
            <pubDate>Sun, 24 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5063225</guid>        </item>
        <item>
            <title>Allele-Specific regulation of FGFR2 expression is cell type-dependent and may increase breast cancer risk through a paracrine stimulus involving FGF10</title>
            <link>http://www.medworm.com/index.php?rid=5037897&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR72</link>
            <description>Conclusions:
The influence of rs2981578 genotypes on FGFR2 mRNA expression levels is cell type-dependent. Expression differences correlated well with signaling levels of the FGFR2 pathway. Our results suggest that the increased breast cancer risk associated with SNP rs2981578 is due to increased FGFR2 signaling activity in stromal fibroblasts, possibly also involving paracrine FGF10 signaling. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5037897</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5037897</guid>        </item>
        <item>
            <title>Correction: An integration of complementary strategies for gene-expression analysis to reveal novel therapeutic opportunities for breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5019927&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2F406</link>
            <description>Blank (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019927</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019927</guid>        </item>
        <item>
            <title>Prospective evaluation of serum tissue inhibitor of metalloproteinase 1 and carbonic anhydrase IX in correlation to circulating tumor cells in patients with metastatic breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5019928&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2FR71</link>
            <description>IntroductionCirculating tumor cells (CTCs) reflect aggressive tumor behavior by hematogenous tumor cell dissemination. The tissue inhibitor of metalloproteinase 1 (TIMP-1) plays a role in tissue invasion and is also involved in angiogenesis, abrogation of apoptosis and in chemoresistance. Carbonic anhydrase IX (CAIX) is a metalloenzyme involved in cell adhesion, growth and survival of tumor cells. The aim of the study was to investigate whether serum concentrations of TIMP-1 and CAIX are associated with the detection of CTC in metastatic breast cancer.
Methods:
Blood was obtained in a prospective multicenter setting from 253 patients with metastatic breast cancer at the time of disease progression. Serum TIMP-1 and CAIX were determined using commercial ELISA-kits (Oncogene Science). CTC we...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019928</comments>
            <pubDate>Sun, 10 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019928</guid>        </item>
        <item>
            <title>Understanding the prognostic value of stromal caveolin-1 as a marker of a lethal tumor microenvironment</title>
            <link>http://www.medworm.com/index.php?rid=5009388&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F4%2F213</link>
            <description>Cancer cells show a broad spectrum of bioenergetic states, with some cells using aerobic glycolysis, while others relying on oxidative phosphorylation as their main source of energy. In addition, there is mounting evidence that metabolic coupling occurs in aggressive tumors, between epithelial cancer cells and the stromal compartment, and between well-oxygenated and hypoxic compartments. We recently showed that oxidative stress in the tumor stroma, due to aerobic glycolysis and mitochondrial dysfunction, is important for cancer cell mutagenesis and tumor progression. More specifically, increased autophagy/mitophagy in the tumor stroma and conversely decreased autophagy in the epithelial compartment, drives a form of parasitic epithelial-stromal metabolic coupling. These findings also expla...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5009388</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5009388</guid>        </item>
        <item>
            <title>Correction: Functional magnetic resonance: biomarkers of response in breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=4985403&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F405</link>
            <description>Upon publication of our article [1], we noticed that the wrong figure had been uploaded for figure 6a. The figure as it should appear can be found overleaf. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4985403</comments>
            <pubDate>Wed, 29 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4985403</guid>        </item>
        <item>
            <title>Reversal of endocrine resistance in breast cancer: interrelationships among 14-3-3zeta, FOXM1, and a gene signature associated with mitosis</title>
            <link>http://www.medworm.com/index.php?rid=4977224&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR70</link>
            <description>Conclusions:
This study reveals that 14-3-3zeta is a key predictive marker for risk of failure on endocrine therapy and serves a pivotal role impacting growth factor signaling, and promoting cell survival and resistance to endocrine therapies. Targeting 14-3-3zeta and its coregulated proteins, such as FOXM1, should prove valuable in restoring endocrine sensitivity and reducing risk of breast cancer recurrence. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4977224</comments>
            <pubDate>Tue, 28 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4977224</guid>        </item>
        <item>
            <title>Microarrays in the 2010s: the contribution of microarray-based gene expression profiling to breast cancer classification, prognostication and prediction</title>
            <link>http://www.medworm.com/index.php?rid=4969766&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F212</link>
            <description>Breast cancer comprises a collection of diseases with distinctive clinical, histopathological and molecular levels features. Importantly, tumours with similar histological features may display disparate clinical behaviours. Gene expression profiling using microarray technologies has improved our understanding of breast cancer biology, and has led to the development of a breast cancer molecular taxonomy and of multigene signatures to predict outcome and response to systemic therapies. The use of these prognostic and predictive signatures in routine clinical decision-making remains controversial. Here, we review the clinical relevance of microarray-based profiling of breast cancer and discuss its impact on patient management. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4969766</comments>
            <pubDate>Sun, 26 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4969766</guid>        </item>
        <item>
            <title>Correction: An integration of complementary strategies for gene-expression analysis to reveal novel therapeutic opportunities for breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=4969765&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR69</link>
            <description>Blank (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4969765</comments>
            <pubDate>Sun, 26 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4969765</guid>        </item>
        <item>
            <title>Correction: Functional magnetic resonance: biomarkers of response in breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=4969764&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR70</link>
            <description>Upon publication of our article [1], we noticed that the wrong figure had been uploaded for figure 6a. The figure as it should appear can be found overleaf. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4969764</comments>
            <pubDate>Sun, 26 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4969764</guid>        </item>
        <item>
            <title>Impact of established prognostic factors and molecular subtype in very young breast cancer patients: pooled analysis of four EORTC randomized controlled trials</title>
            <link>http://www.medworm.com/index.php?rid=4969767&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR68</link>
            <description>Conclusions:
Molecular subtype is a strong independent prognostic factor in breast cancer patients younger than 40 years of age. These data support the use of established prognostic factors as a diagnostic tool to assess disease outcome and to plan systemic treatment strategies in young breast cancer patients. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4969767</comments>
            <pubDate>Thu, 23 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4969767</guid>        </item>
        <item>
            <title>Circulating tumor cells as prognostic and predictive markers in metastatic breast cancer patients receiving first-line systemic treatment</title>
            <link>http://www.medworm.com/index.php?rid=4969768&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR67</link>
            <description>IntroductionCirculating tumor cells (CTCs) represent an independent predictor of outcome in patients with metastatic breast cancer (MBC). We assessed the prognostic impact of CTCs according to different first-line systemic treatments, and explored their potential predictive value in MBC patients.
Methods:
We retrospectively evaluated 235 newly diagnosed MBC patients, treated at the University of Texas MD Anderson Cancer Center. All patients had a baseline CTC assessment performed with CellSearch(R). Progression-free survival (PFS) and overall survival (OS) were compared with Log-Rank test between groups, according to CTC count ( (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4969768</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4969768</guid>        </item>
        <item>
            <title>Sunitinib inhibits lymphatic endothelial cell functions and lymph node metastasis in a breast cancer model through inhibition of vascular endothelial growth factor receptor 3</title>
            <link>http://www.medworm.com/index.php?rid=4954056&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR66</link>
            <description>Conclusions:
The results suggest that sunitinib might be beneficial for the treatment of breast cancer by suppressing lymphangiogenesis and lymph node metastasis, through inhibition, particularly importantly, of VEGFR-3. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4954056</comments>
            <pubDate>Mon, 20 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4954056</guid>        </item>
        <item>
            <title>Cardiovascular disease competes with breast cancer as the leading cause of death for older females diagnosed with breast cancer: a retrospective cohort study</title>
            <link>http://www.medworm.com/index.php?rid=4946238&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR64</link>
            <description>Conclusions:
Comorbid conditions contribute importantly to both total mortality and breast cancer-specific mortality among breast cancer survivors. Attention to reducing the risk of cardiovascular disease should be a priority for the long-term care of women following diagnosis and treatment of breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4946238</comments>
            <pubDate>Sun, 19 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4946238</guid>        </item>
        <item>
            <title>Stat3 and CCAAT/enhancer binding protein beta (C/EBP-beta) regulate Jab1/CSN5 expression in mammary carcinoma cells</title>
            <link>http://www.medworm.com/index.php?rid=4946237&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR65</link>
            <description>Conclusions:
These findings reveal a novel mechanism of Jab1 gene regulation and provide functional and mechanistic links between the Src/Stat3 and IL-6/Stat3 signaling axes that are involved in the activation of Jab1 transcription and regulation of this novel oncogenic protein. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4946237</comments>
            <pubDate>Sun, 19 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4946237</guid>        </item>
        <item>
            <title>Notch-1 and Notch-4 are Novel Gene Targets of PEA3 in Breast Cancer: Novel Therapeutic Implications</title>
            <link>http://www.medworm.com/index.php?rid=4936063&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR63</link>
            <description>Conclusions:
Taken together, results from this study demonstrate for the first time that Notch-1 and Notch-4 are novel transcriptional targets of PEA3 in breast cancer cells. Targeting of PEA3 and/or Notch pathways might provide a new therapeutic strategy for triple-negative and possibly other breast cancer subtypes. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4936063</comments>
            <pubDate>Wed, 15 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4936063</guid>        </item>
        <item>
            <title>The prognostic significance of tumor cell detection in the peripheral blood versus the bone marrow in 733 early-stage breast cancer patients</title>
            <link>http://www.medworm.com/index.php?rid=4936065&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR61</link>
            <description>IntroductionThe detection of circulating tumor cells (CTCs) in the peripheral blood and disseminated tumor cells (DTCs) in the bone marrow are promising prognostic tools for risk stratification in early breast cancer. There is however a need for further validation of these techniques in larger patient cohorts with adequate follow-up periods.
Methods:
We assayed CTCs and DTCs at primary surgery in 733 stage I/II breast cancer patients with a median follow-up time of 7.6 years. CTCs were detected in samples of peripheral blood mononuclear cells previously stored in liquid-nitrogen using a previously-developed multi-marker quantitative PCR (QPCR)-based assay. DTCs were detected in bone marrow samples by immunocytochemical analysis using anti-cytokeratin antibodies.
Results:
CTCs were detected...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4936065</comments>
            <pubDate>Mon, 13 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4936065</guid>        </item>
        <item>
            <title>Analysis of tumor environmental response and oncogenic pathway activation identifies distinct basal and luminal features in HER2-related breast tumor subtypes</title>
            <link>http://www.medworm.com/index.php?rid=4936064&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR62</link>
            <description>Conclusions:
This study demonstrates differences in microenvironmental conditions in HER2 related subgroups defined by distinct oncogenic pathway activities and provides a mechanistic explanation for differences in the observed hypoxia response between these subgroups. Collectively, these data demonstrate the potential of a pathway-based classification strategy as a framework to integrate genetic and non-genetic factors to investigate the basis of tumor heterogeneity. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4936064</comments>
            <pubDate>Mon, 13 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4936064</guid>        </item>
        <item>
            <title>miR-200c at the nexus of epithelial-mesenchymal transition, resistance to apoptosis, and the breast cancer stem cell phenotype</title>
            <link>http://www.medworm.com/index.php?rid=4922990&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F110</link>
            <description>Decreased expression of microRNAs of the miR-200 family has been implicated in the growth and metastasis of breast cancer cells. Of this family, miR-200c has garnered particular attention as a consequence of its ability to target ZEB1 and ZEB2, mediators of epithelial-mesenchymal transition. An article in the current issue of Breast Cancer Research identify additional targets of miR-200c that link increased cancer cell invasiveness, resistance to apoptosis, and induction of breast cancer stem cell characteristics. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922990</comments>
            <pubDate>Thu, 09 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922990</guid>        </item>
        <item>
            <title>Breast cancer growth and metastasis: interplay between cancer stem cells, embryonic signaling pathways and epithelial-to-mesenchymal transition</title>
            <link>http://www.medworm.com/index.php?rid=4913073&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F211</link>
            <description>Induction of epithelial-to-mesenchymal transition (EMT) in cancer stem cells (CSCs) can occur as the result of embryonic pathway signaling. Activation of Hedgehog (Hh), Wnt, Notch, or TGF-beta leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile epithelial-like tumor cells into cells with a mobile, invasive phenotype. To investigate the mechanism of metastatic tumor formation in breast cancer, the CSC hypothesis and EMT are key issues to be studied. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSC and EMT-inducing transcription factors. Understanding these pathways may lead to new opportunities for therapeutic targets to help prevent me...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4913073</comments>
            <pubDate>Thu, 09 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4913073</guid>        </item>
        <item>
            <title>Waking up dormant tumors</title>
            <link>http://www.medworm.com/index.php?rid=4913072&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F310</link>
            <description>As appreciation grows for the contribution of the tumor microenvironment to the progression of cancer, new evidence accumulates to support that the participation of stromal cells can extend beyond the local environment. Recently, Elkabets and colleagues demonstrated a systemic interaction between cancer cells and distant bone marrow cells to support the growth of otherwise indolent tumor cells at a secondary site, raising thought-provoking questions regarding the involvement of stromal cells in maintaining metastatic dormancy. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4913072</comments>
            <pubDate>Thu, 09 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4913072</guid>        </item>
        <item>
            <title>Epithelial-mesenchymal transition markers expressed in circulating tumor cells of early and metastatic breast cancer patients</title>
            <link>http://www.medworm.com/index.php?rid=4913071&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR59</link>
            <description>Conclusions:
CTCs expressing Twist and Vimentin, suggestive of an epithelial-mesenchymal transition, are identified in patients with breast cancer. The high incidence of these cells in patients with metastatic disease compared to early stage breast cancer strongly supports the notion that EMT is involved in the metastatic potential of CTCs. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4913071</comments>
            <pubDate>Thu, 09 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4913071</guid>        </item>
        <item>
            <title>Impact of UGT2B7His268Tyr polymorphism on the outcome of adjuvant epirubicin treatment in breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=4913075&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR57</link>
            <description>Conclusions:
Breast cancer patients carrying the UGT2B7268Tyr/Tyr genotype may benefit most from adjuvant epirubicin-based chemotherapy. These results warrant confirmation in further studies. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4913075</comments>
            <pubDate>Wed, 08 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4913075</guid>        </item>
        <item>
            <title>Chondroitin sulfates play a major role in breast cancer metastasis: a role for CSPG4 and CHST11 gene expression in forming surface P-selectin ligands in aggressive breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=4913074&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR58</link>
            <description>This study was performed to identify the carrier proteoglycan (PG) and the sulfotransferase gene involved in synthesis of the surface P-selectin-reactive CS-GAGs in human breast cancer cells with high metastatic capacity, as well as to determine a direct role for CS-GAGs in metastatic spread.
Methods:
Quantitative real-time PCR (qRT-PCR) and flow cytometry assays were used to detect the expression of genes involved in the sulfation and presentation of chondroitin in several human breast cancer cell lines. Transient transfection of the human breast cancer cell line MDA-MB-231 with the siRNAs for carbohydrate (chondroitin 4) sulfotransferase-11 (CHST11) and chondroitin sulfate proteoglycan 4 (CSPG4 ) was used to investigate the involvement of these genes in expression of surface P-selectin l...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4913074</comments>
            <pubDate>Wed, 08 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4913074</guid>        </item>
        <item>
            <title>Telomerase Expression and Telomere Length in Breast Cancer and their Associations with Adjuvant Treatment and Disease Outcome</title>
            <link>http://www.medworm.com/index.php?rid=4903541&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR56</link>
            <description>Conclusions: Telomerase modified the effect of endocrine therapy on breast cancer survivals, suggesting that telomerase may serve as a marker to guide the selection of adjuvant treatment for breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903541</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903541</guid>        </item>
        <item>
            <title>Elevated pre-treatment levels of plasma C-reactive protein are associated with poor prognosis after breast cancer: a cohort study</title>
            <link>http://www.medworm.com/index.php?rid=4894570&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR55</link>
            <description>We examined whether plasma C-reactive protein (CRP) levels at the time of diagnosis of breast cancer are associated with overall survival, disease-free survival, death from breast cancer, and recurrence of breast cancer.
Methods:
We observed 2,910 women for up to seven years after they were diagnosed with invasive breast cancer (median follow-up time was three years). Plasma levels of high-sensitivity CRP were measured at the time of diagnosis and we assessed the association between CRP levels and risk of reduced overall and disease-free survival, death from breast cancer, and recurrence of breast cancer by using the Kaplan-Meier method and Cox proportional hazards regression. During follow-up, 383 women died (225 of whom died from breast cancer) and 118 women experienced recurrence of bre...</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4894570</comments>
            <pubDate>Thu, 02 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4894570</guid>        </item>
        <item>
            <title>Spotlight on geminin</title>
            <link>http://www.medworm.com/index.php?rid=4884577&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F109</link>
            <description>In the previous issue of Breast Cancer Research, Gardner and co-workers describe a novel interaction between Geminin, a protein that prevents reinitiation of DNA replication, and Topoisomerase IIα (TopoIIα), an enzyme essential for removing catenated intertwines between sister chromatids. Geminin facilitates the action of TopoIIα, thereby promoting termination of DNA replication at the same time it inhibits initiation. In this manner, Geminin ensures that cells duplicate their genome once, but only once, each time they divide. Remarkably, either depletion of Geminin or over-expression of Geminin inhibits the action of TopoIIα, thereby making Geminin an excellent target for cancer chemotherapy. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4884577</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4884577</guid>        </item>
        <item>
            <title>Interpreting Breast International Group (BIG) 1-98: a randomized, double-blind, phase III trial comparing letrozole and tamoxifen as adjuvant endocrine therapy for postmenopausal women with receptor-positive, early breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=4872964&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F209</link>
            <description>The Breast International Group (BIG) 1-98 study is a four-arm trial comparing 5 years of monotherapy with tamoxifen or with letrozole or with sequences of 2 years of one followed by 3 years of the other for postmenopausal women with endocrine-responsive early invasive breast cancer. From 1998 to 2003, BIG -98 enrolled 8,010 women. The enhanced design f the trial enabled two complementary analyses of efficacy and safety. Collection of tumor specimens further enabled treatment comparisons based on tumor biology. Reports of BIG 1-98 should be interpreted in relation to each individual patient as she weighs the costs and benefits of available treatments.Clinicaltrials.gov ID: NCT00004205. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872964</comments>
            <pubDate>Wed, 25 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4872964</guid>        </item>
        <item>
            <title>From Bone to breast and back - the bone cytokine RANKL and breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=4872966&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F107</link>
            <description>Receptor activator of nuclear factor-κB ligand (RANKL) plays a pivotal role in regulating bone homeostasis. Osteoporosis and malignant bone disease secondary to breast cancer are characterized by enhanced RANKL production and increased bone turnover. Thus, denosumab, a monoclonal antibody to RANKL, has been developed and is now approved for various bone loss conditions. Recent results indicate that RANKL may also promote the development and osseous migration of breast cancer. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872966</comments>
            <pubDate>Tue, 24 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4872966</guid>        </item>
        <item>
            <title>Who is in the driver's seat in 8p12 amplifications: ZNF703 in luminal B breast tumors</title>
            <link>http://www.medworm.com/index.php?rid=4872965&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F308</link>
            <description>Two recent reports identify ZNF703 as an oncogene driving selection of frequent chromosome 8p12 amplifications in luminal B breast tumors. The estrogen-responsive ZNF703 gene encodes a transcriptional cofactor that, when overexpressed, induces cell proliferation and interferes with transforming growth factor beta signaling. In MCF7 cells, increased ZNF703 expression results in activation of genes involved in stem cell self-renewal - while in primary human mammary epithelial cells, ZNF703 increases the ratio of luminal to basal progenitors. Expression of the murine homolog of ZNF703 reduces cell adhesion and promotes metastasis. ZNF703 overexpression thus alters regulation of proliferation and differentiation in luminal B tumors. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872965</comments>
            <pubDate>Tue, 24 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4872965</guid>        </item>
        <item>
            <title>Jekyll or Hyde: does Matrigel provide a more or less physiological environment in mammary repopulating assays?</title>
            <link>http://www.medworm.com/index.php?rid=4863652&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F108</link>
            <description>Not applicable (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4863652</comments>
            <pubDate>Tue, 24 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4863652</guid>        </item>
        <item>
            <title>Synergy between trastuzumab and pertuzumab for human epidermal growth factor 2 (Her2) from colocalization: an in silico based mechanism</title>
            <link>http://www.medworm.com/index.php?rid=4853904&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR54</link>
            <description>Conclusions:
If validated, these findings will bring about a new direction in the design of antibodies whereby different epitopes on the same antibody may be targeted to lead to synergistic/cooperative inhibition and contribute to generate more potent therapeutics and to increase clinical efficacy. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4853904</comments>
            <pubDate>Sat, 21 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4853904</guid>        </item>
        <item>
            <title>Endocrine resistance in breast cancer: new roles for ErbB3 and ErbB4.</title>
            <link>http://www.medworm.com/index.php?rid=4842486&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2F106</link>
            <description>Endocrine resistance is a major limitation to the successful treatment of estrogen receptor-positive (ER+) breast cancer and the EGFR and ErbB2 receptor tyrosine kinases are involved in this process. A recent study now implicates the other 2 ErbB family members, ErbB-3 and -4. Exposure of ER+ breast cancer cells to the pure antiestrogen, fulvestrant, increased levels of ErbB-3 or ErbB-4 and sensitivity to the growth stimulatory effects of heregulin beta1, a potent ligand for these receptors. Thus, the initial growth inhibitory effects of fulvestrant appear compromised by cellular plasticity that allows rapid compensatory growth stimulation via ErbB3/4. Further evaluation of pan-erbB receptor inhibitors in endocrine resistant disease appears warranted. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4842486</comments>
            <pubDate>Thu, 19 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4842486</guid>        </item>
        <item>
            <title>Elevated insulin-like growth factor 1 receptor signaling induces anti-estrogen resistance through the MAPK/ERK and PI3K/Akt signaling routes</title>
            <link>http://www.medworm.com/index.php?rid=4842488&amp;cid=s_31084_6_f&amp;fid=31084&amp;url=http%3A%2F%2Fbreast-cancer-research.com%2Fcontent%2F13%2F3%2FR52</link>
            <description>Conclusions:
Our data provide the evidence that the IGF-1/IGF-1R signaling axis may play a causal role in anti-estrogen resistance of breast cancer cells, despite continuous suppression of ER transcriptional function by anti-estrogens. (Source: Breast Cancer Research)</description>
            <author>Breast Cancer Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4842488</comments>
            <pubDate>Wed, 18 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4842488</guid>        </item>
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