Analysis on gene level revealed that a set of 24 genes could clea

Analysis on gene level revealed that a set of 24 genes could clearly discriminate epithelial from mesenchymal cell lines. The identified composite gene expression measure clearly subdivided expression data from clinical samples in 2 groups. Moreover, the composite gene expression measure showed a correlation with the pathological

grade available for the clinical samples. Conclusion: This 24-gene signature revealed that clinical samples consisted of two distinct subpopulations. This suggests that the composite gene measure CBL0137 clinical trial may predict whether a patient biopsy is enriched with epithelial or with mesenchymal cells. It could also give an idea of pathological grade of the sample making this signature a potential biomarker for patient stratification allowing personalized therapy. Poster Selleck SIS 3 No. 125 Loss of R-Cadherin Facilitates Mammary Tumor Progression and Metastasis Rachel Hazan 1 1 Pathology, Albert Einstein College of Medicine, Bronx, NY, USA The mammary epithelium is thought to be stabilized by cell-cell adhesion mediated mainly by E-cadherin. Here we show that another

cadherin, Retinal (R)-cadherin, is critical for maintenance of the epithelial phenotype. R-cadherin is expressed in non-transformed mammary epithelium but absent from tumorigenic cell lines. In vivo, R-cadherin was prominently expressed in the epithelium of both ducts and lobules. In human breast cancer, R-cadherin was downregulated with tumor progression, with high expression in ductal carcinoma in situ and reduced expression in invasive duct carcinomas. By comparison, E-cadherin expression persisted in invasive breast tumors and cell lines where R-cadherin

was lost. Consistent with these findings, R-cadherin knockdown in normal mammary epithelium stimulated invasiveness and disrupted formation of acini despite continued E-cadherin expression. Conversely, R-cadherin overexpression in aggressive cell lines induced glandular morphogenesis and inhibited invasiveness, tumor formation, and lung colonization. R-cadherin also suppressed the MMP1, MMP2, and Cox 2 gene expression, associated with Selleckchem Venetoclax pulmonary metastasis. The data CRISPR/Cas9 activator suggest that R-cadherin is an adhesion molecule of the mammary epithelium that acts as a critical regulator of the normal phenotype. As a result, R-cadherin loss contributes to epithelial suppression and metastatic progression. Poster No. 126 Paradoxical Effect of MUC1/G-TRUNC Expression in Breast Cancer – Metastatic Phenotype Associated with Tumor Abrogation Galit Horn 1,2 , Avital Gaziel1,2, Daniel H. Wreschner1, Marcelo Ehrlich1, Nechama I. Smorodinsky1,2 1 Department of Cell Research and Immunology, Tel-Aviv University, Tel-Aviv, Israel, 2 The Alec and Myra Marmot Hybridoma Unit, Tel-Aviv University, Tel-Aviv, Israel MUC1 is a prominent marker of breast cancer cells endowed with signal transduction potential due to its cytoplasmic domain.

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