WPublication Highlight-- Division of Cancer Research and Training, Center to Eliminate Cancer Health DisparitiesTuesday, February 5, 2013
are glad to announce the most recent publication of a paper titled “Expression of Wnt3 Activates Wnt/β-Catenin Pathway and Promotes EMT-like Phenotype in Trastuzumab-Resistant HER2-Overexpressing Breast Cancer Cells.” (Molecular Cancer Research, Dec 2012 -PMID: 23071104) by Dr. Yanyuan Wu and team at the Center to Eliminate Cancer Health Disparities supported through the CDU/UCLA Cancer Center Partnership Grant (NCI/NIH U54 CA 143931). Dr. Wu and her colleagues ( C. Ginther , J Kim, N Mosher, S Chung, D Slamon, and Center Director and Senior PI on the study -Dr. Jay Vadgama) demonstrated that a basic developmental pathway, involving the protein called Wnt 3, plays a role in the lo ss of therapy-resistance in a certain breast cancer type called “HER2+.” HER2+ breast cancer cells express a certain molecule on the surface that is targeted for therapy with a drug called trastuzumab. Unfortunately, many women who develop the HER2+type of breast cancer experience relapse of the cancer and trastuzumab does not work anymore (called drug-resistance). These women have reduced survival. This study is significant for exploring the molecular pathways that lead to loss of response to trastuzumab so that better molecular targets can be identified in the future for women with this type of cancer. It should be noted that one of the co-authors, N. Mosher, was an undergraduate intern in the Undergraduate Cancer Research Summer Training (UCRTP) Program at CDU.
Full Citation of paper: Wu Y, Ginther C, Kim J, Mosher N, ChungÂ S, Slamon D, Vadgama JV.Expression of Wnt3 Activates Wnt/Î²-Catenin Pathway and Promotes EMT-like Phenotype in Trastuzumab-Resistant HER2-Overexpressing Breast Cancer Cells. Mol Cancer Res. 2012 Dec;10(12):1597-606. doi: 10.1158/1541-7786.MCR-12-0155-T. Epub 2012 Oct 15.