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Abstract B50: MEK inhibitors mount a two-pronged attack to kill estrogen receptor positive (ER+) breast cancer cells undergoing hormonal therapy: Attenuated autophagy and induction of apoptosis
In this study, we hypothesized that the requirement of MEK1/MAPK1/2 for pro-survival autophagy is due, in part, to its role in blocking the intracellular accumulation of dephosphorylated BimEL. To test this hypothesis, we modulated the expression of dephosphorylated BimEL with either a BimEL cDNA expression vector, siRNA targeting of BimEL, or MEK1 blockade with the small molecule inhibitor U0126 and determined the levels of the autophagic flux in ER+ breast cancer cells undergoing antiestrogen treatment. The determination of autophagic flux was made by comparing the levels of two proteins involved in autophagy -the LC3 /A...
Source: Molecular Cancer Research - February 5, 2015 Category: Cancer & Oncology Authors: Takhar, S., Manning, M., Eason, A., Dix, M., Periyasamy-Thandavan, S., Padi, R., Bieberich, E., Hill, W., Browning, D., Ganapathy, V., Thangaraju, M., Schoenlein, P. V. Tags: RAS Targeting: Poster Presentations - Proffered Abstracts Source Type: research

Abstract A24: PBRM1 alteration in clear cell renal cell carcinoma increases tumorigenicity through ALDH1A1 upregulation
In this study, we investigated the mechanisms by which PBRM1 functions as a tumor suppressor in clear cell renal cell carcinoma (ccRCC). PBRM1, also known as BAF180 or Polybromo, is a member of the PBAF SWI/SNF chromatin remodeling complex. Cancer sequencing studies have revealed that SWI/SNF components are widely mutated in cancer. PBRM1 mutations in particular are found in ~40% of ccRCC tumors, making it the second most highly mutated gene in ccRCC (behind VHL). Although many recent studies have looked at how other SWI/SNF components function in cancer control, relatively little is known about the tumor suppressive mecha...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Schoenfeld, D., Su, W., Zairis, S., Mathur, D., Rabadan, R., Parsons, R. Tags: Chromatin Organization Source Type: research