The Role of SF2 in Prostate Cancer Progression
Abstract
Prostate cancer (a leading cause of male mortality) development and progression is dependent upon androgen and androgen receptor (AR) signaling. Current therapies target androgen production and/or AR signaling. Evidence suggests that AR in some tumors may escape therapy through mechanisms that likely involve splicing. Purpose: To better understand splicing during prostate cancer development or progression. Scope: As outlined in the proposal (and recently published) observations suggest that the splicing factor (SF2) may contribute to prostate cancer in part through altered D-cyclin splicing. Findings to date: have been on the generation/characterization of constructs to manipulate SF2 levels in normal- and prostate cancer-derived cell model systems. Simultaneous efforts have been made on the development of robust immunohistochemical methods for detection of SF2 in archived prostate tumor specimens. Additional findings, indicate a potential cross-talk between Dcyclins and androgen/AR that may alter splicing/signaling pathways that impact SF2 function.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2011
- Accession Number
- ADA549702
Entities
People
- Clay Comstock
Organizations
- Thomas Jefferson University