Accession Number:

ADA564541

Title:

Cyclin D1-AR Crosstalk: Potential Implications for Therapeutic Response in Prostate Cancer

Descriptive Note:

Annual summary rept. 1 Apr 2011-31 Mar 2012

Corporate Author:

THOMAS JEFFERSON UNIV PHILADELPHIA PA

Personal Author(s):

• Schiewer, Matthew

Report Date:

2012-04-01

Pagination or Media Count:

9.0

Abstract:

Prostate cancer is dependent on androgens and the androgen receptor AR for disease initiation, maintenance, and progression. Through work by our group and others, it has been shown that there is significant crosstalk between AR and the cell cycle machinery. Most importantly for our study, AR has been shown to induce the G1 to S phase transition in part via regulation of cyclin D1. Cyclin D1 serves as a rheostat to temper the pro-proliferative signaling of AR by directly binding to the receptor and inhibiting it s activity, thus inducing cell cycle arrest. As such, the AR-cyclin D1 crosstalk axis may serve to control the proliferative capacity of prostate cancer cells, and potentially alter the therapeutic efficacy of anti-cancer drugs. The data presented herein will demonstrate that cyclin D1 status does not impinge on the biological outcome in vitro of taxane-based therapy.

Descriptors:

• *ANDROGENS
• *CROSSTALK
• *PROSTATE CANCER
• *RECEPTOR SITES(PHYSIOLOGY)
• CELLS(BIOLOGY)
• DISEASES
• GROWTH(PHYSIOLOGY)
• IN VITRO ANALYSIS
• PHASE TRANSFORMATIONS
• SENSE ORGANS
• THERAPY

Subject Categories:

• Anatomy and Physiology
• Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE