Bin1, Apoptosis, and Prostate Cancer
Abstract
The genetic causes of prostate cancer remain largely unknown. One of the most common chromosomal abnormalities seen in tumors which have acquired invasive and metastatic potential is gain of chromosome 8q, where c-Myc is located (Bova and Isaacs 1996). Gains of 8q of are well-correlated with disease progression insofar as they are found in 85% of lymph node metastases and 89% of recurrent hormone refractive tumors (Cher et at. 1996; Van Den Berg et at. 1995; Visakorpi et at. 1995). c-Myc amplification or overexpression is found in many prostate tumors and is a likely progression marker (Buttyan et at. 1987; Fleming et at. 1986; Jenkins et at. 1997). Oncogenic activation of c-Myc by gene amplification delivers a powerful signal that is sufficient to drive cell cycle progression and malignant growth in many types of cells, including prostate cells (Thompson et at. 1989). However, in premalignant cells, c-Myc can also activate apoptosis such that its oncogenic activation is balanced by apoptotic penalty (Prendergast 1999). Therefore, malignant cells may escape this penalty by inactivating tumor suppressor functions. p53 is an important player but is likely irrelevant to this process in prostate cells because inactivation of p53 does not compromise c-Myc-mediated apoptosis in epithelial cells (Sakamuro et at. 1995; Trudel et at. 1997). Thus, loss or inactivation of molecules other than p53 should be considered.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 1999
- Accession Number
- ADA385677
Entities
People
- Frank J. Rauscher
Organizations
- University of Pennsylvania