The p16 Pathway In Breast Cancer and Senescence Control.
Abstract
The p16INK4a protein, hereafter referred to as pl6, is a known negative regulator of cell cycle progression through its cyclin dependent kinase (CDK) inhibiting function (1). pl6 competes with the activating D type cyclins for association with CDK4 or CDK6, thereby preventing phosphorylation of proteins controlling Ol exit such as the retinoblastoma (Rb) protein (2). Inactivation of p16 has been observed in numerous tumor types (3-8), and lack or reduced expression of p16 has also been shown through a variety of technical approaches to occur in at least 50% of the breast cancer samples examined (9, 10). While these findings suggest that p16 may play an important role in breast tumorigenesis, the consequence of such abberrations of p16 are not yet clear.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 1998
- Accession Number
- ADA358053
Entities
People
- Claudio M. Aldaz
Organizations
- University of Texas at Austin