The Role of Cyclin Dependent Kinase Inhibitor, Cip1, in Breast Cancer.
Abstract
Breast cancer results from inappropriate cell proliferation due to mutations that disrupt normal cell cycle control. Our studies are focused on understanding the role of the p2lCipl protein in cancer. p2l is a member of a family of proteins, including p2l and p57, that inhibit cyclin dependent kinases (Cdks). p2l is regulated by the tumor suppressor protein p53 and is thought to contribute to p53's tumor suppressor function through its interaction with Cdks. p53 is commonly mutated in breast cancer. We have examined the expression of p2l during development and in adult tissues and have found that p21 expression is highly selective and correlates with terminal differentiation. We have also analyzed the phenotype of mice lacking p21. We have found that p21 is responsible for only a subset of p53's function. Specifically, p21 is required for G1 checkpoint function but is not required for the 02 checkpoint or apoptosis induction. Moreover, animals lacking p21 do not readily develop tumors, implying that p21 is not a tumor suppressor. Additional studies have led to a further understanding of the regulation of p21 and the identity of its targets. In addition, we have found that p21 and p21 and p57 collaborate to control lung development.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 1998
- Accession Number
- ADA366917
Entities
People
- J. W. Harper
Organizations
- Baylor College of Medicine