Accession Number : ADA302399
Title : The Role of Cyclin Dependent Kinase Inhibitor, CIP1, in Breast Cancer.
Descriptive Note : Annual rept. 15 Sep 94-14 Sep 95,
Corporate Author : BAYLOR COLL OF MEDICINE HOUSTON TX
Personal Author(s) : Harper, J. W.
PDF Url : ADA302399
Report Date : OCT 1995
Pagination or Media Count : 32
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 growing family of proteins which bind and inhibit cyclin dependent kinases (Cdks). Cdks are required for cell cycle progression. 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 p21 during development and in adult tissues and have found that p2l expression is highly selective and correlates with terminal differentiation. We have also analyzed the phenotype of mice lacking p21. We have found that p2l is responsible for only a subset of pS3's function. Specifically, p2l is required for Gi checkpoint function but is - not required for the G2 checkpoint or apoptosis induction. Moreover, animals lacking p2l do not readily develop tumors, implying that p2l is not a tumor suppressor. Future studies will involve further analysis of checkpoint functions and will examine genetic interactions between oncogenes and loss of p21 in vivo.
Descriptors : *CYCLES, *GENETICS, *MAMMARY GLANDS, CONTROL, TISSUES(BIOLOGY), INTERACTIONS, NEOPLASMS, MUTATIONS, ANIMALS, CELLS(BIOLOGY), ADULTS, CANCER, SUPPRESSORS, PHOSPHORUS TRANSFERASES.
Subject Categories : Medicine and Medical Research
Anatomy and Physiology
Distribution Statement : APPROVED FOR PUBLIC RELEASE