The Mechanism of Retinoblastoma Protein-Mediated Terminal Cell Cycle Arrest
Abstract
A characteristic feature of most cancers is an increase in the percentage of proliferating cells, often referred to as the mitotic index. Upon differentiation most cells in the body enter an irreversible terminal cell cycle arrest. Failure to maintain this growth arrested state is thought to contribute significantly to the development of most forms of human cancer including those of the breast. The retinoblastoma protein (pRb) has been shown to participate in the maintenance of a terminal cell cycle arrest (1), however, the mechanisms by it accomplishes this task are not understood. This is in contrast to the role of pRb in controlling proliferation in a cycling population, which is well characterized. The purpose of these studies are to elucidate the molecular mechanism by which pRb maintains a terminal cell cycle arrest. Initial focus is placed on the study on skeletal muscle differentiation since both in vitro and in vivo studies have clearly demonstrated a role for pRb in maintaining an arrested state following terminal differentiation of this tissue type (1, 2). Information gained from this analysis will then be applied to the study of mammary gland differentiation. Inactivation of the retinoblastoma gene (Rb) is a common event in the development of several human cancers including those of the breast. These studies thus likely have direct bearing of how loss of Rb contributes to the development of cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2002
- Accession Number
- ADA410280
Entities
People
- Duk H. Kim
- Mark E. Ewen
Organizations
- Dana–Farber Cancer Institute