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PMID: 8939849 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

Cancer cell cycles.

Science (New York, N.Y.) ·Vol. 274 ·No. 5293 ·1996-12-06 ·Pages 1672-7

Sherr CJ

Abstract

Uncontrolled cell proliferation is the hallmark of cancer, and tumor cells have typically acquired damage to genes that directly regulate their cell cycles. Genetic alterations affecting p16(INK4a) and cyclin D1, proteins that govern phosphorylation of the retinoblastoma protein (RB) and control exit from the G1 phase of the cell cycle, are so frequent in human cancers that inactivation of this pathway may well be necessary for tumor development. Like the tumor suppressor protein p53, components of this "RB pathway," although not essential for the cell cycle per se, may participate in checkpoint functions that regulate homeostatic tissue renewal throughout life.

MeSH Terms
Animals Carrier Proteins/genetics,metabolism Cell Cycle Cyclin-Dependent Kinase Inhibitor p16 Cyclin-Dependent Kinases/antagonists & inhibitors,metabolism Cyclins/metabolism G1 Phase Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Humans Neoplasms/genetics,metabolism,pathology Proto-Oncogenes Retinoblastoma Protein/metabolism S Phase Signal Transduction Tumor Suppressor Protein p53/metabolism
Chemicals
Carrier Proteins Cyclin-Dependent Kinase Inhibitor p16 Cyclins Retinoblastoma Protein Tumor Suppressor Protein p53 Cyclin-Dependent Kinases
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Sherr C J
Howard Hughes Medical Institute, Department of Tumor Cell Biology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA. [email protected]
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
0036-8075
Published
1996-12-06
Pages
1672-7
Language
English
Region
United States
NLM ID
0404511
Subset
IM
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