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Cyclin D1 regulates proliferation in pancreatic, colonic, and esophageal cancers
Dan Gordon Gastroenterology Volume 114, Issue 4, (April 1998) DOI: /S (98) Copyright © Terms and Conditions
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Transition from the preproliferative G1 to the proliferative S phase of the cell cycle is regulated by phosphorylation of the retinoblastoma (Rb) protein. Phosphorylated Rb activates nuclear transcription factors that lead to cell division. Rb protein is phosphorylated by either of two cyclin dependent kinases, cdk4 or cdk6. These kinases, in turn, are activated by cyclin D1. Thus prevention of cyclin D1 expression is a logical site for antitumor therapy. Most pathways activated by tyrosine kinase growth factor receptors, G protein–coupled receptors, oncogenes, or mutant tumor-suppressor genes converge at the cyclin D1-cdk-Rb proliferation control point. Although abnormal pathways specific for individual tumors may serve as useful therapeutic targets, the cyclin D1-Rb control point appears to have a wider range of potential application. Gastroenterology , DOI: ( /S (98) ) Copyright © Terms and Conditions
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