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Bioessays. 1999 Aug;21(8):704-9.

A node between proliferation, apoptosis, and growth arrest.

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1
Medicine Branch, National Cancer Institute, Bldg. 10, R 12N226, NIH, Bethesda, Maryland 20892, USA. mikhailb@box-m.nih.gov

Abstract

Paradoxically, oncogenes and growth factors can induce proliferation and promote cellular survival but can also cause apoptosis and growth arrest. What determines whether a cell decides to proliferate, arrest growth, or die? Mitogens and activators of mitogen-activated pathways initiate the simultaneous production of proliferative (cyclins) and anti-proliferative (CDK inhibitors such as p21WAF1/CIP1) signals. Quiescent cells may respond to these signals by proliferation whereas proliferating cells may respond by growth arrest. Although pro-apoptotic oncoproteins, which constitute the downstream pathway (cyclin D, E2F, c-myc) directly induce proliferation, the activation of the upstream steps (growth factor receptors, Ras, cytoplasmic kinases) is required to prevent apoptosis.

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