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Scientists discover role for Cdk4 in making cells cancer resistant

A report published in the November 15th issue of Genes & Development details a requirement for cyclin dependent kinase 4 (Cdk4) gene expression in Ras-induced oncogenesis -- highlighting Cdk4 suppression as a potential therapeutic tool to combat the ~30% of human tumors in which the Ras oncogene is activated.

Cancer results from the acquisition of mutations in genes that function as oncogenes (the encoded protein promotes cell growth) or tumor suppressors (the encoded protein regulates the cell growth cycle), leading to their aberrant activation or repression, respectively. Although individual cancer cells have a unique etiology, or blueprint of genetic mutations that confer upon them the ability for unregulated cell proliferation, researchers have identified a few usual suspects: genes that are mutated in a large number of human cancers. For example, the Ras oncogene is activated in roughly one third of all human tumors, while the p53 tumor suppressor gene is inactivated in half.

Dr. Hiroaki Kiyokawa and colleagues have found that expression of a gene called Cdk4 is essential for Ras-induced cancer development, regardless of p53 status or the presence of another frequently mutated tumor suppressor gene, Ink4a/Arf.

The Cdk4 protein promotes progression through the G1 (initial) phase of the cell growth cycle. Accumulating evidence has implicated aberrant Cdk4 activation in the development of a variety of human tumors, including breast cancer, glioblastomas, sarcomas, and melanomas. Thus, Dr. Kiyokawa and colleagues generated mouse cells deficient in Cdk4 in order to determine its role in tumorigenesis.

Dr. Kiyokawa and colleagues deleted the Cdk4 gene in mouse embryonic fibroblast cells (MEFs; connective tissue cells derived from mouse embryos) in a variety of different genetic backgrounds, and assayed these cells for tumorigenicity both in cell culture (via their ability to divide indefinitely, or act "immortal") and in live mice (
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Contact: Heather Cosel
coselpie@cshl.org
Cold Spring Harbor Laboratory
14-Nov-2002


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