Hit for the Cycle

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Science  12 Sep 2003:
Vol. 301, Issue 5639, pp. 1447
DOI: 10.1126/science.301.5639.1447b

A major focus of cancer research is identifying molecular mechanisms that regulate the cell division cycle which often go awry in tumor cells. One molecule believed to be essential for the initiation of cell division is cyclin-dependent kinase 2 (CDK2), an enzyme that phosphorylates protein substrates critical for G1 and S phase progression, centrosome duplication, and DNA synthesis. Drugs that selectively inhibit CDK2 are currently being tested as potential cancer therapies.

Surprising results from a study of CDK2-deficient mice by Ortega et al. cast doubt on whether this enzyme is a master regulator of cell cycle progression after all. Contrary to expectations, mice lacking CDK2 were fully viable and showed no abnormalities in cell division, except in germ cells. The finding that CDK2 is dispensable for normal cell growth and survival-coupled with earlier work by Tetsu and McCormick, who showed that cultured tumor cells can proliferate in the absence of CDK2 activity-will stimulate further discussions about the suitability of CDK2 as a target for cancer therapy. — PAK

Nature Genet. 35, 25 (2003); Cancer Cell 3, 233 (2003).

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