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Cancer drug target Chk1 may also be source of drug resistance

(September 1, 2005, La Jolla, CA) A study published by The Burnham Institute in the September edition of Molecular Cell reports that a cell-cycle checkpoint protein, known to be activated by an important class of anticancer drugs, may play crucial roles in both the hampering of therapeutic actions and aiding cancer cells to "recover" and start dividing again after treatment with these drugs. The study is expected to help academic researchers and biotechnology and pharmaceutical companies design drugs that combat cancer using this checkpoint protein, but with fewer side effects.

Robert Abraham, Ph.D., former director of The Burnham Institute's Cancer Center and now vice president for oncology research at Wyeth Pharmaceuticals, together with his colleagues, found that the Chk1 protein responds with cell-survival activity to stressful conditions induced by hypoxia and certain anticancer drugs. Furthermore these same conditions target Chk1 for eventual destruction. Ironically, stimulation of Chk1 triggers certain repair responses that fight cancer while the simultaneous degradation of Chk1 can allow cancer cells to escape drug-induced death and resume progressive tumor growth.

The study suggests the Chk1 protein is critical for ensuring the repair of mutations and other errors in DNA replication before they can alter the function of a cell. If not repaired, these errors can kill the cell when it attempts to divide and proliferate. In cancer cells, Chk1 is responds as a natural defense to the therapeutic damage done by radiation and chemotherapy and attempts to effect repair to DNA damage caused by the cancer therapy, thus makes the drug therapy less effective.

The researchers also found that the chemotherapy agent campthothecin (CPT), a clinically important anticancer agent, reduced the activity of the Chk1 protein. "These findings lend strong support to the idea that inactivation of Chk1 contributes to the antitumor activity of CPT by allowing
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Contact: Nancy Beddingfield
nbeddingfield@burnham.org
858-646-3146
Burnham Institute
2-Sep-2005


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