New findings suggest balancing Chk1 activity will produce less toxic cancer drugs
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.
Nancy Beddingfield | EurekAlert!
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