Abstract
Background: Dysregulation of the CDK/cyclin complex causes aberrant cell cycle entry and progression that can lead to cancer. For instance, the CDK2/ cyclin E complex governs the G1-S transition and overexpression of cyclin E has been associated with ovarian and breast cancers. Our initial studies have demonstrated that genetic depletion of CDK2 inhibits cell growth and survival in cancer cells overexpressing cyclin E. Furthermore, inhibition of CDK2 may be effective in cancers resistant to clinically approved CDK4/6 therapies as increased CDK2/cyclin E activity has been reported as a compensatory mechanism.
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