Targeting cell cycle kinases for cancer therapy.

摘要: Many tumor-associated mutations result in the abnormal regulation of protein kinases involved progression throughout cell division cycle. The cyclin-dependent kinase (CDK) family has received special attention due to their function as sensors mitogenic signals and central role proliferation. These are frequently upregulated human cancer most overexpression cyclin partners or inactivation CDK inhibitors. A plethora small-molecule inhibitors have been characterized last years some them currently under clinical development. Other serine-threonine such Aurora proteins (mostly B) Polo-like (PLK1) receiving increased putative targets. less studied mitotic TTK (MPS1), BUB NEK might also be relevant candidates new targets interest therapy since they play roles on spindle checkpoint. Although targeting cycle is an efficient procedure arrest proliferation, best strategy potently specifically inhibit tumor proliferation not obvious yet. Thus, may abrogate checkpoints favor apoptotic death cells. New biochemical genetic studies required clarify use these opportunities improve therapy.