Cancer can disrupt the normal regulation of cyclins, which are proteins essential for controlling the cell cycle and promoting cell division. Mutations in oncogenes or tumor suppressor genes can lead to overproduction of cyclins or loss of cyclin inhibitors, resulting in uncontrolled cell proliferation. This dysregulation contributes to tumor growth and progression, as cancer cells bypass the checkpoints that would normally prevent damaged or abnormal cells from dividing. Consequently, targeting cyclins and their pathways is a potential strategy for cancer therapies.
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