Cell cycle interference

Cell cycle interference is a broad therapeutic mechanism rather than a specific molecular target, involving the disruption of the highly regulated phases of cell division (G1, S, G2, and M) [1, 9]. In oncology, this process is exploited to halt the rapid and unscheduled proliferation of malignant cells, which frequently exhibit defects in cell cycle checkpoints [1, 4]. Interference can be achieved through various pharmacological approaches, including the use of antimetabolites that inhibit DNA synthesis, alkylating agents that induce DNA damage, and microtubule-targeting agents that disrupt the mitotic spindle [2, 3]. Modern targeted therapies also focus on specific regulatory proteins within the cell cycle machinery, such as cyclin-dependent kinases (e.g., CDK4/6 inhibitors) and checkpoint kinases [6, 10]. Because these interventions target the fundamental process of division, they often affect healthy tissues with high turnover rates, such as bone marrow and the gastrointestinal tract, leading to characteristic side effects like myelosuppression [2, 3]. Overall, cell cycle interference represents a cornerstone of cancer treatment aimed at arresting tumor growth and inducing programmed cell death [1, 2].

Other names

Cell cycle arrestCell cycle inhibitionCell cycle disruptionMitotic interferenceCell cycle modulation

Disruption of cell cycle progression through the inhibition of DNA replication, induction of DNA damage, or interference with the mitotic spindle, leading to phase-specific arrest and eventual apoptosis [2, 3, 9].