在普遍接受的哺乳动物细胞周期控制范式中，顺序的细胞周期蛋白依赖性激酶 (CDK) 和细胞周期蛋白活性驱动从 G1 到 S 期的有序转变。然而，最近使用不同技术方法并检查多种癌细胞类型的研究正在挑战这一既定范式。另一种模型正在发展，其中细胞周期利用不同的驱动因素并在 G1/S 转变中采取不同的轨迹。我们发现癌细胞尤其可以调整其驱动因素和轨迹，这对抗增殖疗法具有重要意义。这些研究有助于加深对 CDK 抑制如何影响增殖的理解，对于理解细胞生物学和癌症的基本特征具有重要意义。版权所有 © 2023 Elsevier Ltd. 保留所有权利。

In the commonly accepted paradigm for control of the mammalian cell cycle, sequential cyclin-dependent kinase (CDK) and cyclin activities drive the orderly transition from G1 to S phase. However, recent studies using different technological approaches and examining a broad range of cancer cell types are challenging this established paradigm. An alternative model is evolving in which cell cycles utilize different drivers and take different trajectories through the G1/S transition. We are discovering that cancer cells in particular can adapt their drivers and trajectories, which has important implications for antiproliferative therapies. These studies have helped to refine an understanding of how CDK inhibition impinges on proliferation and have significance for understanding fundamental features of cell biology and cancer.Copyright © 2023 Elsevier Ltd. All rights reserved.