Genes & Cancer | CDK4: a master cell cycle regulator and its role in cancer

BUFFALO, NY – December 2, 2022 – A new review has been published in Genes and Cancer on August 25, 2022, entitled “CDK4: a master cell cycle regulator and its role in cancer.”

The mammalian cell cycle is divided into four phases, Gap 1 (G1), Synthesis (S), Gap 2 (G2), and Mitosis (M), the order and timing of which are critical for accurate transmission of information. genetic. Therefore, a number of biochemical pathways have evolved to ensure that the initiation of a particular cell cycle event is dependent on the precise completion of another. These biochemical pathways have been called “checkpoints”.

The cell cycle is regulated in part by cyclins and their associated serine/threonine cyclin-dependent kinases, or CDKs. CDK4, in conjunction with D-type cyclins, mediates progression through the G1 phase as the cell prepares to initiate DNA synthesis. Although Cdk4-null mutant mice are viable and cell proliferation is not significantly affected in vitro due to compensatory roles played by other CDKs, this gene plays a key role in mammalian development and cancer.

In the current position paper, the researchers Stacey J. Baker, Poulikos I. Poulikakos, Hanna Y. Irie, Samir Parekh, and E.Premkumar Reddy of Icahn School of Medicine at Mount Sinai discussed the role played by CDK4 in cell cycle control, normal development and tumorigenesis, as well as the current status and usefulness of approved small molecule CDK4/6 inhibitors that are currently used as therapeutic agents against the cancer. In summary:

“CDK4/6 is a key mediator of cell cycle progression through the G1 phase, the time when a cell prepares to initiate DNA synthesis. The cell’s dependence on this protein as well as its partners in Binding to CYCLINE D and Downstream Target RB for Proliferation Highlights Why CDK4/CYCLINE D/RB Signaling Module is Often Dysregulated in Transformed Cells Approval of 3 CDK4/6 Inhibitors as Breast Cancer Treatments ER+ has paved the way for ongoing clinical studies evaluating the usefulness of these inhibitors in combination with those of other signaling pathways (such as, but not limited to, BRAF, PI3K, and MEK) in multiple tumor types that are dependent on CYCLINE D1/CDK4/RB or other cell cycle components such as p16 and p27 The success of these assays, together with the understanding of the mechanisms that drive resistance to these inhibitors, should provide an answer as to whether know if the inhi Selective CDK4/6 biters may provide therapeutic benefit in a wider range of cancers.

Read the full research paper: DOI: https://doi.org/10.18632/genesandcancer.221

Correspondence: E. Premkumar Reddy – E-mail: ep.reddy@mssm.edu

Key words: CDK4/6, cancer, cell cycle, targeted therapy, checkpoint inhibitor

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