Breaking the Cycle: CDK4/6 Inhibitors Take on Cancers
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: 20 July 2026 | Viewed by 43
Special Issue Editor
Interests: PI3K; targeted therapies; molecular oncology; immunotherapy; biomarkers; CDK4/6
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Cyclin-dependent kinases (CDKs) are a predominant group of serine/threonine protein kinases that are implicated in cell-cycle regulation and progression, which ultimately control the proper cell cycle functionality. These enzymes work by creating complexes with cyclins, and differently than CDKs, cyclins levels fluctuate during the cell cycle progression; therefore, they ensure that the cell cycle progresses in a timely fashion. Moreover, CDKs have been shown to also have roles in regulating cell signaling and transcription of genes. Overall, in humans, there are 20 CDKs and 29 cyclins, supporting the complexity of these molecules. Most crucial for cancer progression are CDK4 and CDK6 (CDK4/6); in fact, their regulation of the cell cycle promotes tumor growth. CDK4/6 are often upregulated in various types of cancer, such as breast cancer (BC) and pancreatic adenocarcinoma (PDAC). Therefore, CDK4/6 inhibitors are often used in cancer treatment to target these proteins. Inhibitors of CDK4/6 block the transition from the G1 to S phase in the cell cycle through the dephosphorylation of the retinoblastoma tumor suppressor. While CDK4/6 inhibitors, such as ribociclib, palbociclib, and abemaciclib, have been approved for the treatment of breast cancer, other inhibitors have shown promise in treating pancreatic cancer (PDAC). To support this, PDAC is often associated with loss of the p16 tumor suppressor protein, which CDK4/6 inhibitors can effectively target. In this Special Issue, we aim to explore the gap in utilizing CDK4/6 inhibitors across various cancer types, such as PDAC, which presents a strong molecular and biological rationale for the use of this drug class. Additionally, we seek to examine the role of the tumor microenvironment in enhancing the efficacy of this targeted therapy.
Dr. Navid Sobhani
Guest Editor
Manuscript Submission Information
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Keywords
- CDK4/6 inhibitors
- p16
- targeted therapy
- tumor microenvironment
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