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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Recent Developments in Targeting the Cell Cycle in Melanoma.

Christie Hung1, Trang T T Nguyen1, Poulikos I Poulikakos2

  • 1Ronald O. Perelman Department of Dermatology, New York University Grossman School of Medicine, Laura and Isaac Perlmutter Cancer Center, NYU Langone Health, New York, NY 10016, USA.

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|April 26, 2025
PubMed
Summary
This summary is machine-generated.

Melanoma treatment faces challenges due to resistance to targeted therapies and immunotherapies. This review examines the dysregulated Cyclin D-CDK4/6-RB pathway in melanoma and strategies to improve CDK4/6 inhibitor efficacy.

Keywords:
AktCDK2CDK4CDK6PI3kRBcell cyclecyclin DimmunotherapyinhibitormTORmelanoma

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Area of Science:

  • Oncology
  • Cancer Biology
  • Molecular Medicine

Background:

  • Melanoma incidence is rising, especially in older adults.
  • Current BRAF/MEK targeted therapies and immunotherapies have limitations, with many patients developing resistance or not responding.
  • The Cyclin D-CDK4/6-RB pathway is frequently activated in melanoma, presenting a therapeutic target.

Purpose of the Study:

  • To review the molecular mechanisms of Cyclin D-CDK4/6-RB pathway dysregulation in melanoma.
  • To discuss the challenges in targeting this pathway clinically.
  • To explore strategies for enhancing the efficacy of CDK4/6 inhibitors.

Main Methods:

  • Literature review of preclinical and clinical studies.
  • Analysis of molecular mechanisms underlying pathway activation and resistance.
  • Exploration of combination therapy approaches.

Main Results:

  • The Cyclin D-CDK4/6-RB pathway is altered in up to 90% of melanomas.
  • Direct targeting of Cyclin-CDK complexes has yielded suboptimal clinical responses.
  • Resistance mechanisms to CDK4/6 inhibition are being elucidated.

Conclusions:

  • Understanding Cyclin D-CDK4/6-RB pathway dysregulation is crucial for melanoma treatment.
  • Combination therapies may overcome resistance and improve outcomes for patients with melanoma.
  • Further research is needed to optimize CDK4/6 inhibitor strategies in melanoma.