Related Experiment Video

Updated: May 4, 2026

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Overview of cyclins D1 function in cancer and the CDK inhibitor landscape: past and present

Mathew C Casimiro1, Marco Velasco-Velázquez, Charmina Aguirre-Alvarado

  • 1Thomas Jefferson University & Hospital, Department of Cancer Biology , 233 South 10th Street, Philadelphia, PA 19107 , USA.

Expert Opinion on Investigational Drugs
|January 7, 2014
PubMed
Abstract

Insights

Targeting cyclin D1, a key cell-cycle regulator, is crucial for cancer treatment. Newer, specific cyclin D1/CDK4/CDK6 inhibitors show promise, unlike earlier broad-spectrum drugs.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • Cyclins are critical mediators of cell-cycle progression.
  • Cyclin D1 oncogene activation drives various human tumors, including breast and squamous cell cancers.
  • Inhibiting cyclin kinase activity is a focus of cancer research.

Purpose of the Study:

  • To review the role of cyclins and cyclin-dependent kinases in cell-cycle progression and transcription.
  • To focus on the cyclin D1/CDK4/CDK6 complex in the G1 to S phase transition.
  • To evaluate the efficacy of different generations of cyclin-dependent kinase inhibitors.

Main Methods:

  • Review of scientific literature on cyclin function and inhibition.
  • Analysis of the cyclin D1/CDK4/CDK6 pathway in cell cycle regulation.
  • Comparison of first-generation pan-CDK inhibitors with second-generation specific inhibitors.

Main Results:

  • First-generation pan-cyclin-dependent kinase inhibitors had limited success.
  • Second-generation inhibitors targeting cyclin D1/CDK4/CDK6 demonstrate improved efficacy.
  • Cyclin D1's role in tumorigenesis may involve both kinase-dependent and independent functions.

Conclusions:

  • Specific inhibition of cyclin D1/CDK4/CDK6 is a promising therapeutic strategy.
  • Further research is needed to understand cyclin D1's kinase-independent roles in early tumorigenesis.
  • Overexpression of cyclin D1 may promote genomic instability in pre-neoplastic lesions.

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