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Related Concept Videos

Inhibition of Cdk Activity02:34

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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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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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M cyclin...
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
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Related Experiment Video

Updated: Apr 13, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
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Molecular Pathways: Targeting the Cyclin D-CDK4/6 Axis for Cancer Treatment.

Todd VanArsdale1, Chris Boshoff2, Kim T Arndt3

  • 1Oncology Research Unit, Pfizer Worldwide Research and Development, San Diego, California.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|May 6, 2015
PubMed
Summary
This summary is machine-generated.

Cancer cells hijack the cell cycle using cyclin D-CDK4/6. Inhibiting this pathway with drugs like palbociclib shows promise for treating various cancers, validating a long-held hypothesis.

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Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Cancer cells exhibit uncontrolled proliferation by bypassing normal cell-cycle checkpoints.
  • The retinoblastoma protein (pRb) is crucial for the G1-S phase transition, preventing cell division without proper signals.
  • Dysregulation of pRb, often through cyclin-dependent kinase (CDK) 4/6 and D-type cyclins, is common in cancer.

Purpose of the Study:

  • To investigate the therapeutic potential of targeting the cyclin D-CDK4/6 pathway in cancer.
  • To review the clinical development of selective CDK4/6 inhibitors.

Main Methods:

  • Review of preclinical and clinical data on CDK4/6 inhibitors.
  • Analysis of the role of the pRb pathway in cancer cell proliferation.

Main Results:

  • Cyclin D-CDK4/6 activity drives cancer cell proliferation by inactivating pRb.
  • Selective CDK4/6 inhibitors (palbociclib, ribociclib, abemaciclib) are in clinical trials for pRb-positive tumors.
  • Positive clinical data support the targeting of this pathway.

Conclusions:

  • The cyclin D-CDK4/6 pathway is a validated therapeutic target for cancer.
  • CDK4/6 inhibitors represent a promising new class of anti-cancer drugs.