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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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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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DNA Damage can Stall the Cell Cycle02:37

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Negative Regulator Molecules01:23

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: May 26, 2025

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
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Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

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p16 expression confers sensitivity to CDK2 inhibitors.

Chance Sine, Lotte Watts, Brianna Fernandez

    Biorxiv : the Preprint Server for Biology
    |February 24, 2025
    PubMed
    Summary

    The tumor suppressor p16 inhibits CDK4/6, enhancing sensitivity to CDK2 inhibitors in ovarian cancers. This finding identifies p16 as a potential biomarker for predicting patient response to CDK2-targeted cancer therapy.

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    Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
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    Area of Science:

    • Oncology
    • Molecular Biology
    • Cell Cycle Regulation

    Background:

    • Cyclin-Dependent Kinase 2 (CDK2) is a key target for cancer therapy, but its inhibition can be circumvented by compensatory CDK4/6 activity.
    • This compensatory mechanism allows cancer cells to maintain proliferation and CDK2 reactivation, limiting the efficacy of CDK2 inhibitors.

    Purpose of the Study:

    • To investigate the hypothesis that sensitivity to CDK2 inhibition is associated with the absence of CDK4/6-mediated compensation.
    • To identify potential biomarkers for predicting patient response to CDK2 inhibitors in ovarian cancer.

    Main Methods:

    • Analysis of ovarian cancer cell lines co-expressing Cyclin E1 and the tumor suppressor p16.
    • Assessment of sensitivity to CDK2 inhibitors in cells with and without p16.
    • Multiplexed immunofluorescence staining of 225 ovarian patient tumors to evaluate Cyclin E1 and p16 expression levels.

    Main Results:

    • Ovarian cancer cells expressing p16 demonstrated heightened sensitivity to CDK2 inhibitors.
    • Depletion of p16 significantly increased resistance to CDK2 inhibitors.
    • At least 18% of analyzed ovarian tumors showed high expression of both Cyclin E1 and p16.

    Conclusions:

    • The presence of p16, which inhibits CDK4/6, is linked to increased sensitivity to CDK2 inhibitors in ovarian cancer.
    • p16 may serve as a predictive biomarker for identifying ovarian cancer patients who will benefit from CDK2 inhibitor therapy.