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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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Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold...
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Related Experiment Video

Updated: Jul 24, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
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MCAK Inhibitors Induce Aneuploidy in Triple Negative Breast Cancer Models.

John C Smith, Stefan Husted, Jay Pilrose

    Biorxiv : the Preprint Server for Biology
    |July 3, 2023
    PubMed
    Summary

    Targeting MCAK, a protein overexpressed in triple negative breast cancer (TNBC), offers a new therapeutic strategy. Inhibiting MCAK sensitizes TNBC cells to paclitaxel, potentially improving treatment outcomes for this lethal cancer subtype.

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    Area of Science:

    • Oncology
    • Molecular Biology
    • Genetics

    Background:

    • Triple negative breast cancer (TNBC) is an aggressive subtype with limited treatment options.
    • Current therapies like paclitaxel induce aneuploidy but cause resistance and neuropathy.
    • MCAK (mitotic centromere-associated kinesin) regulates microtubule dynamics and limits aneuploidy.

    Conclusions:

    • MCAK is a potential prognostic biomarker and therapeutic target for TNBC.
    • Novel MCAK inhibitors demonstrate efficacy in preclinical TNBC models.
    • Targeting MCAK offers a promising strategy to overcome taxane resistance and improve TNBC treatment.