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Related Concept Videos

M-Cdk Drives Transition Into Mitosis02:15

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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.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
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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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Abnormal Proliferation02:23

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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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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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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Positive Regulator Molecules02:39

Positive Regulator Molecules

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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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mTOR Signaling and Cancer Progression03:03

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Generation of Prostate Cancer Patient Derived Xenograft Models from Circulating Tumor Cells
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Characterizing CDK12-Mutated Prostate Cancers.

Pasquale Rescigno1,2, Bora Gurel1, Rita Pereira1

  • 1The Institute of Cancer Research, Sutton, London, United Kingdom.

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|September 29, 2020
PubMed
Summary
This summary is machine-generated.

Cyclin-dependent kinase 12 (CDK12) alterations in metastatic castration-resistant prostate cancer (mCRPC) are linked to poorer survival and distinct tumor microenvironments. These tumors show enrichment of CD4+FOXP3- cells, potentially indicating an immunosuppressive role.

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Area of Science:

  • Oncology
  • Genetics
  • Immunology

Background:

  • Cyclin-dependent kinase 12 (CDK12) aberrations are potential biomarkers for immunotherapy response in metastatic castration-resistant prostate cancer (mCRPC).
  • Characterizing CDK12-mutated mCRPC is crucial for understanding its clinical implications and tumor microenvironment.

Purpose of the Study:

  • To characterize the clinical, genomic, and tumor-infiltrating lymphocyte (TIL) data of mCRPC with CDK12 mutations.
  • To investigate the prognostic significance of CDK12 alterations in mCRPC.

Main Methods:

  • Genomic analysis of mCRPC biopsies using targeted next-generation sequencing and exome sequencing.
  • Assessment of TIL subsets (CD4+, CD8+, FOXP3+) using immunocytochemistry and artificial intelligence-based multiplex immunofluorescence.
  • Comparison of CDK12-altered mCRPC with a control cohort.

Main Results:

  • CDK12 alterations were found in 4.7% of 913 mCRPC patients.
  • CDK12-altered mCRPCs exhibited distinct genomic features, including high chromosomal break numbers.
  • Biallelic CDK12 alterations correlated with shorter overall survival (5.1 vs. 6.4 years; P=0.02).
  • CDK12-altered tumors showed a trend towards higher CD3+ cell density, significantly enriched for CD4+FOXP3- cells (P<0.0001).

Conclusions:

  • CDK12-altered mCRPCs are associated with a worse prognosis.
  • These tumors are characterized by a specific immune infiltrate, primarily CD4+FOXP3- cells.
  • The CD4+FOXP3- cell population may contribute to an immunosuppressive tumor microenvironment and associate with worse outcomes.