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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

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...
Positive Regulator Molecules02:39

Positive Regulator Molecules

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.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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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Related Experiment Video

Updated: May 22, 2026

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
10:54

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations

Published on: September 17, 2012

Cyclin d1 induces chromosomal instability.

Mathew C Casimiro1, Richard G Pestell

  • 1Department of Cancer Biology, Thomas Jefferson University and Hospital, Kimmel Cancer Center, Philadelphia, USA.

Oncotarget
|April 28, 2012
PubMed
Summary
This summary is machine-generated.

Cyclin D1 expression can induce chromosomal instability (CIN) in mouse models, leading to mammary gland tumors. This instability is linked to specific breast cancer subtypes, suggesting targeted therapies.

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Related Experiment Videos

Last Updated: May 22, 2026

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
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Published on: September 17, 2012

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Investigated the role of cyclin D1 in inducing chromosomal instability (CIN) using mammary gland-specific mouse models.
  • Utilized Tet-inducible and MMTV-targeted models for acute and continuous cyclin D1 expression studies.

Discussion:

  • Acute cyclin D1 expression enriched for CIN-related genes.
  • Continuous cyclin D1 expression in MMTV models led to mammary tumors with a CIN signature.
  • Compared gene expression profiles with a breast cancer database.

Key Insights:

  • Cyclin D1 promotes chromosomal instability in vivo.
  • High cyclin D1 and CIN gene expression strongly correlate with the luminal B subtype of breast cancer.
  • CIN gene signatures are enriched in luminal breast cancer subtypes.

Outlook:

  • The identified link between CIN and luminal B breast cancer provides a rationale for targeted therapies.
  • Exploiting CIN in tumors is a growing area of clinical interest.
  • Suggests potential for using CDK and CIN inhibitors for luminal B breast cancer treatment.