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Related Concept Videos

M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

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.
M cyclin...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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.
There are several types of targeted therapies against specific...
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...
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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 daughter...

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Related Experiment Video

Updated: May 8, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
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Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

Targeting Cdc42 in cancer.

Luis E Arias-Romero1, Jonathan Chernoff

  • 1Cancer Biology Program, Fox Chase Cancer Center , Philadelphia, PA , USA +1 215 728 5319 ; +1 215 728 3616 ; Jonathan.Chernoff@fccc.edu.

Expert Opinion on Therapeutic Targets
|August 21, 2013
PubMed
Summary
This summary is machine-generated.

Cdc42, a Rho GTPase, is overexpressed in many cancers and linked to poor prognosis. Targeting Cdc42 or its effectors may offer new therapeutic strategies for cancers with activating Ras mutations.

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Last Updated: May 8, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

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Published on: May 14, 2016

Assessing Cellular Target Engagement by SHP2 (PTPN11) Phosphatase Inhibitors
08:45

Assessing Cellular Target Engagement by SHP2 (PTPN11) Phosphatase Inhibitors

Published on: July 17, 2020

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Oncology

Background:

  • Rho GTPases are key regulators of cellular processes, acting as molecular switches.
  • Cdc42, a Rho family member, is implicated in various human cancers.
  • Aberrant Cdc42 expression correlates with poor prognosis in some malignancies.

Purpose of the Study:

  • To describe key regulators and effectors of Cdc42.
  • To analyze molecular alterations in Cdc42 signaling.
  • To explore Cdc42's role in tumorigenesis and potential therapeutic targeting.

Main Methods:

  • Review of literature on Cdc42 regulators and effectors.
  • Analysis of molecular alterations in Cdc42 signaling pathways.
  • Examination of Cdc42's role in Ras-mediated tumorigenesis.

Main Results:

  • Cdc42 mutations are not reported in human cancer.
  • Aberrant Cdc42 expression is observed in diverse tumor types.
  • Cdc42 activation by oncogenic Ras is critical for tumorigenesis.

Conclusions:

  • Targeting Cdc42 or its downstream effectors presents a potential therapeutic strategy.
  • This approach is particularly relevant for tumors with activating Ras mutations.
  • Cdc42 represents a promising target for novel cancer therapies.