Related Experiment Video

Updated: May 11, 2026

Isolation and Expansion of Cytotoxic Cytokine-induced Killer T Cells for Cancer Treatment
11:11

Isolation and Expansion of Cytotoxic Cytokine-induced Killer T Cells for Cancer Treatment

Published on: January 24, 2020

Cyclin-dependent kinase inhibitor therapy for hematologic malignancies

Prithviraj Bose1, Gary L Simmons, Steven Grant

  • 1Virginia Commonwealth University, Internal Medicine, 1101 E Marshall St, Sanger Hall, Richmond, VA 23298, USA.

Expert Opinion on Investigational Drugs
|May 8, 2013
PubMed
Abstract

Insights

Cyclin-dependent kinase (CDK) inhibitors show promise for treating blood cancers by halting cell growth and triggering cell death. Combinations of CDK inhibitors with other targeted therapies are being explored for improved anticancer efficacy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Cyclin-dependent kinases (CDKs) regulate cell cycle and transcription.
  • Aberrant CDK expression is common in malignancies, making them key anticancer targets.
  • Hematologic malignancies are particularly sensitive to CDK inhibition-induced apoptosis.

Purpose of the Study:

  • To review the development and efficacy of CDK inhibitors for cancer treatment.
  • To highlight the role of CDK7 and CDK9 in cell cycle regulation and transcription.
  • To explore the potential of CDK inhibitors in hematologic malignancies.

Main Methods:

  • Profiling of various CDK inhibitors, including pan-CDK inhibitors (e.g., flavopiridol) and selective inhibitors (e.g., PD0332991).
  • Review of early-phase clinical trial data for flavopiridol, dinaciclib, and PD0332991.
  • Analysis of CDK inhibitor mechanisms, including cell cycle arrest and transcriptional repression.

Main Results:

  • Flavopiridol induces cell cycle arrest and global transcription repression via CDK9 inhibition.
  • Early trials show encouraging efficacy of flavopiridol in hematologic malignancies.
  • Promising early results observed with dinaciclib and PD0332991.

Conclusions:

  • CDK inhibitor monotherapy exhibits modest antitumor efficacy.
  • Rational combinations of CDK inhibitors with other targeted agents are under investigation.
  • Broad-spectrum CDK inhibition may be necessary for treating most cancers, while selective CDK4/6 inhibitors show potential for specific malignancies.

More Related Videos

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors10:33

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

Published on: October 26, 2015

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia10:49

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia

Published on: September 18, 2013

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...
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.
There are several types of targeted therapies against specific...
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.
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...