Related Experiment Video

Updated: Jun 16, 2026

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
12:40

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

JAK2 kinase inhibitors and myeloproliferative disorders

Andrew T Chen1, Josef T Prchal

  • 1Hematology and Medical Oncology, University of Utah, Salt Lake City, Utah, USA.

Current Opinion in Hematology
|January 21, 2010
PubMed
Abstract

Insights

Targeting the JAK2V617F mutation in Philadelphia-chromosome negative myeloproliferative disorders is a key focus. While JAK2 inhibitors show promise, their efficacy and role in therapy are still under investigation.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Philadelphia-chromosome negative myeloproliferative disorders (MPNs) are characterized by the JAK2V617F mutation.
  • This mutation is highly prevalent in polycythemia vera, essential thrombocythemia, and primary myelofibrosis.

Purpose of the Study:

  • To review and assess the progress of JAK2V617F inhibitors in treating MPNs.
  • To evaluate the potential of targeted JAK2 inhibition for disease control.

Main Methods:

  • Review of preclinical and clinical trial data for JAK2 inhibitors.
  • Analysis of current research on JAK2V617F as a therapeutic target.

Main Results:

  • Numerous agents targeting JAK2V617F have undergone preclinical studies, with a few advancing to clinical trials.
  • Clinical trial data are limited, primarily available through abstracts and reviews.

Conclusions:

  • JAK2V617F is a significant target in MPNs, but it's a secondary somatic mutation, unlike the causative bcr/abl in CML.
  • As JAK2 inhibitors progress to Phase III trials, their therapeutic role is becoming clearer, yet many questions remain.
  • Further research is needed to fully understand the efficacy and long-term impact of JAK2 inhibitors in MPNs.

More Related Videos

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells10:21

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells12:04

Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells

Published on: March 10, 2023

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...
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...
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...
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...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...