Skip NavigationSkip to Content

The promise of Janus kinase inhibitors in the treatment of hematological malignancies

  1. Author:
    Senkevitch, Emilee
    Durum, Scott
  2. Author Address

    NCI, Cytokines & Immun Sect, Canc & Inflammat Program, NIH, Frederick, MD 21702 USA.
    1. Year: 2017
    2. Date: Oct
  1. Journal: Cytokine
  2. ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD,
    1. 98
    2. Special Issue
    3. Pages: 33-41
  3. Type of Article: Article
  4. ISSN: 1043-4666
  1. Abstract:

    The Janus kinases (JAK) are a family of kinases that play an essential role in cytokine signaling and are implicated in the pathogenesis of autoimmune diseases and hematological malignancies. As a result, the JAKs have become attractive therapeutic targets. The discovery of a JAK2 point mutation (JAK2 V617F) as the main cause of polycythemia vera lead to the development and FDA approval of a JAK1/2 inhibitor, ruxolitinib, in 2011. This review focuses on the various JAK and associated components aberrations implicated in myeloproliferative neoplasms, leukemias, and lymphomas. In addition to ruxolitinib, other JAM inhibitors are currently being evaluated in clinical trials for treating hematological malignancies. The use of JAK inhibitors alone or in combination therapy should be considered as a way to deliver targeted therapy to patients. Published by Elsevier Ltd.

    See More

External Sources

  1. DOI: 10.1016/j.cyto.2016.10.012
  2. PMID: 28277287
  3. WOS: 000411539000005

Library Notes

  1. Fiscal Year: FY2017-2018
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel