JAK-STAT pathway activation in malignant and nonmalignant cells contributes to MPN pathogenesis and therapeutic response Academic Article uri icon

Overview

MeSH Major

  • Cell Transformation, Neoplastic
  • Janus Kinases
  • Myeloproliferative Disorders
  • STAT Transcription Factors
  • Signal Transduction

abstract

  • Our results demonstrate that JAK-STAT3-mediated cytokine production from malignant and nonmalignant cells contributes to MPN pathogenesis and that JAK inhibition in both populations is required for therapeutic efficacy. These findings provide novel insight into the mechanisms by which JAK kinase inhibition achieves therapeutic efficacy in MPNs. Cancer Discov; 5(3); 316-31. ©2015 AACR. See related commentary by Belver and Ferrando, p. 234 This article is highlighted in the In This Issue feature, p. 213.

publication date

  • January 2015

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC4355105

Digital Object Identifier (DOI)

  • 10.1158/2159-8290.CD-14-0736

PubMed ID

  • 25572172

Additional Document Info

start page

  • 316

end page

  • 31

volume

  • 5

number

  • 3