A "RANning" leap with "XPOrt" into TKI resistance

Blood. 2015 Mar 12;125(11):1686-8. doi: 10.1182/blood-2015-01-622217.

Abstract

In this issue of Blood, Khorashad et al show that genetic (eg, short hairpin RNA [shRNA]-mediated) or pharmacologic (eg, KPT-330 [selinexor]) inhibition of nucleocytoplasmic protein trafficking restored sensitivity to tyrosine kinase inhibitors (TKIs) and impaired clonogenic potential of chronic myeloid leukemia (CML) cell lines with BCR-ABL1 kinase-independent TKI resistance (see figure).

Publication types

  • Comment

MeSH terms

  • Active Transport, Cell Nucleus*
  • Fusion Proteins, bcr-abl / metabolism*
  • Humans
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism*
  • RNA, Small Interfering / genetics*

Substances

  • BCR-ABL1 fusion protein, human
  • RNA, Small Interfering
  • Fusion Proteins, bcr-abl