BCR-ABL (Ph)-like acute leukemia-Pathogenesis, diagnosis and therapeutic options

Blood Rev. 2017 Mar;31(2):11-16. doi: 10.1016/j.blre.2016.09.001. Epub 2016 Sep 16.

Abstract

Recent comprehensive genetic studies revealed numerous genetic aberrations underlying a group of high-risk leukemias that share a specific activated kinase gene expression pattern. These ALLs were first recognized by the expression profile similar to that of Philadelphia chromosome-positive ALL and currently can be sub-classified by the main aberrantly activated kinase in the leukemic cells. We herein review the biological mechanisms and diagnostic and clinical challenges presented by these leukemias.

Keywords: BCR-ABL-like ALL; JAK inhibitors; Kinase-driven ALL; Ph-like ALL; Tyrosine kinase inhibitors.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Fusion Proteins, bcr-abl / genetics*
  • Fusion Proteins, bcr-abl / metabolism
  • Gene Deletion
  • Genetic Association Studies
  • Genetic Predisposition to Disease
  • Humans
  • Ikaros Transcription Factor / genetics
  • Ikaros Transcription Factor / metabolism
  • Janus Kinases / metabolism
  • Phenotype
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • STAT Transcription Factors / metabolism
  • Signal Transduction

Substances

  • STAT Transcription Factors
  • Ikaros Transcription Factor
  • Fusion Proteins, bcr-abl
  • Janus Kinases