The molecular basis of T cell acute lymphoblastic leukemia

J Clin Invest. 2012 Oct;122(10):3398-406. doi: 10.1172/JCI61269. Epub 2012 Oct 1.

Abstract

T cell acute lymphoblastic leukemias (T-ALLs) arise from the malignant transformation of hematopoietic progenitors primed toward T cell development, as result of a multistep oncogenic process involving constitutive activation of NOTCH signaling and genetic alterations in transcription factors, signaling oncogenes, and tumor suppressors. Notably, these genetic alterations define distinct molecular groups of T-ALL with specific gene expression signatures and clinicobiological features. This review summarizes recent advances in our understanding of the molecular genetics of T-ALL.

Publication types

  • Review

MeSH terms

  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / physiology
  • Cell Lineage
  • Cell Transformation, Neoplastic / genetics
  • Chromatin Assembly and Disassembly / genetics
  • Chromatin Assembly and Disassembly / physiology
  • Cyclin-Dependent Kinase Inhibitor p16 / physiology
  • Genes, p16
  • Hematopoietic Stem Cells / pathology
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / physiology
  • Humans
  • Molecular Targeted Therapy
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / physiology*
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • Prognosis
  • Receptors, Notch / physiology
  • Signal Transduction / genetics
  • Signal Transduction / physiology
  • T-Lymphocytes / pathology
  • Transcription Factors / physiology
  • Transcriptome
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / physiology

Substances

  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p16
  • Homeodomain Proteins
  • Neoplasm Proteins
  • Receptors, Notch
  • Transcription Factors
  • Tumor Suppressor Proteins