Revisiting β-Catenin Signaling in T-Cell Development and T-Cell Acute Lymphoblastic Leukemia

Bioessays. 2020 Feb;42(2):e1900099. doi: 10.1002/bies.201900099. Epub 2019 Dec 19.

Abstract

β-Catenin/CTNNB1 is critical for leukemia initiation or the stem cell capacity of several hematological malignancies. This review focuses on a general evaluation of β-catenin function in normal T-cell development and T-cell acute lymphoblastic leukemia (T-ALL). The integration of the existing literature offers a state-of-the-art dissection of the complexity of β-catenin function in leukemia initiation and maintenance in both Notch-dependent and independent contexts. In addition, β-catenin mutations are screened for in T-ALL primary samples, and it is found that they are rare and with little clinical relevance. Transcriptional analysis of Wnt family members (Ctnnb1, Axin2, Tcf7, and Lef1) and Myc in different publicly available T-ALL cohorts indicates that the expression of these genes may correlate with T-ALL subtypes and/or therapy outcomes.

Keywords: LIC activity; Myc; Notch pathway; T-cell acute leukemia; Wnt signaling; β-catenin.

Publication types

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

MeSH terms

  • Animals
  • Humans
  • Mutation / genetics
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • T-Lymphocytes / physiology*
  • Transcription, Genetic / genetics
  • Wnt Signaling Pathway / genetics
  • beta Catenin / genetics*

Substances

  • beta Catenin