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

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  • Anna Bigas
    Cancer Research Program, CIBERONC Institut Mar d'Investigacions Mèdiques (IMIM) Doctor Aiguader 88 08003 Barcelona Spain
  • Yolanda Guillén
    Cancer Research Program, CIBERONC Institut Mar d'Investigacions Mèdiques (IMIM) Doctor Aiguader 88 08003 Barcelona Spain
  • Leonie Schoch
    Cancer Research Program, CIBERONC Institut Mar d'Investigacions Mèdiques (IMIM) Doctor Aiguader 88 08003 Barcelona Spain
  • David Arambilet
    Cancer Research Program, CIBERONC Institut Mar d'Investigacions Mèdiques (IMIM) Doctor Aiguader 88 08003 Barcelona Spain

Abstract

<jats:title>Abstract</jats:title><jats:p>β‐Catenin/<jats:italic>CTNNB1</jats:italic> 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 (<jats:italic>Ctnnb1</jats:italic>, <jats:italic>Axin2</jats:italic>, <jats:italic>Tcf7</jats:italic>, and <jats:italic>Lef1</jats:italic>) and <jats:italic>Myc</jats:italic> in different publicly available T‐ALL cohorts indicates that the expression of these genes may correlate with T‐ALL subtypes and/or therapy outcomes.</jats:p>

Journal

  • BioEssays

    BioEssays 42 (2), 2019-12-19

    Wiley

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