Scientific article

γ-Catenin-Dependent Signals Maintain BCR-ABL1+ B Cell Acute Lymphoblastic Leukemia

Published inCancer Cell, vol. 35, no. 4, p. 649-663.e10
Publication date2019

The BCR-ABL1 fusion protein is the cause of chronic myeloid leukemia (CML) and of a significant fraction of adult-onset B cell acute lymphoblastic leukemia (B-ALL) cases. Using mouse models and patient-derived samples, we identified an essential role for γ-catenin in the initiation and maintenance of BCR-ABL1+ B-ALL but not CML. The selectivity was explained by a partial γ-catenin dependence of MYC expression together with the susceptibility of B-ALL, but not CML, to reduced MYC levels. MYC and γ-catenin enabled B-ALL maintenance by augmenting BIRC5 and enforced BIRC5 expression overcame γ-catenin loss. Since γ-catenin was dispensable for normal hematopoiesis, these lineage- and disease-specific features of canonical Wnt signaling identified a potential therapeutic target for the treatment of BCR-ABL1+ B-ALL.

  • B cell acute lymphoblastic leukemia (B-ALL)
  • BCR-ABL1
  • BIRC5 (Survivin)
  • MYC
  • Chronic myeloid leukemia (CML)
  • Junction plakoglobin
  • Β-catenin
  • γ-catenin
Citation (ISO format)
LUONG-GARDIOL, Noemie et al. γ-Catenin-Dependent Signals Maintain BCR-ABL1+ B Cell Acute Lymphoblastic Leukemia. In: Cancer Cell, 2019, vol. 35, n° 4, p. 649–663.e10. doi: 10.1016/j.ccell.2019.03.005
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ISSN of the journal1535-6108

Technical informations

Creation11/22/2019 10:22:00 PM
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