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Title

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

Authors
Luong-Gardiol, Noemie
Siddiqui, Imran
Pizzitola, Irene
Jeevan-Raj, Beena
Charmoy, Mélanie
Irmisch, Anja
Curtet, Sara
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Published in Cancer Cell. 2019, vol. 35, no. 4, p. 649-663.e10
Abstract 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.
Keywords B cell acute lymphoblastic leukemia (B-ALL)BCR-ABL1BIRC5 (Survivin)MYCChronic myeloid leukemia (CML)Junction plakoglobinΒ-cateninγ-catenin
Identifiers
PMID: 30991025
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Structures
Research group Leucémie et transplantation allogénique de cellules souches hématopoïétiques (982)
Projects FNS: 310030_159598
FNS: 310030-133108 and 310030_166627/1
FNS: CRSII3_136245
FNS: 310030_159598 and 310030B_179570
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(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 https://archive-ouverte.unige.ch/unige:135511

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Deposited on : 2020-05-03

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