| First Author | Luong-Gardiol N | Year | 2019 |
| Journal | Cancer Cell | Volume | 35 |
| Issue | 4 | Pages | 649-663.e10 |
| PubMed ID | 30991025 | Mgi Jnum | J:274197 |
| Mgi Id | MGI:6295055 | Doi | 10.1016/j.ccell.2019.03.005 |
| Citation | Luong-Gardiol N, et al. (2019) gamma-Catenin-Dependent Signals Maintain BCR-ABL1(+) B Cell Acute Lymphoblastic Leukemia. Cancer Cell 35(4):649-663.e10 |
| abstractText | 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 gamma-catenin in the initiation and maintenance of BCR-ABL1(+) B-ALL but not CML. The selectivity was explained by a partial gamma-catenin dependence of MYC expression together with the susceptibility of B-ALL, but not CML, to reduced MYC levels. MYC and gamma-catenin enabled B-ALL maintenance by augmenting BIRC5 and enforced BIRC5 expression overcame gamma-catenin loss. Since gamma-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. |
