| Title: |
γ-Catenin-Dependent Signals Maintain BCR-ABL1+ B Cell Acute Lymphoblastic Leukemia |
| Authors: |
Luong-Gardiol N.; Siddiqui I.; Pizzitola I.; Jeevan-Raj B.; Charmoy M.; Huang Y.; Irmisch A.; Curtet S.; Angelov G. S.; Danilo M.; Juilland M.; Bornhauser B.; Thome M.; Hantschel O.; Chalandon Y.; Cazzaniga G.; Bourquin J. -P.; Huelsken J.; Held W. |
| Contributors: |
Luong-Gardiol, N; Siddiqui, I; Pizzitola, I; Jeevan-Raj, B; Charmoy, M; Huang, Y; Irmisch, A; Curtet, S; Angelov, G; Danilo, M; Juilland, M; Bornhauser, B; Thome, M; Hantschel, O; Chalandon, Y; Cazzaniga, G; Bourquin, J; Huelsken, J; Held, W |
| Publisher Information: |
Cell Press |
| Publication Year: |
2019 |
| Collection: |
Università degli Studi di Milano-Bicocca: BOA (Bicocca Open Archive) |
| Subject Terms: |
B cell acute lymphoblastic leukemia (B-ALL); BCR-ABL1; BIRC5 (Survivin); chronic myeloid leukemia (CML); junction plakoglobin; MYC; β-catenin; γ-catenin; Animal; Fusion Proteins; bcr-abl; Gene Expression Regulation; Leukemic; Human; K562 Cell; Mice; Inbred NOD; SCID; Transgenic; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma; Proto-Oncogene Proteins c-myc; Survivin; beta Catenin; gamma Catenin; Wnt Signaling Pathway |
| Description: |
Luong-Gardiol et al. show that Wnt pathway activity mediated by γ-catenin is critical for BCR-ABL1 + B-ALL, in contrast to β-catenin being important in CML. B-ALL is more sensitive to partial reduction of MYC expression level than CML, and γ-catenin regulates the expression of MYC and Survivin in B-ALL. |
| Document Type: |
article in journal/newspaper |
| Language: |
English |
| Relation: |
info:eu-repo/semantics/altIdentifier/pmid/30991025; info:eu-repo/semantics/altIdentifier/wos/WOS:000464931000012; volume:35; issue:4; firstpage:649; lastpage:663.e10; journal:CANCER CELL; https://hdl.handle.net/10281/272289 |
| DOI: |
10.1016/j.ccell.2019.03.005 |
| Availability: |
https://hdl.handle.net/10281/272289; https://doi.org/10.1016/j.ccell.2019.03.005 |
| Rights: |
info:eu-repo/semantics/openAccess |
| Accession Number: |
edsbas.AFBAC1AD |
| Database: |
BASE |