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

被引：23

作者：

Luong-Gardiol, Noemie ^{[1
,8
]}

Siddiqui, Imran ^{[1
]}

Pizzitola, Irene ^{[1
]}

Jeevan-Raj, Beena ^{[1
]}

Charmoy, Melanie ^{[1
]}

Huang, Yun ^{[2
,3
]}

Irmisch, Anja ^{[4
,9
]}

Curtet, Sara ^{[1
]}

Angelov, Georgi S. ^{[1
]}

Danilo, Maxime ^{[1
,10
]}

Juilland, Melanie ^{[5
]}

Bornhauser, Beat ^{[2
,3
]}

Thome, Margot ^{[5
]}

Hantschel, Oliver ^{[4
]}

Chalandon, Yves ^{[6
]}

Cazzaniga, Gianni ^{[7
]}

Bourquin, Jean-Pierre ^{[2
,3
]}

Huelsken, Joerg ^{[4
]}

Held, Werner ^{[1
]}

机构：

[1] Univ Lausanne, Dept Oncol UNIL CHUV, Epalinges, Switzerland

[2] Univ Childrens Hosp Zurich, Dept Pediat Oncol, Zurich, Switzerland

[3] Univ Childrens Hosp Zurich, Childrens Res Ctr, Zurich, Switzerland

[4] Fed Univ Technol Lausanne EPFL, Swiss Inst Expt Canc Res ISREC, Lausanne, Switzerland

[5] Univ Lausanne, Dept Biochem, Epalinges, Switzerland

[6] Hop Univ Geneve, Serv Hematol, Geneva, Switzerland

[7] Pediat Clin Univ Milano Bicocca, Ctr Ric Tettamanti, Monza, Italy

[8] Debiopharm Int SA, Ch Messidor 5-7, CH-1002 Lausanne, Switzerland

[9] Univ Hosp Zurich, Clin Dermatol, Wagistr 14, CH-8952 Schlieren, Switzerland

[10] Phi Pharma SA, Pl Midi 36, CH-1950 Sion, Switzerland

来源：

CANCER CELL | 2019年 / 35卷 / 04期

基金：

瑞士国家科学基金会;

关键词：

CHRONIC MYELOID-LEUKEMIA; BETA-CATENIN; STEM-CELLS; C-MYC; BCR-ABL; TRANSCRIPTIONAL REGULATION; TRANSLOCATION PRODUCTS; SURVIVIN; PATHWAY; KINASE;

D O I：

10.1016/j.ccell.2019.03.005

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：649 / +

页数：25

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