Tumor-specific HSP90 inhibition as a therapeutic approach in JAK-mutant acute lymphoblastic leukemias-Reference-Cited by-同舟云学术

Tumor-specific HSP90 inhibition as a therapeutic approach in JAK-mutant acute lymphoblastic leukemias

Published:2015-11-26 Issue:22 Volume:126 Page:2479-2483
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Kucine Nicole¹²,Marubayashi Sachie¹,Bhagwat Neha¹³,Papalexi Efthymia¹,Koppikar Priya¹,Sanchez Martin Marta⁴,Dong Lauren¹,Tallman Marty S.⁵,Paietta Elisabeth⁶,Wang Kai⁷,He Jie⁷,Lipson Doron⁷,Stephens Phil⁷,Miller Vince⁷,Rowe Jacob M.⁸,Teruya-Feldstein Julie⁹,Mullighan Charles G.¹⁰,Ferrando Adolfo A.⁴,Krivtsov Andrei¹¹¹²,Armstrong Scott¹¹¹²,Leung Laura¹,Ochiana Stefan O.¹³,Chiosis Gabriela¹³,Levine Ross L.¹⁵¹²,Kleppe Maria¹

Affiliation:

1. Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY;

2. Department of Pediatrics, Division of Hematology/Oncology, Weill Cornell Medical College, New York, NY;

3. Gerstner Sloan Kettering Graduate School in Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, NY;

4. Institute for Cancer Genetics, Columbia University, New York, NY;

5. Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY;

6. Division of Hemato-Oncology, Department of Medicine (Oncology), Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY;

7. Foundation Medicine, Cambridge, MA;

8. Department of Hematology and Bone Marrow Transplantation, The Rambam Medical Center, Haifa, Israel;

9. Department of Pathology, Icahn School of Medicine, Mount Sinai, New York, NY;

10. Department of Pathology and Hematological Malignancies Program, St. Jude Children’s Research Hospital, Memphis, TN; and

11. Cancer Biology and Genetics Program,

12. Center for Epigenetics Research, and

13. Molecular Pharmacology and Chemistry Program, Memorial Sloan Kettering Cancer Center, New York, NY

Abstract

Key Points PU-H71, a novel purine scaffold inhibitor, shows potent therapeutic efficacy in JAK-mutant ALL cells and mouse models. HSP90 inhibition retains therapeutic efficacy in ruxolitinib-persistent JAK-mutant ALL cells.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/126/22/2479/1390311/2479.pdf

Reference18 articles.

1. A gain-of-function mutation of JAK2 in myeloproliferative disorders.;Kralovics;N Engl J Med,2005

2. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.;Levine;Cancer Cell,2005

3. Rearrangement of CRLF2 in B-progenitor- and Down syndrome-associated acute lymphoblastic leukemia.;Mullighan;Nat Genet,2009

4. JAK mutations in high-risk childhood acute lymphoblastic leukemia.;Mullighan;Proc Natl Acad Sci USA,2009

5. Somatically acquired JAK1 mutations in adult acute lymphoblastic leukemia.;Flex;J Exp Med,2008

Cited by 32 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Co-targeting HSP90 alpha and CDK7 overcomes resistance against HSP90 inhibitors in BCR-ABL1+ leukemia cells;Cell Death & Disease;2023-12-06

2. High-throughput screening as a drug repurposing strategy for poor outcome subgroups of pediatric B-cell precursor Acute Lymphoblastic Leukemia;Biochemical Pharmacology;2023-11

3. Epichaperome inhibition targets TP53-mutant AML and AML stem/progenitor cells;Blood;2023-09-21

4. The role of ruxolitinib treatment in JAK-mutated Ph-like acute lymphoblastic leukemia;Annals of Hematology;2023-09-20

5. Epichaperomes as a Gateway to Understanding, Diagnosing, and Treating Disease Through Rebalancing Protein–Protein Interaction Networks;Protein Homeostasis in Drug Discovery;2022-11-14