Targeting the Inactive Conformation of JAK2 in Hematological Malignancies

Olli Silvennoinen; Stevan R Hubbard

doi:10.1016/j.ccell.2015.06.010

Targeting the Inactive Conformation of JAK2 in Hematological Malignancies

Cancer Cell. 2015 Jul 13;28(1):1-2. doi: 10.1016/j.ccell.2015.06.010.

Authors

Olli Silvennoinen¹, Stevan R Hubbard²

Affiliations

¹ School of Medicine, University of Tampere, Biokatu 8, 33014 Tampere, Finland; Clinical Hematology, Department of Internal Medicine, Tampere University Hospital, Medisiinarinkatu 3, 33520 Tampere, Finland. Electronic address: olli.silvennoinen@uta.fi.
² Kimmel Center for Biology and Medicine at the Skirball Institute and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.

PMID: 26175407
DOI: 10.1016/j.ccell.2015.06.010

Abstract

Activating JAK2 mutants cause hematological malignancies. Current clinical type I JAK2 inhibitors effectively relieve symptoms but fail to resolve the disease. In this issue of Cancer Cell, two articles by Wu and colleagues and Meyer and colleagues characterize a type II JAK2 inhibitor that is effective in preclinical models of JAK2-dependent myeloproliferative neoplasms and B cell acute lymphoblastic leukemia.

Publication types

Comment

MeSH terms

Aminopyridines / administration & dosage*
Animals
Antineoplastic Agents / administration & dosage*
Benzimidazoles / administration & dosage*
Dexamethasone / administration & dosage*
Drug Resistance, Neoplasm / drug effects*
Humans
Janus Kinase 2 / antagonists & inhibitors*
Janus Kinase 2 / genetics*
Myeloproliferative Disorders / drug therapy*
Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy*
Protein Kinase Inhibitors / administration & dosage*

Substances

Aminopyridines
Antineoplastic Agents
Benzimidazoles
Protein Kinase Inhibitors
Dexamethasone
Janus Kinase 2