Mechanisms of Resistance to JAK2 Inhibitors in Myeloproliferative Neoplasms.

Meyer, Sara C. (2017). Mechanisms of Resistance to JAK2 Inhibitors in Myeloproliferative Neoplasms. Hematology/oncology clinics of North America, 31(4), pp. 627-642. Elsevier 10.1016/j.hoc.2017.04.003

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Myeloproliferative neoplasms are driven by activated JAK2 signaling due to somatic mutations in JAK2, the thrombopoietin receptor MPL or the chaperone calreticulin in hematopoietic stem/progenitor cells. JAK2 inhibitors have been developed, but despite clinical benefits, they do not signficantly reduce the mutant clone. Loss of response to JAK2 inhibitors occurs and several mechanisms of resistance, genetic and functional, have been identified. Resistance mutations have not been reported in MPN patients suggesting incomplete target inhibition. Alternative targeting of JAK2 by HSP90 inhibitors or type II JAK2 inhibition overcomes resistance to current JAK2 inhibitors. Additional combined therapy approaches are currently being evaluated.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Clinic of Haematology and Central Haematological Laboratory

UniBE Contributor:

Meyer, Sara Christina

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1558-1977

Publisher:

Elsevier

Language:

English

Submitter:

Julia Elisa Garcia

Date Deposited:

22 Dec 2023 06:22

Last Modified:

22 Dec 2023 06:31

Publisher DOI:

10.1016/j.hoc.2017.04.003

PubMed ID:

28673392

Uncontrolled Keywords:

JAK2 JAK2 inhibition Myeloproliferative neoplasms Resistance

BORIS DOI:

10.48350/190300

URI:

https://boris.unibe.ch/id/eprint/190300

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