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Therapy with JAK 1/2 inhibitors for myelofibrosis

Therapy with JAK 1/2 inhibitors for myelofibrosis review memo (2013) 6:109–113 DOI 10.1007/s12254-013-0077-9 Franz Romeder, Richard Greil, Alexander Egle Received: 22 November 2012 / Accepted: 28 February 2013 / Published online: 4 April 2013 © Springer-Verlag Wien 2013 Abstract Introduction Purpose Myelofibrosis (MF) is currently the myelopro- liferative disorder with the most severe prognosis. A mu- Myeloproliferative neoplasms (MPN) are an inhomoge- tation of the JAK2 (V617F) enzyme is present in about neous group of hematologic malignancies characterized 65 % of patients. Inhibition of JAK-kinases was therefore by deregulated production of maturing regular blood a proposed treatment for the disease. The purpose of this cells [1]. The classic Philadelphia-chromosome negative article is to give an updated overview about the recent MPNs include polycythemia vera (PV), essential throm- developments in the therapy of MF with JAK-inhibitors. bocythemia (ET), and primary myelofibrosis (PMF). Materials and methods We did a research through the Clinically, patients with MF, as compared to PV and ET, literature to identify the JAK 1/2 inhibitors which are show a substantial reduction in life expectancy with a already approved for treating MF or currently undergo- median survival of 5 years after initial diagnosis and were ing clinical trials. The most important clinical data con- therefore http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png memo - Magazine of European Medical Oncology Springer Journals

Therapy with JAK 1/2 inhibitors for myelofibrosis

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Publisher
Springer Journals
Copyright
Copyright © 2013 by Springer-Verlag Wien
Subject
Medicine & Public Health; Oncology; Medicine/Public Health, general
ISSN
1865-5041
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1865-5076
DOI
10.1007/s12254-013-0077-9
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Abstract

review memo (2013) 6:109–113 DOI 10.1007/s12254-013-0077-9 Franz Romeder, Richard Greil, Alexander Egle Received: 22 November 2012 / Accepted: 28 February 2013 / Published online: 4 April 2013 © Springer-Verlag Wien 2013 Abstract Introduction Purpose Myelofibrosis (MF) is currently the myelopro- liferative disorder with the most severe prognosis. A mu- Myeloproliferative neoplasms (MPN) are an inhomoge- tation of the JAK2 (V617F) enzyme is present in about neous group of hematologic malignancies characterized 65 % of patients. Inhibition of JAK-kinases was therefore by deregulated production of maturing regular blood a proposed treatment for the disease. The purpose of this cells [1]. The classic Philadelphia-chromosome negative article is to give an updated overview about the recent MPNs include polycythemia vera (PV), essential throm- developments in the therapy of MF with JAK-inhibitors. bocythemia (ET), and primary myelofibrosis (PMF). Materials and methods We did a research through the Clinically, patients with MF, as compared to PV and ET, literature to identify the JAK 1/2 inhibitors which are show a substantial reduction in life expectancy with a already approved for treating MF or currently undergo- median survival of 5 years after initial diagnosis and were ing clinical trials. The most important clinical data con- therefore

Journal

memo - Magazine of European Medical Oncology – Springer Journals

Published: Apr 3, 2013

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