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2015 ; 56
(10
): 2768-78
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Novel therapies for myelofibrosis
#MMPMID25860240
Stein BL
; Cervantes F
; Giles F
; Harrison CN
; Verstovsek S
Leuk Lymphoma
2015[]; 56
(10
): 2768-78
PMID25860240
show ga
Myelofibrosis (MF), including primary, post-essential thrombocythemia and
post-polycythemia vera MF, associates with a reduced quality of life and
shortened life expectancy. Dysregulation of the Janus kinase (JAK)/signal
transducer and activator of transcription (STAT) pathway is prominent, even in
the absence of the JAK2(V617F) mutation. Therefore, all symptomatic MF patients
may potentially derive benefit from JAK inhibitors. Despite the efficacy of JAK
inhibitors in controlling signs and symptoms of MF, they do not eradicate the
disease. Therefore, JAK inhibitors are currently being tested in combination with
other novel therapies, a strategy which may be more effective in reducing disease
burden, either by overcoming JAK inhibitor resistance or targeting additional
mechanisms of pathogenesis. Additional targets include modulators of epigenetic
regulation, pathways that work downstream from JAK/STAT (i.e. mammalian target of
rapamycin/AKT/phosphoinositide 3-kinase) heat shock protein 90, hedgehog
signaling, pro-fibrotic factors, abnormal megakaryocytes and telomerase. In this
review, we discuss novel MF therapeutic strategies.
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