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Therapeutic approaches in myelofibrosis and myelodysplastic/myeloproliferative
overlap syndromes
#MMPMID27143923
Sochacki AL
; Fischer MA
; Savona MR
Onco Targets Ther
2016[]; 9
(?): 2273-86
PMID27143923
show ga
The discovery of JAK2 (V617F) a decade ago led to optimism for a rapidly
developing treatment revolution in Ph(-) myeloproliferative neoplasms. Unlike
BCR-ABL, however, JAK2 was found to have a more heterogeneous role in
carcinogenesis. Therefore, for years, development of new therapies was slow,
despite standard treatment options that did not address the overwhelming symptom
burden in patients with primary myelofibrosis (MF), post-essential
thrombocythemia MF, post-polycythemia vera MF, and myelodysplastic syndrome
(MDS)/myeloproliferative neoplasm (MPN) syndromes. JAK-STAT inhibitors have
changed this, drastically ameliorating symptoms and ultimately beginning to show
evidence of impact on survival. Now, the genetic foundations of myelofibrosis and
MDS/MPN are rapidly being elucidated and contributing to targeted therapy
development. This has been empowered through updated response criteria for
MDS/MPN and refined prognostic scoring systems in these diseases. The aim of this
article is to summarize concisely the current and rationally designed
investigational therapeutics directed at JAK-STAT, hedgehog, PI3K-Akt, bone
marrow fibrosis, telomerase, and rogue epigenetic signaling. The revolution in
immunotherapy and novel treatments aimed at previously untargeted signaling
pathways provides hope for considerable advancement in therapy options for those
with chronic myeloid disease.
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