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Therapeutic approaches in myelofibrosis and myelodysplastic/myeloproliferative overlap syndromes. | LitMetric

Therapeutic approaches in myelofibrosis and myelodysplastic/myeloproliferative overlap syndromes.

Onco Targets Ther

Department of Internal Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Vanderbilt-Ingram Cancer Center, Nashville, TN, USA.

Published: May 2016

AI Article Synopsis

  • - The discovery of JAK2 (V617F) sparked hope for new treatments in myeloproliferative neoplasms, but progress was slow due to its complex role in cancer development and limited existing therapies.
  • - JAK-STAT inhibitors have improved symptoms in conditions like primary myelofibrosis and myelodysplastic syndromes, and new genetic insights are paving the way for more targeted therapies.
  • - This article outlines current investigational therapies that target various pathways, highlighting a promising shift towards novel immunotherapy and treatment options for chronic myeloid diseases.

Article Abstract

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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844455PMC
http://dx.doi.org/10.2147/OTT.S83868DOI Listing

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