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• W3016444371 abstract "Over the last decade, the Janus kinase1/2 (JAK1/2) inhibitor ruxolitinib has emerged as a cornerstone of myelofibrosis (MF) management. Ruxolitinib improves splenomegaly and symptoms regardless of driver mutation status, and confers a survival advantage in patients with intermediate-2/high risk MF. However, cytopenias remain problematic, and evidence for a robust anti-clonal effect is lacking. Furthermore, the median duration of spleen response to ruxolitinib in clinical trials is approximately 3 years, and ruxolitinib does not appear to affect the risk of leukemic transformation. There is no therapy approved specifically for patients whose disease 'progresses' on ruxolitinib, defining which remains challenging. The recent regulatory approval of the JAK2 inihibitor fedratinib partially fulfills this unmet need, but much remains to be done. Other JAK inhibitors and a plethora of novel agents are being studied in the ruxolitinib 'failure' setting, as well as 'add-on' therapies to ruxolitinib in patients having a 'sub-optimal' response." @default.
• W3016444371 created "2020-04-24" @default.
• W3016444371 creator A5013173470 @default.
• W3016444371 creator A5085521139 @default.
• W3016444371 date "2020-04-16" @default.
• W3016444371 modified "2023-10-18" @default.
• W3016444371 title "Management of myelofibrosis after ruxolitinib failure" @default.
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• W3016444371 doi "https://doi.org/10.1080/10428194.2020.1749606" @default.
• W3016444371 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8565616" @default.
• W3016444371 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32297800" @default.
• W3016444371 hasPublicationYear "2020" @default.
• W3016444371 type Work @default.

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