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- W2023278718 abstract "Myeloproliferative neoplasms (MPNs) are a group of clonal disorders that arise from the transformation of hematopoietic stem cells. In 2005, several groups reported a single acquired point mutation in the Janus kinase 2 (Jak2) gene in the majority of patients with Philadelphia chromosome (Ph)-negative MPN.1 The mutation is believed to have a critical role in the pathogenesis of these disorders,2, 3 and it has been suggested that most patients harbor mutations (some of which remain to be identified) that potentially serve as a molecular target for selective Jak2 inhibition.4 Although small molecule Jak2 inhibitors are entering clinical trials, their ultimate efficacy is unclear.5 In addition to the concern of insufficient inhibition of mutated Jak2 in vivo or the emergence of resistance through activation of complementary pathways, many MPNs contain other mutational events (for example, mutation in exon12 of Mpl,6 or the KIT D618V mutation in patients with systemic mastocytosis7), and thus are not sensitive to Jak inhibitors. Therefore, the development of inhibitors to common mediators of diverse signaling pathways in this disease is very desirable." @default.
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- W2023278718 date "2011-12-02" @default.
- W2023278718 modified "2023-10-14" @default.
- W2023278718 title "Dual inhibition of Jak2 and STAT5 enhances killing of myeloproliferative neoplasia cells" @default.
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- W2023278718 doi "https://doi.org/10.1038/leu.2011.338" @default.
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