NS-018, a selective JAK2 inhibitor, preferentially inhibits CFU-GM colony formation by bone marrow mononuclear cells from high-risk myelodysplastic syndrome patients

Abstract JAK2/STAT signaling promotes survival and expansion of myelodysplastic syndrome (MDS) clones, but little is known about the potential of JAK2/STAT as a therapeutic target in MDS. We investigated the effect of NS-018, a novel antagonist for JAK2, on the colony-forming ability of bone marrow...

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Published inLeukemia research Vol. 38; no. 5; pp. 619 - 624
Main Authors Kuroda, Junya, Kodama, Ayumi, Chinen, Yoshiaki, Shimura, Yuji, Mizutani, Shinsuke, Nagoshi, Hisao, Kobayashi, Tsutomu, Matsumoto, Yosuke, Nakaya, Yohei, Tamura, Ayako, Kobayashi, Yutaka, Naito, Haruna, Taniwaki, Masafumi
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.05.2014
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Summary:Abstract JAK2/STAT signaling promotes survival and expansion of myelodysplastic syndrome (MDS) clones, but little is known about the potential of JAK2/STAT as a therapeutic target in MDS. We investigated the effect of NS-018, a novel antagonist for JAK2, on the colony-forming ability of bone marrow mononuclear cells (BMMNCs) from high-risk MDS patients. NS-018 decreased colony-forming unit-granulocyte/macrophage (CFU-GM) colony numbers from MDS-derived BMMNCs in a dose-dependent manner, and this effect was significantly more potent than against normal BMMNCs. In addition, NS-018 suppressed the phosphorylation of STAT3 in colony-forming cells from MDS patients. Collectively, NS-018 could be a new therapeutic option for high-risk MDS.
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ISSN:0145-2126
1873-5835
DOI:10.1016/j.leukres.2014.03.001