Now showing items 1-3 of 3

    • Heterodimeric JAK-STAT Activation as a Mechanism of Persistence to JAK2 Inhibitor Therapy 

      Koppikar, Priya; Bhagwat, Neha; Kilpivaara, Outi; Manshouri, Taghi; Adli, Mazhar; Hricik, Todd; Liu, Fan; Saunders, Lindsay M.; Mullally, Ann; Abdel-Wahab, Omar; Leung, Laura; Weinstein, Abby; Marubayashi, Sachie; Goel, Aviva; Gönen, Mithat; Estrov, Zeev; Ebert, Benjamin L.; Chiosis, Gabriela; Nimer, Stephen D.; Bernstein, Bradley E.; Verstovsek, Srdan; Levine, Ross L. (2012)
      The identification of somatic activating mutations in JAK21–4 and in the thrombopoietin receptor (MPL)5 in the majority of myeloproliferative neoplasm (MPN) patients led to the clinical development of JAK2 kinase inhibitors6,7. ...
    • IDH1 and IDH2 Mutation Studies in 1473 Patients with Chronic-, Fibrotic- or Blast-Phase Essential Thrombocythemia, Polycythemia Vera or Myelofibrosis 

      Tefferi, A; Lasho, T L; Abdel-Wahab, O; Guglielmelli, P; Caramazza, D; Pieri, L; Finke, C M; Kilpivaara, O; Mai, M; Gilliland, Dwight; Pardanani, A; Vannucchi, A M; Patel, J.; Wadleigh, Martha; McClure, R. F.; Levine, Robert A. (Nature Publishing Group, 2010)
      In a multi-institutional collaborative project, 1473 patients with myeloproliferative neoplasms (MPN) were screened for isocitrate dehydrogenase 1 (IDH1)/IDH2 mutations: 594 essential thrombocythemia (ET), 421 polycythemia ...
    • Kinase domain mutations confer resistance to novel inhibitors targeting JAK2V617F in myeloproliferative neoplasms 

      Deshpande, Anagha; Reddy, Mamatha M.; Schade, Georg O.M.; Ray, Arghya; Chowdary, Tirumala K.; Griffin, James D.; Sattler, Martin (2011)
      The transforming JAK2V617F kinase is frequently associated with myeloproliferative neoplasms (MPNs) and thought to be instrumental for the overproduction of myeloid lineage cells. Several small molecule drugs targeting ...