Improved targeting of JAK2 leads to increased therapeutic efficacy in myeloproliferative neoplasms.
Bhagwat, Neha; Koppikar, Priya; Keller, Matthew; Marubayashi, Sachie; Shank, Kaitlyn; Rampal, Raajit; Qi, Jun; Kleppe, Maria; Patel, Hardik J; Shah, Smit K; Taldone, Tony; Bradner, James E; Chiosis, Gabriela; Levine, Ross L.
; 123(13): 2075-83, 2014 Mar 27.
Artigo em Inglês | MEDLINE | ID: mdl-24470592
Increasing therapeutic efficacy in MPN.
The promise of Janus kinase inhibitors in the treatment of hematological malignancies.
Germ-line JAK2 mutations in the kinase domain are responsible for hereditary thrombocytosis and are resistant to JAK2 and HSP90 inhibitors.
Ruxolitinib reduces JAK2 p.V617F allele burden in patients with polycythemia vera enrolled in the RESPONSE study.
A comparison of qPCR and ddPCR used for quantification of the JAK2 V617F allele burden in Ph negative MPNs.
[Small molecular compounds for BCR/ABL-negative myeloproliferative neoplasms].
New generation small-molecule inhibitors in myeloproliferative neoplasms.
Clarifying the use of ruxolitinib in patients with myelofibrosis.
What is next beyond janus kinase 2 inhibitors for primary myelofibrosis?
JAK2 is dispensable for maintenance of JAK2 mutant B-cell acute lymphoblastic leukemias.