title: Advancing the STATus of MPN pathogenesis.
abstract: In this issue of Blood, Yan et al and Walz et al exploit mouse genetics to investigate the contribution of signal transducer and activator of transcription 5 (STAT5) to the abnormal in vivo growth of hematopoietic cells expressing JAK2(V617F) or BCR-ABL. Eliminating STAT5 expression had dramatic effects in both contexts, and this new work and other recent studies support the therapeutic potential of targeting pathways regulated by this important signaling molecule in patients with myeloproliferative neoplasms (MPNs).
authors.affiliation: University of California, San Francisco, CA, USA.
authors.forename: Neil P
authors.initials: NP
authors.lastname: Shah
authors.forename: Kevin
authors.initials: K
authors.lastname: Shannon
mesh_terms: D000818:Animals; D016313:Genes, abl / Q000502:physiology*; D006801:Humans; D053614:Janus Kinase 2 / Q000502:physiology*; D009196:Myeloproliferative Disorders / Q000235:genetics*; D011087:Polycythemia Vera / Q000235:genetics* / Q000473:pathology*; D050799:STAT5 Transcription Factor / Q000502:physiology*
chemical_list: D050799:STAT5 Transcription Factor; C494093:Stat5a protein, mouse; C494096:Stat5b protein, mouse; C507926:Jak2 protein, mouse; D053614:Janus Kinase 2