Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders.
By E. Baxter, L. Scott, Peter J. Campbell, C. East, N. Fourouclas, S. Swanton, G. Vassiliou, A. Bench, Elaine M. Boyd, N. Curtin and 3 more. The Lancet, 2005
3,720 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Oncology
View Paper: https://www.semanticscholar.org/paper/f8b9cafb281b260d2f935da2fc9a9510af510425
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Citations in the corpus
- MPLW515L Is a Novel Somatic Activating Mutation in Myelofibrosis with Myeloid Metaplasia (2006, background): “Although clonal hematopoiesis was observed in these disorders more than three decades ago, the molecular etiology of these disorders was not known until recently when several groups reported a somatic mutation in the JAK2 tyrosine kinase (JAK2V617F) in most patients with PV and in a subset of patien”
- Kinase-targeted cancer therapies: progress, challenges and future directions (2018, background): “The oncogenic mutations in JAK2 kinase such as single point mutation (Val617Phe) and JAK2 exon 12 mutations are implicated in both myeloproliferative disorders and myelodysplastic syndromes [38, 39].”
- JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis. (2012, neutral): “Grade 0 134 (92) 44 (30) 33 (23) 7 (5) 3 (2)”
- Pegylated interferon-alfa-2a induces complete hematologic and molecular responses with low toxicity in polycythemia vera. (2008, background): “of phlebotomies in the past 3 mo* 3 (3-5)”
- Classification and diagnosis of myeloproliferative neoplasms: The 2008 World Health Organization criteria and point-of-care diagnostic algorithms (2008, methodology): “Accordingly, the 2008 revision of the WHO document on the classification and diagnosis of CMPDs (now referred to as myeloproliferative neoplasms) has incorporated new information on the molecular pathogenesis of both BCR–ABL -negative classic MPD”
- Mechanisms and consequences of Jak-STAT signaling in the immune system (2017, background): “STAT-targeting small interfering RNAs (siRNAs) (10) and STAT-binding”