The JAK2 V617F tyrosine kinase mutation in myelodysplastic syndromes (MDS) developing myelofibrosis indicates the myeloproliferative nature in a subset of MDS patients
Author:
Publisher
Springer Science and Business Media LLC
Subject
Oncology,Cancer Research,Hematology
Link
http://www.nature.com/articles/2403989.pdf
Reference7 articles.
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2. Levine RL, Wadleigh M, Cools J, Ebert BL, Wernig G, Huntly BJ et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and agnogenic myeloid metaplasia. Cancer Cell 2005; 7: 387–397.
3. James C, Ugo V, Le Couedic JP, Staerk J, Delhommeau F, Lacout C et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 2005; 484: 1144–1148.
4. Baxter EJ, Scott LM, Campbell PJ, East C, Fourouclas N, Swanton S et al. Cancer genome project. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet 2005; 365: 1054–1061.
5. Steensma DP, Dewald GW, Lasho TL, Powell HL, McClure RF, Levine RL et al. The JAK2 V617F activating tyrosine kinase mutation is an infrequent event in both ‘atypical’ myeloproliferaive disorders and myelodysplastic syndromes. Blood 2005; 106: 1207–1209.
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1. DÜŞÜK VE YÜKSEK JAK2V617F ALLEL YÜKÜ OLAN MİYELOPROLİFERATİF NEOPLAZİ ÖN TANILI HASTALARIN KLİNİK VE HEMATOLOJİK PARAMETRELER AÇISINDAN KARŞILAŞTIRILMASI;Kocatepe Tıp Dergisi;2024-01-17
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3. Machine learning demonstrates that somatic mutations imprint invariant morphologic features in myelodysplastic syndromes;Blood;2020-11-12
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