A der(18)t(9;18)(p13;p11) and a der(9;18)(p10;q10) in polycythemia vera associated with a hyperproliferative phenotype in transformation to postpolycythemic myelofibrosis
Author:
Publisher
Elsevier BV
Subject
Cancer Research,Genetics,Molecular Biology
Reference21 articles.
1. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders;Baxter;Lancet,2005
2. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera;James;Nature,2005
3. A gain-of-function mutation of JAK2 in myeloproliferative disorders;Kralovics;N Engl J Med,2005
4. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis;Levine;Cancer Cell,2005
5. Gains on 9p are common genomic aberrations in idiopathic myelofibrosis: a comparative genomic hybridization study;Al-Assar;Br J Haematol,2005
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1. Late appearance of JAK2 mutated polycythaemia vera in a patient with typical chronic myeloid leukaemia on imatinib: Speculations about role of therapeutic pressure and of secondary genetic events;Leukemia Research;2023-03
2. A Novel Acquired t(2;4)(q36.1;q24) with a Concurrent Submicroscopic del(4)(q23q24) in An Adult with Polycythemia Vera;Cancers;2018-06-25
3. Concomitant presence of JAK2V617F mutation and BCR‑ABL translocation in two patients: A new entity or a variant of myeloproliferative neoplasms (Case report);Molecular Medicine Reports;2018-05-17
4. Translocation t(1;9) is a recurrent cytogenetic abnormality associated with progression of essential thrombocythemia patients displaying the JAK2 V617F mutation;Leukemia Research;2011-09
5. Cytogenetic Findings in Classical MPNs;Myeloproliferative Neoplasms;2010-09-28
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