Literature DB >> 16772604

Progenitors homozygous for the V617F mutation occur in most patients with polycythemia vera, but not essential thrombocythemia.

Linda M Scott1, Mike A Scott, Peter J Campbell, Anthony R Green.   

Abstract

An acquired V617F JAK2 mutation occurs in patients with polycythemia vera (PV) or essential thrombocythemia (ET). In a proportion of V617F-positive patients, mitotic recombination produces mutation-homozygous cells that come to predominate with time. However, the prevalence of homozygosity is unclear, as previous reports studied mixed populations of wild-type, V617F-heterozygous, and V617F-homozygous mutant cells. We therefore analyzed 1766 individual hematopoietic colonies from 34 patients with PV or ET in whom granulocyte sequencing demonstrated that the mutant peak did not predominate. V617F-positive erythroid burst-forming units (BFU-Es) were more frequent in patients with PV compared with patients with ET (P = .022) and, strikingly, V617F-homozygous BFU-Es were detected in all 17 patients with PV, but in none of the patients with ET (P < .001). Moreover, mutation-homozygous cells were present in 2 patients with ET after polycythemic transformation. These results demonstrate that V617F-homozygous erythroid progenitors are present in most patients with PV but occur rarely in those with ET.

Entities:  

Mesh:

Substances:

Year:  2006        PMID: 16772604     DOI: 10.1182/blood-2006-04-018259

Source DB:  PubMed          Journal:  Blood        ISSN: 0006-4971            Impact factor:   22.113


  84 in total

Review 1.  Pathogenesis and consequences of uniparental disomy in cancer.

Authors:  Hideki Makishima; Jaroslaw P Maciejewski
Journal:  Clin Cancer Res       Date:  2011-04-25       Impact factor: 12.531

2.  JAK2-V617F-mutated myeloproliferative neoplasms reveal different allele burden within hematopoietic cell lineages: a microdissection study of bone marrow trephine biopsies.

Authors:  Andreas Kreft; Thomas Kindler; Erik Springer; Charles James Kirkpatrick
Journal:  Virchows Arch       Date:  2011-10-18       Impact factor: 4.064

Review 3.  Do we know more about essential thrombocythemia because of JAK2V617F?

Authors:  Claire Harrison
Journal:  Curr Hematol Malig Rep       Date:  2009-01       Impact factor: 3.952

4.  STATistical power of clonal analysis: differential STAT1 pathway activation downstream of the JAK2V617F mutation.

Authors:  Ann Mullally; Benjamin L Ebert
Journal:  Cancer Cell       Date:  2010-11-16       Impact factor: 31.743

Review 5.  JAK2 and genomic instability in the myeloproliferative neoplasms: a case of the chicken or the egg?

Authors:  Linda M Scott; Vivienne I Rebel
Journal:  Am J Hematol       Date:  2012-05-28       Impact factor: 10.047

Review 6.  JAK2 inhibitors: what's the true therapeutic potential?

Authors:  Fabio P S Santos; Srdan Verstovsek
Journal:  Blood Rev       Date:  2010-11-20       Impact factor: 8.250

7.  Pediatric essential thrombocythemia (ET) from the Czech Republic.

Authors:  Scott J Samuelson; Josef T Prchal
Journal:  Leuk Res       Date:  2007-09-07       Impact factor: 3.156

8.  Clinical relevance of JAK2 (V617F) mutant allele burden.

Authors:  Francesco Passamonti; Elisa Rumi
Journal:  Haematologica       Date:  2009-01       Impact factor: 9.941

9.  Inherited predisposition to myeloproliferative neoplasms.

Authors:  Amy V Jones; Nicholas C P Cross
Journal:  Ther Adv Hematol       Date:  2013-08

Review 10.  Molecular pathways: molecular basis for sensitivity and resistance to JAK kinase inhibitors.

Authors:  Sara C Meyer; Ross L Levine
Journal:  Clin Cancer Res       Date:  2014-02-28       Impact factor: 12.531

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.