Literature DB >> 19657484

Comparison of JAK2V617F mutation assessment employing different molecular diagnostic techniques.

Dino Veneri1, Enrico Capuzzo, Giovanna de Matteis, Massimo Franchini, Elisabetta Baritono, Marco Benati, G Pietro Solero, Achille Ambrosetti, Giulia Quaresmini, Giovanni Pizzolo.   

Abstract

BACKGROUND: The JAK2(V617F) mutation is present in the majority of patients with polycythaemia vera and in approximately half of patients with essential thrombocythaemia and primary myelofibrosis. In this study we compare the results of JAK2(V617F) mutation detection using three different molecular techniques in the same group of patients affected by essential thrombocythaemia. PATIENTS AND METHODS: The JAK2 mutation was investigated with a qualitative method in 115 consecutive outpatients with a diagnosis of essential thrombocythaemia made according to WHO 2001 criteria. In 48/115 (41.7%) the allele burden was also evaluated with two different qualitative methods, of which one was a method developed in-house and the other was a commercially available method.
RESULTS: The JAK2(V617F) mutation was detected by the qualitative method in 81/115 (69.6%) of the patients. Among the 48/115 patients in whom all three methods were applied, the qualitative method detected the mutation in 38 (79%). According to the quantitative method developed in-house, the mutation was present in 35/48 (73%) of the patients: of these, 2/35 (5.7%) patients were homozygous for the JAK2(V617F) mutation. The commercial quantitative method showed the mutation in 37/48 (77%) patients: of these, 9/37 (18%) patients were homozygous. Three of the 13 patients in whom no mutation was detected by the in-house method were positive for the JAK2(V617F) according to the commercial method. In one patient the search for the JAK2(V617F) mutation was positive with the in-house method but negative with the commercial kit.
CONCLUSION: Detection of the JAK2(V617F) mutation may depend on the molecular technique used. Considering that detection of this mutation will not only have a diagnostic value, but also a role in treatment given the development of JAK2(V617F) pathway inhibiting drugs, indications on a reference molecular diagnostic technique for JAK2(V617F) assessment and quantification of its allele burden from a panel of experts are warranted.

Entities:  

Keywords:  JAK2V617F mutation; essential thrombocythaemia; molecular diagnostic techniques

Mesh:

Substances:

Year:  2009        PMID: 19657484      PMCID: PMC2719272          DOI: 10.2450/2009.0070-08

Source DB:  PubMed          Journal:  Blood Transfus        ISSN: 1723-2007            Impact factor:   3.443


  24 in total

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3.  The V617F JAK2 mutation is uncommon in cancers and in myeloid malignancies other than the classic myeloproliferative disorders.

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4.  The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia.

Authors:  Ross L Levine; Marc Loriaux; Brian J P Huntly; Mignon L Loh; Miroslav Beran; Eric Stoffregen; Roland Berger; Jennifer J Clark; Stephanie G Willis; Kim T Nguyen; Nikki J Flores; Elihu Estey; Norbert Gattermann; Scott Armstrong; A Thomas Look; James D Griffin; Olivier A Bernard; Michael C Heinrich; D Gary Gilliland; Brian Druker; Michael W N Deininger
Journal:  Blood       Date:  2005-08-04       Impact factor: 22.113

5.  A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera.

Authors:  Chloé James; Valérie Ugo; Jean-Pierre Le Couédic; Judith Staerk; François Delhommeau; Catherine Lacout; Loïc Garçon; Hana Raslova; Roland Berger; Annelise Bennaceur-Griscelli; Jean Luc Villeval; Stefan N Constantinescu; Nicole Casadevall; William Vainchenker
Journal:  Nature       Date:  2005-04-28       Impact factor: 49.962

6.  Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.

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Journal:  Cancer Cell       Date:  2005-04       Impact factor: 31.743

7.  Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders.

Authors:  Amy V Jones; Sebastian Kreil; Katerina Zoi; Katherine Waghorn; Claire Curtis; Lingyan Zhang; Joannah Score; Rachel Seear; Andrew J Chase; Francis H Grand; Helen White; Christine Zoi; Dimitris Loukopoulos; Evangelos Terpos; Elisavet-Christine Vervessou; Beate Schultheis; Michael Emig; Thomas Ernst; Eva Lengfelder; Rüdiger Hehlmann; Andreas Hochhaus; David Oscier; Richard T Silver; Andreas Reiter; Nicholas C P Cross
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8.  The JAK2 V617F activating tyrosine kinase mutation is an infrequent event in both "atypical" myeloproliferative disorders and myelodysplastic syndromes.

Authors:  David P Steensma; Gordon W Dewald; Terra L Lasho; Heather L Powell; Rebecca F McClure; Ross L Levine; D Gary Gilliland; Ayalew Tefferi
Journal:  Blood       Date:  2005-04-28       Impact factor: 22.113

9.  Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders.

Authors:  E Joanna Baxter; Linda M Scott; Peter J Campbell; Clare East; Nasios Fourouclas; Soheila Swanton; George S Vassiliou; Anthony J Bench; Elaine M Boyd; Natasha Curtin; Mike A Scott; Wendy N Erber; Anthony R Green
Journal:  Lancet       Date:  2005 Mar 19-25       Impact factor: 79.321

10.  JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia.

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2.  The Burden of JAK2V617F Mutated Allele in Turkish Patients With Myeloproliferative Neoplasms.

Authors:  Ipek Yonal-Hindilerden; Aynur Daglar-Aday; Basak Akadam-Teker; Ceylan Yilmaz; Meliha Nalcaci; Akif Selim Yavuz; Deniz Sargin
Journal:  J Clin Med Res       Date:  2014-12-29

3.  Jak2a regulates erythroid and myeloid hematopoiesis during zebrafish embryogenesis.

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