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Vol. 126, No. 1, 2011
Issue release date: June 2011
Section title: Original Paper
Acta Haematol 2011;126:54–62
(DOI:10.1159/000324436)

Proteolytic Matrix Metallopeptidases and Inhibitors in BCR-ABL1-Negative Myeloproliferative Neoplasms: Correlation with JAK2V617F Mutation Status

Vadikolia C.M.a · Tsatalas C.a · Anagnostopoulos K.b · Trypsianis G.c · Pantelidou D.a · Bazdiara I.a · Anastasiadis A.a · Spanoudakis E.a · Kotsianidis I.a · Margaritis D.a · Kortsaris A.b · Bourikas G.a
Departments of aHematology, bClinical Biochemistry and cMedical Statistics, Democritus University Medical School, Alexandroupolis, Greece

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 11/10/2010
Accepted: 1/17/2011
Published online: 4/7/2011
Issue release date: June 2011

Number of Print Pages: 9
Number of Figures: 2
Number of Tables: 5

ISSN: 0001-5792 (Print)
eISSN: 1421-9662 (Online)

For additional information: http://www.karger.com/AHA

Abstract

Background/Aims: Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) share the same acquired lesion JAK2V617F and may exhibit substantial overlap. Variability in JAK activation and allele burden, complemented by host, genetic and non-genetic modifiers, determine the phenotype. The aim of this study was to investigate the presence of the JAK2 mutation in association with the ratio of metallopeptidases inhibitors (TIMPs) to tissue metallopeptidases (MMPs) in MPNs, where inhibitory rather than proteolytic activity in marrow microenvironment appears to predominate. Methods: 94 patients with polycythemia vera, essential thrombocythemia and primary myelofibrosis, and 102 healthy individuals were evaluated. Allele-specific PCR and RFLP were used to detect JAK2 and genomic status. Serum concentrations of MMP and TIMP were measured by ELISA. The parameters were assessed with covariance analysis, and adjusted for gender, age and co-morbidity. Results: Mutation frequency was 81.91%. Abnormal TIMP/MMP ratios were identified in all three diseases. JAK2 mutation was correlated with significant changes in TIMP concentrations. Conclusions: Identification of an abnormal TIMP/MMP ratio in all three diseases, regardless of the JAK2 status, indicates invariable marrow remodeling. In this particular group of patients, presence of a JAK2V617F mutation, being associated with even higher ratios, appears to be a concurring participant in bone marrow-reforming processes. Additional research may delineate correlates with the JAK2 allelic burden.

© 2011 S. Karger AG, Basel


  

Author Contacts

Prof. C. Tsatalas
Hematology Department
Democritus University Hospital
GR–68100 Alexandroupolis (Greece)
Tel. +30 6945 10 34 94, E-Mail ktsatala@med.duth.gr and c.vadikolia@gmail.com

  

Article Information

Received: November 10, 2010
Accepted after revision: January 17, 2011
Published online: April 7, 2011
Number of Print Pages : 9
Number of Figures : 2, Number of Tables : 5, Number of References : 33

  

Publication Details

Acta Haematologica

Vol. 126, No. 1, Year 2011 (Cover Date: June 2011)

Journal Editor: Ben-Bassat I. (Qiryat-Ono)
ISSN: 0001-5792 (Print), eISSN: 1421-9662 (Online)

For additional information: http://www.karger.com/AHA


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 11/10/2010
Accepted: 1/17/2011
Published online: 4/7/2011
Issue release date: June 2011

Number of Print Pages: 9
Number of Figures: 2
Number of Tables: 5

ISSN: 0001-5792 (Print)
eISSN: 1421-9662 (Online)

For additional information: http://www.karger.com/AHA


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