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Angiogenesis and vascular endothelial growth factor-/receptor expression in myeloproliferative neoplasms: correlation with clinical parameters and JAK2-V617F mutational status

Medinger, Michael and Skoda, Radek and Gratwohl, Alois and Theocharides, Alexandre and Buser, Andreas and Heim, Dominik and Dirnhofer, Stephan and Tichelli, André and Tzankov, Alexandar. (2009) Angiogenesis and vascular endothelial growth factor-/receptor expression in myeloproliferative neoplasms: correlation with clinical parameters and JAK2-V617F mutational status. British Journal of Haematology, 146 (2). pp. 150-157.

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Official URL: http://edoc.unibas.ch/43927/

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Abstract

Data on angiogenesis in the bone marrow of BCR-ABL1-negative myeloproliferative neoplasm (MPN) patients suggest an increase of the microvessel density (MVD) and vascular endothelial growth factor (VEGF) expression, but relations to the JAK2-V617F status remain controversial. We performed immunohistochemical studies of MVD and VEGF-expression in 100 MPN, including 24 essential thrombocythemia- (ET), 46 polycythemia vera- (PV), 26 primary myelofibrosis- (PMF), four myelodysplastic (MDS)/MPN- and 20 control reactive bone marrow cases, and correlated these findings with biological and clinical key data and the JAK2-V617F status. We found significantly increased MVD, particularly that assessed by CD105, and VEGF expression in MPN compared to controls (PMF > PV > MDS/MPN > ET). We observed stronger association between CD105-MVD and VEGF expression, fibrosis, and JAK2-V617F mutant allele burden, compared to CD34-MVD. MVD was strongly increased in MPN with high JAK2-V617F mutant allele burden. Our study highlights the importance of newly formed CD105+ vessels in the bone marrow of MPN patients, and indicates that assessment of CD105-MVD better reflects angiogenic activity in MPN. In addition, it provides evidence that despite the fact that angiogenesis is generally independent of the JAK2-V617F status in MPN, new vessel formation might be linked to Jak2 effects in some cases with high JAK2-V617F mutant allele burden.
Faculties and Departments:03 Faculty of Medicine
UniBasel Contributors:Medinger, Michael
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Wiley
ISSN:0007-1048
e-ISSN:1365-2141
Note:Publication type according to Uni Basel Research Database: Journal article
Identification Number:
Last Modified:04 Oct 2017 10:02
Deposited On:04 Oct 2017 10:02

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