Vascular Endothelial Growth Factor and Thrombopoietin in Patients with Essential Thrombocythemia and Polycythemia vera and Thrombotic Complications

2003 ◽  
Vol 110 (4) ◽  
pp. 202-203 ◽  
Author(s):  
Rossella R. Cacciola ◽  
Ernesto Di Francesco ◽  
Carmen Ferlito ◽  
Giuliana G. Guarnaccia ◽  
Rosario Giustolisi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Polycythemia Vera ◽  
Essential Thrombocythemia ◽  
Vascular Endothelial ◽  
Thrombotic Complications ◽  
Endothelial Growth Factor

scholarly journals Selected Parameters of Angiogenesis and the JAK2, CALR, and MPL Mutations in Patients With Essential Thrombocythemia

2018 ◽  
Vol 24 (7) ◽  
pp. 1056-1060 ◽  
Author(s):  
Grażyna Gadomska ◽  
Alicja Bartoszewska-Kubiak ◽  
Joanna Boinska ◽  
Karolina Matiakowska ◽  
Katarzyna Ziołkowska ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Essential Thrombocythemia ◽  
Leukemia Virus ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Vascular Endothelial ◽  
High Concentration ◽  
Endothelial Growth Factor ◽  
Calr Mutation

The aim of the study was to evaluate selected angiogenic factors in patients with essential thrombocythemia (ET) depending on JAK2V617F, calreticulin gene (CALR) and myeloproliferative leukemia virus oncogene (MPL) mutations. Sixty ET patients and 20 healthy volunteers were enrolled in the study. The following tests were performed: vascular endothelial growth factor- A (VEGF-A), soluble vascular endothelial growth factor receptor-1 (sVEGFR-1),soluble vascular endothelial growth factor receptor-2 (sVEGFR-2), platelet-derived growth factor( PDGF-BB), and stromal-derived factor-1α (SDF-1α). We observed an increased PDGF-BB level in patients with ET compared to the controls. Patients with CALR mutation had significantly higher concentration of PDGF-BB and lower concentration of SDF-1α than patients with JAK2V617F mutation. High concentration of PDGF-BB and low concentration of SDF-1α in patients with CALR(+) ET may indicate a contribution of these chemokines in disturbed Ca2+ metabolism in platelets.

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