J 2023

JAK2V617F mutation and circulating extracellular vesicles in essential thrombocythemia

ASWAD, Mohamed Hussam, Jarmila KISSOVÁ, Petra OVESNÁ, Lucie ŘÍHOVÁ, Miroslav PENKA et. al.

Basic information

Original name

JAK2V617F mutation and circulating extracellular vesicles in essential thrombocythemia

Authors

ASWAD, Mohamed Hussam (760 Syrian Arab Republic, guarantor, belonging to the institution), Jarmila KISSOVÁ (203 Czech Republic, belonging to the institution), Petra OVESNÁ (203 Czech Republic, belonging to the institution), Lucie ŘÍHOVÁ (203 Czech Republic, belonging to the institution) and Miroslav PENKA (203 Czech Republic, belonging to the institution)

Edition

CLINICAL HEMORHEOLOGY AND MICROCIRCULATION, AMSTERDAM, IOS PRESS, 2023, 1386-0291

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30205 Hematology

Country of publisher

Netherlands

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 2.100 in 2022

RIV identification code

RIV/00216224:14110/23:00130986

Organization unit

Faculty of Medicine

UT WoS

001076811500002

Keywords in English

Essential thrombocythemia; thrombosis; risk factor; JAK2V617F mutation; extracellular vesicles

Tags

International impact, Reviewed
Změněno: 25/1/2024 14:05, Mgr. Tereza Miškechová

Abstract

V originále

The clinical course of essential thrombocythemia (ET) is complicated with thrombosis which significantly impacts patients’ mortality. Studies have identified JAK2V617F mutation as an independent risk factor for thrombosis. Circulating extracellular vesicles (EVs) were evaluated in several studies regarding myeloproliferative neoplasms and thrombosis as potential biomarkers. The present study investigates the relationship between JAK2V617F mutation and EVs levels in 119 ET patients. Our analyses revealed that JAK2V617F-positive patients are at a significantly increased risk of thrombosis within five years before the ET diagnosis (hazard ratio [95% CI]: 11.9 [1.7–83.7], P = 0.013), and that JAK2V617F mutation is an independent risk factor for thrombosis at ET diagnosis or during the follow-up (hazard ratio [95% CI]: 3.56 [1.47–8.62], P = 0.005). ET patients have higher levels of platelet-EVs, erythrocyte-EVs and procoagulant activity of EVs than the healthy population. Absolute and relative counts of platelet-EVs are increased in the presence of JAK2V617F mutation (P = 0.018, P = 0.024, respectively). In conclusion, our results support the role of JAK2V617F mutation in the pathogenesis of thrombosis in essential thrombocythemia through enhancing platelet activation.