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A proteomic study on adhesion molecules in JAK2-V617F and CALR mutated chronic myeloproliferative neoplasia (CMN) patients)
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Deutsche Forschungsgemeinschaft (DFG) ;
Genomic analysis has revealed the occurrence of JAK2-V617F and Calreticulin (CALR) mutations in CMN, where granulocytes, monocytes and erythrocytes are known to be the key players in the induction of venous thrombosis. Previously, our group found that JAK2-V617F aberrantly activates ß1 and ß2 integrins on leukocytes in CMN and identified some of the critical inside-out signaling molecules involved (e.g., small GTPase Rap1, CALDAG-GEF1). However, their context-specific pathophysiology, including the underlying cytokine and chemokine network, is not sufficiently understood. Moreover, it is known that the inter- and intracellular molecular networks classically communicate through proteins produced during granulopoiesis. These proteins are generally stored in granules, or generated on demand, and the differences in expression of these protein could contribute to the pathological thrombus formation in veins as well as in arteries. Therefore, study of the proteome could be an imperative tool for determining new prognostic biomarkers, allowing more classifications and diagnosis of patients with medically unexplained symptoms, and for the identification of novel therapeutic targets.

This study aimed to reveal the pathogenic role of aberrant protein expression in the granulocytes of JAK2-V617F and CALR mutated CMN patients towards the development of a pro-thrombotic state.

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