Figure 5.
Figure 5. Hemostatic alterations in JAK2V617F+ and JAK2V617F− MPN patients. Abnormalities of platelets, erythrocytes, leukocytes, and endothelial cells lead to systemic hypercoagulability as represented by an increased production of procoagulant microparticles and the occurrence of an acquired APC resistance. Studies addressing whether the JAK2V617F mutation may specifically affect the hemostatic system indicate that both cellular (ie, platelets and leukocytes) and plasma compartments of hemostasis are more activated in MPN patients positive for the JAK2V617F mutation. Therefore, the expression of the JAK2V617F mutation may represent a molecular lesion relevant to promote the cellular procoagulant phenotype. N indicates not different from healthy control subjects; ↗, elevated compared with healthy control subjects; ↗↗, elevated compared with JAK2V617F− patients.

Hemostatic alterations in JAK2V617F+ and JAK2V617F MPN patients. Abnormalities of platelets, erythrocytes, leukocytes, and endothelial cells lead to systemic hypercoagulability as represented by an increased production of procoagulant microparticles and the occurrence of an acquired APC resistance. Studies addressing whether the JAK2V617F mutation may specifically affect the hemostatic system indicate that both cellular (ie, platelets and leukocytes) and plasma compartments of hemostasis are more activated in MPN patients positive for the JAK2V617F mutation. Therefore, the expression of the JAK2V617F mutation may represent a molecular lesion relevant to promote the cellular procoagulant phenotype. N indicates not different from healthy control subjects; ↗, elevated compared with healthy control subjects; ↗↗, elevated compared with JAK2V617F patients.

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