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01) (data not shown). Three PV patients, wild type for JAK2V617F, were carriers of exon-12 JAK2 mutation. At the time of enrolment, 46% of ET and 58% of PV patients were on cytoreductive treatment with HU. Twenty seven patients (15 ET and 12 PV) had a positive history for at least one major thrombotic event (i.e., acute myocardial infarction, ictus/transient ischemic attack, venous thromboembolism); 22 ET patients (28%) and 20 PV patients (33%) experienced microcirculatory symptoms (i.e., headache, paraesthesia, erythromelalgia). Figure 2 shows representative TG curves of PRP from ET and PV patients and healthy controls, triggered in the presence (left panel) and absence (right panel) of exogenous 1 pM TF. For all study subjects, the quantity of thrombin generated by PRP in http://www.selleck.cn/products/Methazolastone.html the absence of exogenous TF was lower compared to that triggered by the addition of 1 pM TF. However, in both experimental conditions, the TG peak and slope were significantly increased (P http://www.selleckchem.com/products/ABT-737.html patients and particularly in those carriers of the http://www.selleckchem.com/products/Nutlin-3.html JAK2V617F mutation. In addition, TG triggered by exogenous TF in PRP from ET patients on ASA showed lower peak (155 �� 33 nM) and slope (29 �� 12 nM min?1) compared to ET patients not taking any treatment (peak: 167 �� 57 nM; slope: 37 �� 27 nM min?1), without reaching a statistical significance. Similar results were observed in the absence of exogenous TF (data not shown). To evaluate the contribution of JAK2V617F mutation in determining the TG potential of PRP, the groups of patients not on HU therapy at the time of the study were analyzed according to JAK2V617F allele burden. These patients, all heterozygous for the mutation, were divided in three groups: i.e., negative (0%),