Cristal Reyna Thompson's research while affiliated with Boston University and other places

Publications (5)

Article
Objective The risk of thrombosis in myeloproliferative neoplasms, such as primary myelofibrosis varies depending on the type of key driving mutation (JAK2 [janus kinase 2], CALR [calreticulin], and MPL [myeloproliferative leukemia protein or thrombopoietin receptor]) and the accompanying mutations in other genes. In the current study, we sought to...
Article
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Excessive accumulation of extracellular matrix (ECM) is a hallmark of bone marrow (BM) milieu in primary myelofibrosis (PMF). As cells have the ability to adhere to the surrounding ECM through integrin receptors, we examined the hypothesis that an abnormal ECM-integrin receptor axis contributes to BM megakaryocytosis in JAK2V617F+ PMF. Secretion of...
Article
Full-text available
Excessive accumulation of extracellular matrix (ECM) is a hallmark of bone marrow (BM) milieu in Primary Myelofibrosis (PMF). Myelofibrosis was long regarded as a bystander of disease in PMF. However, as cells have the ability to sense the surrounding ECM through integrin receptors, we examined the hypothesis that abnormal ECM in myelofibrosis, med...
Article
Patients with malignancy are at 4- to 7-fold higher risk of venous thromboembolism (VTE), a potentially fatal, yet preventable complication. Although general mechanisms of thrombosis are enhanced in these patients, malignancy-specific triggers and their therapeutic implication remain poorly understood. Here we examined a colon cancer-specific VTE m...
Article
Full-text available
Thrombosis is at the heart of cardiovascular complications observed in specific diseases. A heightened thrombosis risk above that in general population in diseases such as myelofibrosis and chronic kidney disease implicates disease-specific mediators of thrombosis. This relative lack of information regarding the mechanisms of thrombosis in specific...

Citations

... Moreover, leukocytosis is an independent predictor of hemorrhagic complications in MPNs [14]. A third possibility is that the JAK2 V617F mutation itself decreased platelet aggregation when adding collagen and thrombin [15]. Collectively, despite long-term treatment with ruxolitinib, our case might have developed abnormal hemostasis and inhibition of platelet aggregation caused by these possible mechanisms, which led to prolonged bleeding time and subsequent recurrent and multiple ICHs. ...
... Recently, Matsuura et al. (4) examined integrin-mediated adhesion to fibronectin of megakaryocytes (MKs) carrying the JAK2 V627F mutation, in order to expand the present understanding of megakaryocytosis in this pathology. Integrins are adhesion receptors that link cells to components of the extracellular matrix (ECM) and are, thereby, responsible for intracellular signal transduction (5,6). ...
... Finally, indoxyl sulfate can be included in the family of uremic endotheliotoxins, meaning that this compound induces endothelial dysfunction, one central element implicated in cardiovascular morbidity and mortality, taking into account that the risk of cardiovascular dysfunctions is associated with chronic kidney disease [104]. From in vivo and in vitro preclinical studies, indoxyl sulfate has been shown to promote both pro-thrombotic processes, notably through mechanisms involving the aryl hydrocarbon receptor [105][106][107] and prooxidant processes [108][109][110][111]. Clinical data obtained in patients with chronic kidney disease indicate that indoxyl sulfate is likely to represent one of the links between impaired renal function and adverse cardiovascular events, notably regarding hemostatic disorders [112] and thrombotic events [113]. ...
... Mutations in the Janus kinase 2 (JAK2), myeloproliferative leukemia virus (MPL) and calreticulin (CALR) genes are found in the majority of patients with these three classic MPNs and all lead to hyperactivity of the JAK-STAT signaling pathway normally involved in inflammatory signaling and hematopoietic cell proliferation [59]. Thrombotic and hemorrhagic complications are commonly seen in these patients with approximately 18% of patients developing thrombotic events during a 10 year period [60][61][62]. In a study of 891 patients with ET, the presence of the JAK2 V617F mutation, the most common mutation in MPNs, was associated with a two-fold increase in the risk of VTE and arterial thrombosis compared to patients without a JAK 2V617F mutation (hazard ratio of 2.04 with 95% confidence interval of 1.19-3.48) ...