Circulating activated platelets in myeloproliferative disorders

Wehmeier, A.; Tschöpe, D; Esser, Jennifer S.; Menzel, Claudia; Nieuwenhuis, H. K.; Schneider, Wolfgang

doi:10.1016/0049-3848(91)90103-4

Cited by 64 publications

(41 citation statements)

References 10 publications

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“…It became apparent that this aggregation correlates with the metastatic potential of cancer cells in vivo (Karpatkin et al, 1988;Joseph, 1995;Al-Mondhiry, 1983). Compared with those in complete remission, patients with active malignant disease have elevated levels of beta-thromboglobulin and platelet factor 4 (Al-Mondhiry, 1983) Circulating activated platelets have also been evidenced in cancer patients by detection of the platelet membrane antigens CD62 (p-selecting) and CD63 (Wehmeier et al, 1991). Tumor cells or membrane vesicles that have been shed spontaneously from tumor cells can directly aggregate platelets in vitro (Jamieson and Scipio, 1982) and can induce platelet aggregation through the release of proaggregatory mediators including adenosine diphosphate, thrombin and a cathepsin-like cysteine proteinase (Grignani and Jamieson, 1988).…”

Section: Iii-b Platelet Activation Markersmentioning

confidence: 99%

Platelets, Coagulation and Cancer: Multifaceted Interactions

Goubran

Burnouf²

2012

American Medical Journal

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Approach: Literature review of the multifaceted interactions between platelets, coagulation and cancer. Results: Over the years, the links existing between cancer development, progression and occurrence of metastasis on one side and coagulation on the other have become obvious. Tumors seems to activate platelets whereas, platelets, on the other hand, through their capacity to activate and release soluble factors and microparticles, interact with tumor cells and influence immune regulation. They appear to be key regulators of many cancer events. Furthermore, coagulation with its different facets also interplays and significantly crosstalks with malignancy. The objectives of this article are to review the mechanisms through which cancer interacts with platelets and the coagulation, triggering thrombosis and the role played by platelets and coagulation factors in the regulation of cancer and to underline the perspectives that are now open in the development of novel diagnostic tools and new cancer treatment strategies. Conclusion/Recommendations: Challenging issues and unresolved questions still need to be addressed to understand the complexity existing between coagulation factors and platelet components and the different stages of cancer progression. Recent discoveries are leading clinicians to consider new therapeutic applications of anticoagulant therapies or new drugs targeting specific platelet functions in cancer patients' management. Furthermore, markers of coagulation and platelet activity may prove to serve as biomarkers for dormant tumors.

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Section: Iii-b Platelet Activation Markersmentioning

confidence: 99%

Platelets, Coagulation and Cancer: Multifaceted Interactions

Goubran

Burnouf²

2012

American Medical Journal

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“…The causes of these abnormalities may include: 1. defects in arachidonic acid metabolism (decrease in agonist-induced release of arachidonic acid from membrane phospholipids; reduced conversion of arachidonic acid to prostaglandine endoperoxides or lipoxygenase products; reduced platelet responsiveness to tromboxane A 2 ) [9][10][11]; 2. abnormalities of platelet granules (increased platelet alpha-granule secretion and an aquired storage pool defect of dense granules) [3,12,13]; 3. decreased number of á 2 -adrenergic receptors, abnormalities of specific platelet membrane glycoproteins (GP) such as GPIIb/IIIa, GP Ib/IX or increased number of GPIV molecules and receptors for the Fc component of IgG [3,[14][15][16]]. An aquired von Willebrand disease [17,18], a reduction of platelet procoagulant activity and an aquired form of Bernard-Soulier syndrome were also reported in these disorders [19].…”

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confidence: 99%

Abnormalities of platelet aggregation in chronic myeloproliferative disorders

Avram

Lupu

Angelescu

et al. 2001

J Cellular Molecular Medi

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A large variety of platelet dysfunctions has been described in chronic myeloproliferative disorders. These abnormalities may be due to deficiency of platelet granules, arahidonic acid metabolism defects or platelet membrane glycoproteins abnormalities. In this study we intend to detect the incidence of platelet function defects in 76 patients with various types of chronic myeloproliferative disorders. The platelet activity was studied in vitro by measuring platelet aggregation in response to ADP, epinephrine, collagen, arachidonic acid and ristocetin. These results were subsequently correlated with bleeding time and clinical aspects (bleeding or thrombosis). We found complex changes in platelet response with all agonists, in varied proportions. These abnormalities include absent, decreased or abnormal platelet aggregation response. In a few cases we found a markedly decreased, almost absent platelet response to all agonists while in some patients a normal platelet aggregation was noted. The correlation between these results and template bleeding time, thrombotic or hemorrhagic events and the type of diseases was difficult to establish and sometimes conflictual. Despite this fact, we consider that investigating platelet aggregation may be useful not only for the assesment of the hemostatic balance in chronic myeloproliferative disorders but also for a better insight into cell abnormalities occuring in these pathologic conditions.

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“…However, the degree of platelet count has not been significantly correlated with thrombosis risk in PV [20,21].…”

Section: Quantitative Platelet Abnormalitiesmentioning

confidence: 99%

Polycythemia Vera and Acute Coronary Syndromes: Pathogenesis, Risk Factors and Treatment

Gouri¹

2013

J Hematol Thrombo Diseases

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Polycythemia vera is a chronic myeloproliferative disorder marked by significant thrombotic complications. Myocardial infarction and heart failure is the most common cause of death. Mechanisms involved in the pathogenesis of these complications are not yet well elucidate; erythrocytosis and quantitative platelet abnormalities may play a major role in the development of thrombosis and ischemia. Age older than 60 years and prior history of thrombosis are the two main risk factors. Evidence for the prevention and treatment of specific cardiovascular complications in PV is too scarce. However, current evidence supports the use of hydroxyurea as the initial choice of cytoreductive agent in PV patients with acute coronary syndrome.

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Circulating activated platelets in myeloproliferative disorders

Cited by 64 publications

References 10 publications

Platelets, Coagulation and Cancer: Multifaceted Interactions

Platelets, Coagulation and Cancer: Multifaceted Interactions

Abnormalities of platelet aggregation in chronic myeloproliferative disorders

Polycythemia Vera and Acute Coronary Syndromes: Pathogenesis, Risk Factors and Treatment

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