Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombotic complications in non-Hodgkin's lymphoma often originate in the large veins. We describe a patient with refractory advanced high-grade lymphoma who presented with the rare complication of extensive cutaneous necrosis due to thrombosis of dermal vessels; there was also a recent new peak of monoclonal IgM-kappa protein. Direct immunofluorescence demonstrated immune deposits with complement in the dermal vessel wall. Based on these observations and on published data, we suggest that these complexes were the trigger for the thrombotic events and that the monoclonal IgM acted as xenoreactive antibodies, initiating a cascade of events. The first step of this cascade was activation of the complement and the membrane attack complex, which caused secretion of IL-1 alpha by endothelial cells, followed by overexpression of tissue factor on the surface of the dermal vessel wall endothelium. Dermal vessel thrombosis was the final event in this cascade.
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PMID:Cutaneous necrosis as a terminal paraneoplastic thromboembolic event in a patient with non-Hodgkin's lymphoma. 1020 93

Thromboembolism affects many patients with solid tumors and clonal hematologic malignancies. Pathogenetic mechanisms include inflammatory- and tissue factor-mediated coagulation, natural anticoagulant deficiencies, fibrinolytic alterations, hyperviscosity, and activation of platelets, endothelial cells, and leukocytes. High rates of venous thromboembolism (VTE) occur with advanced pancreatic, breast, ovarian, germ cell, lung, prostate, and central nervous system cancers. Hodgkin disease, non-Hodgkin's lymphoma, myeloma, paroxysmal nocturnal hemoglobinuria, and certain leukemias also predispose to venous thromboembolism. Arterial and venous events occur with polycythemia vera and essential thrombocythemia. Central venous catheters and prothrombotic antitumor regimens augment the risk in some patients. Part 1 of this two-part article addresses pathophysiology, clinical presentations, and risk of malignancy-associated thrombosis. Part 2, which will appear in next month's issue, covers prophylaxis and treatment of these thromboembolic complications.
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PMID:Thromboembolic complications of malignancy. Part 1: Risks. 1605 35

Patients with haematological malignancies carry increased risk of venous thrombosis (VT). However, the mechanisms that link these malignancies to activated coagulation have not been fully identified. Since anti-haemostatic agents are studied in clinical trials for their potential to prolong survival in cancer patients, a detailed characterisation of haemostatic markers in cancer subtypes is needed. Hence, in this study, we measured the plasma concentrations and mRNA expression in blood mononuclear cells of haemostatic parameters in 93 patients with haematological neoplasias (acute myeloid leukaemia, chronic lymphatic leukaemia, multiple myeloma, and non-Hodgkin's lymphoma) before start and after completion of cancer therapy. At diagnosis we found activation of coagulation and fibrinolysis, especially in patients with acute myeloid leukaemia. This hypercoagulation was not associated with increased levels of tissue factor (TF) or factor VII (fVII) antigen or mRNA, or levels of activated fVII. In conclusion we found a hypercoagulable state in patients with haematological malignancy that did not seem to be initiated by TF.
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PMID:Hypercoagulability in patients with haematological neoplasia: no apparent initiation by tissue factor. 1852 6