Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibrinogen survival using 125I-labelled homologous fibrinogen was studied in 17 adults with acute leukemia. Five patients in complete remission had normal fibrinogen survival and turnover rate. Five of 6 patients undergoing induction therapy and 4 of 6 in relapse had shortened fibrinogen survival; the turnover rate was increased in all 12 patients. Nine of 12 patients with active disease had elevated levels of fibrinogen degradation products in the serum. Serial coagulation studies did not support the diagnosis of overt disseminated intravascular coagulation. There was no correlation between the morphological type of leukemia, chemotherapy, the presence of fever and sepsis, or liver dysfunction and fibrinogen survival. Other possible causes of the accelerated fibrinogen turnover in patients with active disease are discussed.
Cancer 1975 Feb
PMID:Fibrinogen survival and fibrinolysis in acute leukemia. 105 37

Eight sublines of the radiation-induced lymphoma S-1033 of C57BL/10 (hereafter called B10) origin were established by exposing the cells in vivo to eight antineoplastic agents for a number of transplant generations. The parental and drug-treated sublines were tested for immunogenic properties, i.e., the ability to elicit allograft reactions in the host of origin and in congenic-resistant mice differing for the S-D or K-I-S regions of the H-2 complex. Lymphoma S-1033 and all drug-treated sublines except one were found to be essentially nonimmunogenic for B10 mice. The S-DIC subline, when exposed for 8 to 12 transplant generations to dimethyltriazenoimidazolecarboxamide, became immunogenic for syngeneic B10 mice, as judged from prolongation of survival time. Large i.v. inocula (10(7) cells) of S-1033 and of the drug-treated sublines, with the possible exception of the cyclophosphamide-treated and dimethyltriazenoimideazolecarboxamide-treated lymphomas, were more effectively rejected by K-I-S- than by S-D-incompatible mice. Dilution escape (i.e., tumor rejection after challenge with large inocula, and lethal tumor growth after injection of small inocula of lymphoma cells in allogeneic recipients) occurred in K-I-S-incompatible mice that were inoculated with S-1033 and three drug-treated (5-fluorouracil, cyclophosphamide, and pyrazocarboxamideamino) sublines. No dilution escape occurred with dimethyltriazenoimidazolecarboxamide or bischloroethylnitrosourea sublines. These data favor the hypothesis that various types of immunogenic changes of neoplastic cells may occur in tumor-bearing hosts following treatment with antineoplastic agents in vivo.
Cancer Res 1975 Aug
PMID:Changes of the immunogenic properties of a radiation-induced mouse lymphoma following treatment with antitumor drugs. 114 19

Highly immunogenic sublines of L1210 and LSTRA lymphomas were obtained from athymic (nude) mice treated with 4(5)-(3,3-dimethyl-1-triazeno)imidazole-5(4)carboxamide (DIC) in vivo. Conventional mice, compatible with the parent tumor, rejected the DIC-treated sublines and were relatively resistant to a subsequent challenge with the parent lines. The DIC-treated sublines were not rejected by athymic mice, which indicated that the transplantation resistance to these tumors in conventional mice was thymus-cell dependent. In addition, there was marginal or no increase of tumor-cell immunogenicity when the parent lines were passaged in nude mice without DIC treatment. This indicated that the DIC-dependent immunogenic changes in DIC-treated leukemic conventional mice could not be ascribed merely to protection by naturally occurring antigenic clones that resulted from DIC-induced immunodepression.
J Natl Cancer Inst 1975 Jul
PMID:Increased immunogenicity of two lymphoma lines after drug treatment of athymic (nude) mice. 115 15

Disturbances in the blood coagulation mechanism are seen by the obstetrician and gynecologist as rare complications of abruptio placentae, retained dead fetus syndrome, amniotic fluid embolism, toxemia, saline amnioinfusion, and septic abortion. Two cases of disseminated intravascular coagulation complicating gynecologic malignancy are presented. Laboratory studies showed thrombocytopenia, hypofibrinogenemia, and increased fibrin degradation products. Derangements of hemostasis in patients with malignancy are discussed from a clinical viewpoint.
 ...
PMID:Disseminated intravascular coagulation in gynecologic cancer. 119 68

New antigenic properties of experimental lymphomas have been reported previously following in vivo treatment with antitumor agents. 5-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide (DIC) induced new antigenic characteristics on L1210 and L5178Y lymphomas, that were previously investigated in studies in animals compatible with the original untreated parental tumors. Here the L1210/DIC and L5178Y/DIC susceptibility to the cytotoxic effects of allogeneic and xenogeneic lymphocytes and sera obtained from animals sensitized to DBA/2 histocompatibility antigens were studied. The original and the DIC tumors showed the same sensitivity to anti-DBA/2 cellular and humoral cytotoxicity. The immune response electied in allogeneic mice by the original and DIC sublines was evaluated by in vitro cell-mediated and humoral cytotoxic assay. Beyond the immune response to histocompatibility antigens, a specific, anti-DIC-antigen immunoreaction was not found. Inhibition assay of the cell-mediated cytotoxicity and absorption of the humoral cytotoxicity demonstrated that DIC-induced antigens are not reciprocally related in cell-surface concentration to the natural DBA/2 histocompatibility antigens associated with tumor cells of DIC lines. An experiment was conducted in which specific activity against the DIC-treated L5178Y/DIC cells was observed with anti-L5178Y/DIC rabbit immune serum absorbed with the parental L5178Y lymphoma. This finding provides additional support to previous studies indicating that treatment with DIC induced new antigens on the lymphoma cells.
Cancer Res 1976 Jan
PMID:Immunosensitivity and histocompatibility antigens in drug-altered leukemic cells. 124 1

Immunologic alteration of the L5178Y lymphoma was obtained in vivo after treatment with 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DIC). A single dose of 1,3-bis(2-chlorethyl)-1-nitrosourea (BCNU) "CURED" MICE CHALLENGED WITH L5178Y cells that had been treated with DIC (L5178Y/DIC) for four transplant generations; BCNU did not cure mice bearing the parent tumor. The L5178Y/DIC, treated in vivo for five transplant generations, id not grow in syngeneic mice. L5178Y/OIC cell growth and incidences of death were similar to those of parent cells when inoculated into heavily immunosuppressed mice. Adoptive transfer of lymphocytes from spleens of mice sensitized to the drug-altered tumor specifically protected immunosuppressed mice bearing the L5178Y/DIC tumor. Little protection was afforded by lymphocytes immune to the parent L5178Y tumor, whereas nonimmune lymphocytes or lymphocytes immune against unrelated tumors were completely ineffective. Anti-L5178Y/DIC lymphocytes did not cure mice challenged with the parent L5178Y tumor. Irradiated (400 R) mice previously sensitized to L5178Y/DIC cells rejected 10(2)-10(7) inocula of L5178Y/DIC cells and died when the parent L5178Y was used for challenge. It was concluded that antigeni( alterations of L5178Y cells occurred in (BALB/ctcr X DBA/2Cr)F1 mice after treatment with DIC in vivo.
J Natl Cancer Inst 1976 Jan
PMID:Antigenic changes of L5178Y lymphoma after treatment with 5-(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide in vivo. 125 54

Disseminated intravascular coagulation (DIC) is a syndrome caused by the systemic generation of thrombin. Most cases are due to pathological activation of the intrinsic coagulation systems (e.g. in sepsis), and/or the extrinsic system (e.g. in malignancy and head trauma). Diagnosis is made by finding abnormalities in at least 3 of 4 laboratory values, namely prothrombin time, platelet count, fibrinogen and fibrinogen/fibrin degradation products. The most common clinical manifestation of DIC is bleeding, with thrombosis in less than 10% of acute cases but more frequently encountered in chronic DIC associated with malignancy. Acute DIC must first be treated by specific therapy of the underlying disease and general support measures. If serial clinical and laboratory monitoring improves, no further treatment is required. If severe or life-threatening haemorrhage occurs or a thrombotic event ensues, heparin anticoagulation followed by aggressive replacement with platelets, fresh plasma and possibly cryoprecipitate is indicated. Heparin doses should be 'therapeutic' (i.e. adequate to overcome the coagulant forces that may have produced a relative heparin-resistant state in the blood). Chronic DIC with haemorrhage, or more usually thrombosis, should also be treated with heparin; warfarin is ineffective. If DIC persists because, for example, a tumour does not regress, long term outpatient subcutaneous heparin therapy may be required.
 ...
PMID:Disseminated intravascular coagulation. Approach to treatment. 128 66

About 15% of patients with cancer have cerebrovascular lesions, resulting from 4 kinds of disorders sometimes intermingled in advanced disseminated cancer: coagulation disorders, direct effects of the tumor, infections and therapeutic measures. Infarction, hardly less frequent than hemorrhage, mostly complicates lymphoma and carcinoma. Hypercoagulation states, such as chronic disseminated intravascular coagulation, nonbacterial thrombotic endocarditis, and nonmetastatic cerebral venous thrombosis account for about 50% of cases. Tumor emboli, as seen in intravascular malignant lymphomatosis, arteritis related to aspergillus, granulomatous angiitis with or without herpes zoster and radiation-induced atherosclerosis are rarer. Cerebral hemorrhages, excluding bleeding from the metastases of choriocarcinoma and melanoma are mainly associated with leukemia by acute disseminated intravascular coagulation as in promyelocytic leukemia, by leukostasis or by pancytopenia. Both infarction and hemorrhage rarely reveal the neoplasia. Lesions are often small and disseminated, and therefore produce a picture of diffuse acute or subacute encephalopathy rather than acute focal deficits. Finally, there may be no relationship between the cerebrovascular event and the neoplasia, and atherosclerosis or traumatic subdural hematoma may well be the causal factor.
 ...
PMID:[Cerebrovascular complications of cancers]. 130 55

Acute promyelocytic leukemia is a clonal expansion of malignant cells blocked at a specific stage of myeloid differentiation. The disease is associated with a specific translocation between chromosome 17 and chromosome 15 [t(15;17)] and with a bleeding diathesis previously attributed to disseminated intravascular coagulation, which has recently also been related to primary fibrinolysis. The high percentage of early deaths, about 20%, experienced by acute promyelocytic leukemia patients, is generally due to the hemorrhagic syndrome. A new finding is the high effectiveness of treatment with all-trans retinoic acid, a vitamin A derivative, for inducing complete remission. The induction of cellular maturation by this agent represents the first model of differentiation therapy. Furthermore, recent molecular studies revealed that the breakpoints of the t(15;17) translocation are clustered in the gene of retinoic acid receptor-alpha, generating a hybrid gene product. Gene transfection experiments disclosed the impairment of gene transactivation due to the hybrid gene products, opening new concepts for understanding leukemogenesis. Understanding the mechanisms of action of retinoic acid could extend differentiation therapy to other malignancies with aberrant gene transcription.
 ...
PMID:Retinoic acid in acute promyelocytic leukemia: a model for differentiation therapy. 131 15

Circulating thrombomodulin is a novel endothelial cell marker, which may reflect the endothelial injury. Plasma levels of thrombomodulin were quantitated by an enzyme-linked immunosorbent assay (ELISA) in patients with hematological malignancies, liver disease, diabetes mellitus, collagen disease, thrombotic disease, and disseminated intravascular coagulation (DIC), and the thrombomodulin values were compared with those of von Willebrand factor antigen (vWf:Ag) and tissue-type plasminogen activator (t-PA) which are released from stimulated or damaged endothelial cells. The mean plasma concentrations of thrombomodulin in these disease states were elevated as compared with healthy subjects. A relatively high mean thrombomodulin level was observed in DIC, liver disease, and collagen disease. Abnormally high thrombomodulin values (greater than normal mean value + 3 SD) were found in 32.3% of patients with hematological malignancies, 57.7% of patients with liver disease, 39.3% of patients with diabetes mellitus, 30.0% of patients with collagen disease, 23.1% of patients with thrombotic disease, and 69.0% of patients with DIC. Plasma concentrations of both vWf:Ag and t-PA were also elevated in these patients. On the whole, the plasma thrombomodulin concentration was positively correlated with vWf:Ag (r = 0.441, P less than 0.001) and t-PA (r = 0.398, P less than 0.001). These findings indicate that the elevation of plasma thrombomodulin is frequently seen in a variety of diseases and circulating thrombomodulin is possibly useful for evaluating the endothelial damage in selected disease states.
 ...
PMID:Circulating thrombomodulin as a novel endothelial cell marker: comparison of its behavior with von Willebrand factor and tissue-type plasminogen activator. 132 30


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>