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

It has previously been demonstrated that an in vitro antineoplastic treatment may induce new antigenic specificities in murine lymphomas. L1210 leukemia has been altered by DIC (L1210/DIC); drug-treated L1210 subline has been rejected by syngeneic animals. Here spleen cells from mice, normal or immune to L1210/DIC, have been stimulated in vitro by the L1210/DIC cells as measured by 3-h-thymidine uptake. Spleen cell stimulation did not occur with other syngeneic tumor cells and, as expected, spleen cells have been triggered by allogeneic cells. DIC-induced antigens stimulating syngeneic lymphocytes, as allogeneic cells did, have been demonstrated on L1210/DIC cells.
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PMID:[Pharmacological alteration of the antigenic properties of experimental leukemias detected by lymphocyte transformation]. 102 82

Analysis of four cases of hemangiosarcoma of the liver and review of the literature indicate that these tumors are either predominantly cystic and fairly well differentiated or are more solid and poorly differentiated. Well-differentiated hemangiosarcomas may resemble peliosis hepatis or other benign conditions. The tumor was associated disseminated intravascular coagulation and fibrinolysis syndrome in one of our cases. One of our patients had received thorium dioxide (Thorotrast) but none seemed to have been exposed to arsenicals or to vinyl chloride.
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PMID:Hemangiosarcoma of the liver. Spectrum of morphologic changes and clinical findings. 109 26

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.
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PMID:Changes of the immunogenic properties of a radiation-induced mouse lymphoma following treatment with antitumor drugs. 114 19

A newborn infant with congenital neuroblastoma complicated by disseminated intravascular coagulation is described. At birth the infant showed liver and spleen enlargement and shortly thereafter malignant cells were found in the bone marrow. On the fifth day of life the infant started to bleed and coabulation analysis indicated disseminated intravascular coagulation. Heparin therapy corrected the coagulation anomaly and irradiation and chemotherapy temporarily improved the general condition of the infant. The infant finally succumbed from tis primary neoplastic disease.
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PMID:Disseminated intravascular coagulation and congenital neuroblastoma. 115 89

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.
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PMID:Increased immunogenicity of two lymphoma lines after drug treatment of athymic (nude) mice. 115 15

An infant with a large occipital hemangioendothelioma with thrombocytopenia, anemia, and hypofibrinogenemia--Kasabach-Merritt syndrome--was reported. The case, a male neonate is unique, for this is the first report with this syndrome in whom the large hemangioma was noted at birth on the midocciput simulating the occipital encephalomeningocele. With the development of thrombocytopenia of 84,000 per mm3, hypofibrinogenemia of 92 mg/dl, anemia (erythrocyte 193 X 10(4) per mm3, hemoglobin 5.9 g/dl, hematocrit 16 vol%), hepato-splenomegalia, enlargement and bluish discoloration of the tumor noted on the 21/2 months of life, total excision was intended prior to the expected occurence of the systemic purpura. The patient received fresh whole blood transfusion immediately prior to surgery, and the total excision was successfully performed. Excessive bleeding was not encountered. Abrupt rise in the platelet count, red blood cell count, hemoglobin and hematocrit to normal range was noted at the first postoperative day; he was discharged on the 17th day after surgery. Nineteen months' follow-up showed normal hematologic findings with good somatic and mental development. The specimen weighing 250 g. revealed benigh hemangioendothelioma. Silver impregnation demonstrated lobular aggregates of small vascular channels. Papillary projection of interstitial cells into the lumen, reaction of the endothelium of the vessels, newly formed thrombus, ishemic necrosis and hemorrhage, hyaline degeneration of interstitial tissue were noted. These findings suggested the disseminated intravascular coagulation within the tumor followed by fibrinolysis accounts for loss of blood corpuscles, platelet, fibrinogen and clotting factors, which leads ultimately to the consumption coagulopathy and diffuse bleeding.
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PMID:[Giant occipital hemangioendothelioma with thrombocytopenia, anemia and hypofibrinogenemia treated by total excision (author's transl)]. 123 5

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.
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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.
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PMID:Antigenic changes of L5178Y lymphoma after treatment with 5-(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide in vivo. 125 54

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.
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PMID:[Cerebrovascular complications of cancers]. 130 55

Preoperative hemostatic data were obtained on 42 brain tumor patients and correlated with the subsequent occurrence of venous thrombosis detected with 125I-labeled fibrinogen leg scans. The occurrence of thrombosis correlated significantly with an increased prothrombin time, plasminogen, and total fibrinolytic activity and a decreased fibrinogen level. This overall trend in the group of patients with postoperative thrombosis indicates that the hemostatic disorder noted in brain tumor patients is most closely related to a subclinical form of chronic disseminated intravascular coagulation syndrome. Differences in hemostatic parameters seen with the various types of brain tumors suggest that biological factors specific to each tumor are likely responsible for the described hemostatic disorder and support the need for further research directed at the tumor tissue level.
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PMID:Postoperative venous thromboembolism and brain tumors: Part II. Hemostatic profile. 133 49


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