Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

New antigenic specificities, not detectable on parental cells and transmissible after the withdrawal of the drug treatment, have been induced in mouse lymphomas. Studies were conducted of proliferative stimulation of syngeneic lymphocytes and the generation of cytotoxic lymphocytes (CL's) in a mixed lymphocyte-tumor cell culture system by 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC)-induced antigens in L1210 and EL4 leukemia sublines. The DTIC-induced antigens were observed to stimulate [3H]thymidine uptake by normal and primed syngeneic lymphocytes and to generate specific CL's to DTIC-altered cells. The specificity of the in vitro immune reactivity was demonstrated. Characteristics of lymphocyte triggering, including the optimal ratio of stimulating cells to responding cells, the kinetics of CL activation, and the quantitation of CL activity, were also evaluated. DTIC antigens on leukemic cells can activate syngeneic lymphocytes and can act as target antigens in cell-mediated immunity. The experimental data support the transplantation antigen-like nature of DTIC-induced antigens.
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PMID:In vitro lymphocyte stimulation and the generation of cytotoxic lymphocytes with drug-induced antigenic lymphomas. 7 62

Murine leukemia cells transformed by in vivo treatment with 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC) are rejected by histocompatible recipients following inocula of 10(7) cells i.p. Progressive tumor growth or tumor growth and regression was monitored measuring the extent of DNA synthesis in the peritoneal cavity of mice using the [125I]5-iodo-2'-deoxyuridine uptake method. In addition, the results were confirmed by cell count and mortality data. Comparable growth rate was found initially in both DTIC and parental lines in histocompatible hosts. Later, mice challenged with parental lines died, whereas hosts inoculated with DTIC-treated sublines rejected the tumor. On the other hand, lethal growth occurred in mice inoculated with DTIC-treated sublines when immunodepressed by cyclophosphamide given before tumor challenge, or by methotrexate given after challenge of a methotrexate-resistant DTIC-treated subline. The similarity between the growth rate of the parental and DTIC-treated lines in histocompatible hosts does not support the hypothesis of impaired "oncogenic potential" of such DTIC-treated lines. Furthermore, the growth and rejection pattern of a parental line in H-2-incompatible hosts was similar to that observed for DTIC-treated lines in histocompatible hosts, suggesting that comparable immune mechanisms were involved in both cases.
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PMID:Growth and rejection patterns of murine lymphoma cells antigenically altered following drug treatment in vivo. 14 82

Cell-mediated cytotoxic response in vitro to a Moloney strain of murine leukemia virus-induced tumor (LSTRA) altered by 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC) was investigated with the use of mixed-leukocyte tumor cell cultures (MLTC). As assessed by means of a short-term 51Cr-release assay, minimal or no cytolytic activity was generated in primary MLTC. In contrast, high specific cytotoxic response against the altered tumor was obtained in secondary MLTC. Partial cross reactivity was found between the LSTRA and LSTRA/DTIC tumor lines.
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PMID:Secondary cytotoxic response in vitro against Moloney lymphoma cells antigenically altered by drug treatment in vivo. 14 46

Changes of prekallikrein in the cases with DIC were investigated, i.e., DIC cases including disseminated metastasis of gastric cancer, acute promyelocytic leukemia and endotoxin shock. Therefore, the trigger substances for this paper were the pathologic cells of the leukemia, the cultured well differentiated adenocarcinoma cells and endotoxin. (1) The lysates of the pathologic cells of the leukemia and the cultured cells showed prekallikrein activation. Endotoxin showed prekallikrein activation via factor XII. (2) Serine proteases (factor Xa, thrombin, plasmin and trypsin) activated prekallikrein in the plasma and the purified prekallikrein. (3) Antithrombin III, aprotinin and FOY inhibited prekallikrein activation. Antithrombin III was promoted by heparin in its inhibitory effect.
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PMID:Changes of prekallikrein in the cases with disseminated intravascular coagulation syndrome. 16 Jan 91

Acute myelomonocytic leukemia developed in a patient 18 months after treatment with cyclophosphamide, vincristine, adriamycin, and DTIC, a chemotherapeutic regimen used for the treatment of metastatic sarcoma. The patient had had no prior history of radiation. More than 400 patients received this treatment and none of them developed leukemia. The occurrence of leukemia in this relatively short period of time may have been caused by the combined chemotherapeutic agents. However, confirmation of this will require long-term followup studies in cancer patients receiving chemotherapy to determine the true risk of second malignancies.
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PMID:Acute myelomonocytic leukemia following a chemotherapeutic regimen for metastatic sarcoma. 28 Apr 18

Graded doses of LSTPA or L1210 leukemia cells were injected ip or iv into fully compatible hosts or mice incompatible for Multiple Minor Histocompatibility Loci (MMHL). Three days later the animals were treated with single doses of BCNU, NM, DTIC and VCR. The results showed that NM and VCR could synergize with the weak anti-tumor immune responses of MMHL-histocompatible mice only upon ip injection of the tumor. If the same tumor has been injected iv, only BCNU could synergize with the host's antitumor response. On DTIC treatment, no synergistic effects were detectable for either route of tumor's challenge.
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PMID:[Experimental models of immunochemotherapeutic synergism: study of the influence of the treatment schedule]. 55 36

The treatment in vivo with anti-tumour drugs can induce an antigenic alteration of L1210 leukemia resulting in the rejection of an inoculum of 10 X 10(6) viable cells in syngeneic mice. As drug-induced antigens appeared in excess of any pre-existing tumour-associated transplantation antigens (TATA), viable altered cells have been used to sensitize syngeneic animals. Experiments showed that viable altered cells elicited stronger anti-TATA reaction than X-inactivated parental cells, as measured by host survival to a challenge of L1210 leukemia. TATA immunogenicity of parental cells has been preminent, in the strain of animals used, to determine the sensitizing effectiveness of 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide (DTIC) cells. Host protection to an inoculum of parental tumours has been more proficient with the DTIC subline derived from highly immunogenic L1210Ha cells than from poorly immunogenic L1210Cr cells. Immunoprophylactic inocula, proper chemotherapeutic treatments and adoptive transfer of immune lymphocytes used in combination exerted a synergic host protection.
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PMID:Vaccination of leukemic mice with viable drug-altered leukemic cells. 74 93

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

A case of Vibrio cholerae non-O1 septicemia is described in this paper. A 45-year-old male with a three year history of liver cirrhosis, was admitted to our division with hematemesis, abdominal pain, high fever and a loss of consciousness. Three days before onset of symptoms, he traveled to Ishigaki Island and ate a raw lobster. Two days after, his temperature rose to 39.7 degrees C and the blood pressure dropped to 36/- mmHg. By endoscopic examination, an ulcer was found in the stomach, and the bleeding was stopped by electrical coagulation. Blood culture showed growth of V. cholerae non-O1. The organism was found to be sensitive to OFLX, CZX, MINO, LMOX and CP. Although DIC, infections of fungus and MRSA occurred as complications, he recovered by adequate procedures. Subsequently, he left this division after eight weeks. There are various reports related to V. cholerae non-O1 septicemia in foreign countries, but few cases have been reported in Japan. And these cases had severe underlying diseases such as leukemia and liver cirrhosis.
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PMID:[A case of Vibrio cholerae non-O1 septicemia with liver cirrhosis]. 140 1

Automated platelet counts in a patient with newly diagnosed AML M5 with extreme leukocytosis were reported as 129, 166 and 121 x 10(9)/1. Routine blood films showed a corresponding number of platelet-sized particles, judged to be platelets. The patient was treated for DIC with low-dose heparin infusion. Platelet transfusions were not given initially. The patient died 14 h after admission from intracerebral haematoma. The origin of the platelet-sized particles seen in routine stained blood films was examined by cytochemical and immunological staining for peroxidase, non-specific esterase, CD 13 and CD 33. About 1/3 of the fragments had the same staining characteristics as the leukaemia cells, indicating leukaemia cell origin. Staining for platelet-specific antigen GpIIIa was positive only in 4% of the platelet-sized fragments, with a calculated true platelet count of 4 x 10(9)/1. The presence of cell fragments masquerading as platelets should be suspected in leukaemia patients with bleeding symptoms and normal or near normal platelet counts.
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PMID:Spurious platelet counts in acute leukaemia with DIC due to cell fragmentation. 145 3


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