Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several anticancer chemicals containing a quinone group were found to stimulate the aerobic oxidation of NADPH by liver microsomes. The enzyme responsible for the above reaction was identified as NADPH-cytochrome c reductase (EC 1.6.2.4), one of the microsomal flavoproteins. The fact that a catalytic amount (20 micronM) of these anticancer chemicals was sufficient to oxidize all the NADPH (100 micronM) indicates that they function as electron carries from the flavoprotein to molecular oxygen. As a corollary, Mitomycin-C and Carbazilquinone stimulated oxygen uptake by Ehrlich ascites tumor cells in the presence of glucose that Daunomycin and Adriamycin failed to do so, although the reason for it remains to be elucidated. Carbazilquinone, in contrast to others, also stimulated the microsomal NADH oxidation.
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PMID:Stimulation of microsomal NADPH oxidation by quinone group-containing anticancer chemicals. 1 20

Recent studies have demonstrated that nitroso chemical carcinogens activate guanylate cyclase (EC 4.6.1.2) which catalyzes the production of guanosine 3',5'-monophosphate. This nucleotide is thought to be involved in normal and abnormal cell growth. We examined the effect of 3 major classes of anticancer chemotherapeutic agents, the antimetabolites (methotrexate and 6-mercaptopurine), antitumor antibiotics (adriamycin and actinomycin D), and alkylating agents (cytoxan, uracil mustard, isophosphamide, chlornaphazine, and 1-propranol-3,3'-iminodimethane sulfonate) on the activation of guanylate cyclase by nitroso chemical carcinogens. The anticancer chemotherapeutic agents noncompetitively blocked the activation of rat hepatic guanylate cyclase by N'-nitro-N-nitroso-N-propylguanidine (NNPG) and hydrazine. Adriamycin, methotrexate, and uracil mustard were the most effective inhibitors completely abolishing the effect of 1 mM NNPG on guanylate cyclase activity. The remainder of the anticancer chemotherapeutic agents abolished the NNPG activation of guanylate cyclase 40--70%. Since a previously described guanylate cyclase inhibitor has been shown to terminate the growth of an undifferentiated prostatic cancer in tissue culture the present data may indicate that one of the mechanisms by which anticancer chemotherapeutic agents exert their effects is by inhibition of tumor guanylate cyclase activity.
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PMID:Inhibition of nitroso chemical carcinogen activation of rat hepatic guanylate cyclase by anticancer agents. 3 20

Experience with 70 patients having osteogenic sarcomas treated between 1968 and 1973 demonstrated the importance of persistence in the management of the disease of these patients. Resection for pulmonary metastases in one or both lungs, often on more than one occasion, will salvage a number of these patients, thus improving the cure rate. Adriamycin has proved an effective palliative agent and a useful adjuvant to surgical therapy. Although the cure rate of tumors arising distal to the knee is much higher than that of more proximally situated tumors, resection of osteogenic sarcomas of the distal part of the femur does not require removal of the entire femur when care is taken to resect well above the site of the apparent tumor. Some osteogenic sarcomas are sensitive to adequate dosages of radiation therapy, but the exact role of this method is yet to be determined. No definite beneficial result could be attributed to any of a variety of modalities of immune stimulation therapy.
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PMID:Improvement in the results of treatment of osteogenic sarcoma. 4 34

Nineteen Zambian and 22 American patients with hepatocellular carcinoma were treated with Adriamycin every three weeks in intravenous doses ranging from 20-75 mg/m2 (depending upon their initial serum bilirubin levels). Four of 16 (25%) "good risk" Zambian and American patients who received 75 mg/m2 had objective responses, while in five additional patients there was evidence of either transient tumor regression or disease stabilization. In contrast three of 25 "poor risk" patients who received 20-60 mg/m2 had objective responses. Even in this latter group, however, transient, objective signs of tumor regression were noted in four patients. The results of the present study confirm previous reports suggesting anti-tumor activity for high doses of Adriamycin in hepatocellular carcinoma. Since those responses seen were generally incomplete and transient, further clinical trials of this agent used in combination or sequentially with other agents are indicated.
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PMID:A phase II study of adriamycin (NSC 123127) in patients with hepatocellular carcinoma from Zambia and the United States. 6 74

Spleen cell populations from mice treated with Adriamycin or daunorubicin were found to develop a greater complement-independent cellular cytotoxic immune response during culture with allogeneic tumor cells than spleen cells from untreated or cyclophosphamide-treated animals. A temporal and drug dose dependence of this effect was demonstrated. The changes in spleen cell population occurring in the donor mice consequent to drug treatment were evident in the nylon woll-adherent fraction of the spleen cells. The results are consistent with the possibility that the concentration of specific progenitor or accessory cells in the spleen is increased consequent to drug treatment.
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PMID:Increased primary cell-mediated immunity in culture subsequent to adriamycin or daunorubicin treatment of spleen donor mice. 6 85

Acetoxymethyl-methyl-nitrosamine (AMMN) induced only carcinomas of the forestomach in female Sprague-Dawley rats after an induction time of about 100 days when applied orally twice weekly in single doses (d) of 3.5 mg/kg body weight, Butyl-butanol-nitrosamine (BBN) selectively produced bladder tumors in female Sprague-Dawley rats after about 280 days when given in daily oral single doses (d) of 10 mg/kg body weight. The reactions of a total of 520 rats with chemically induced tumors were tested using 4-drug combination chemotherapy with different equitoxic doses of Adriamycin (Adm), Methotrexate (Mtx), 5-Fluorouracil (5-FU) and Bleomycin (Blm). The influences of combined therapy on mean sruvival time, tumor weight, histology of tumors, and adverse side effects of therapy are herein described. The results showed to be tumorspecific. In addition, the comparability of experimental chemotherapy in autochthonous rat tumors to clinical experience is discussed.
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PMID:Chemotherapy studies in autochthonous rat tumors. Forestomach and bladder cancer. 7 Aug 91

Thirteen patients with osteogenic sarcoma were treated with multiple drug chemotherapy consisting of bleomycin, cyclophosphamide and dactinomycin. The dosage schedule used was: bleomycin 12 mg/m2/day, cyclophosphamide 600 mg/m2/day, and dactinomycin 450 microgram/m2/day. All drugs were given intravenously for two consecutive days. Treatment was repeated every 2 weeks. Toxicity included severe nausea and vomiting (managed with antiemetics and intravenous hydration) and manifestations of bone marrow depression. Of 13 patients, eight were previously treated with high dose methotrexate with citrovorum factor rescue, cyclophosphamide and Adriamycin. Of these eight, three patients had objective evidence of tumor regression (37.5%). Five of five previously untreated patients had objective evidence of tumor regression. The overall response rate in osteogenic sarcoma patients to BCD was 61.5%. The combination of BCD appears to be more active against osteogenic sarcoma than cyclophosphamide alone or Adriamycin alone. The relative safety with which BCD can be administered makes this combination a valuable adjunct to high dose methotrexate with citrovorum factor rescue and Adriamycin in the treatment of osteogenic sarcoma.
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PMID:Combination chemotherapy with bleomycin, cyclophosphamide and dactinomycin for the treatment of osteogenic sarcoma. 7 9

Five permanent tumor cell lines derived originally from either a solid or an ascites biopsy of rat hepatoma exhibited differential sensitivities to bleomycin, Adriamycin, 1-beta-D-arabinofuranosylcytosine, hydroxyurea, 1-trans-(2)-chloroethyl)-3-(4-methoylcyclohexyl)-1-nitrosourea, and 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea. The cells were least sensitive to hydroxyurea and 1-beta-D-arabinofurano-sylcytosine, with some cell lines being almost totally resistant to these drugs. However, from 25- to 700-fold differences in survival were obtained between cell lines treated with either bleomycin or Adriamycin.
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PMID:Differential sensitivities of five rat hepatoma cell lines to anticancer drugs. 7 57

Effect of clinically available chemotherapeutic agents on transplantable and tissue culture bladder carcinoma cell line, BC-47, which were syngeneic to host animals, was confirmed. Adriamycin, vincristine, and bleomycin possessed predominant antitumor activity. 1,3-Bis(2-chloroethyl)-1-nitrosourea (BCNU) also reduced the tumor load of the host after which the tumor began to grow at the site of inoculation. Alkylating agents such as nitrogen mustard N-oxide (Nitromin), cyclophosphamide, 3,3'-dimesyloxydipropylamine tosylate (864T), and mitomycin-C possessed a weak activity, while antimetabolites such as 5-fluorouracil, 1-(1'=furyl)-5-fluorouracil (FT-207), cytosine arabinoside, and behenoylcytosine arabinoside possessed no activity.
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PMID:Effect of chemotherapeutic agents on the growth of rat bladder cancer, BC-47. 7 84

Exposure of cells in tissue culture to bleomycin or Adriamycin during 43 degrees C hyperthermia increased cytotoxicity dramatically compared to exposure at 37 degrees C. This study was designed to test whether this interaction was useful in tumor-bearing animals. C3H mice bearing the KHT tumor were treated with bleomycin (7 or 15 mg/kg) or with Adriamycin (2.5 or 5 mg/kg) with or without local heating of the tumor to 43 degrees C for 30 minutes by 13.56 MHz radiofrequency fields. The effects were assessed by growth delay (mean tumor diameter doubling time) and cure rate. In separate experiments, BALB/c mice bearing EMT6 tumors were treated identically, but tumors were excised 2 hours after treatment and tumor cell survival was assayed by colony formation. Antitumor effects of systemic bleomycin were potentiated by local hyperthermia. The two modalities had to be administered close together in time to observe the potentiation, suggesting a true interaction. There was a "threshold" for bleomycin potentiation in vivo between 42 degrees C and 43 degrees C, just as observed in tissue culture experiments. The antitumor activity of Adriamycin was not potentiated in vivo in these tumor systems except in cell survival experiments at doses higher than those compatible with survival of the host. The toxicity of drug combined with heat was greater than that of either modality alone. Hyperthermia did not adversely affect the incidence or severity of spontaneous lung metastases from KHT tumors. In fact, groups treated with heat and bleomycin had less severe lung metastases than groups treated with bleomycin alone. We conclude that local heating of tumors may be a useful adjunct to systemic bleomycin therapy. In vivo potentiation of Adriamycin by heat, however, could not be demonstrated in these tumor systems.
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PMID:Effects of systemically administered bleomycin or adriamycin with local hyperthermia on primary tumor and lung metastases. 8 6


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