Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytotoxic T-lymphocytes (CTL's) harvested from mixed splenic lymphocyte cultures (DBA/2 + C57BL) were tested for their ability to lyse allogeneic P815 mastocytoma cells under various tumor-like assay conditions, with or without previous exposure to ionizing radiation or hyperthermia (43 degrees). There was little or no decrease of immune cytolysis when CTL's were assayed by 51Cr release under tumor-like conditions (plateau-phase target cells, low pH, or anoxia) or after irradiation, but cytolytic activity was greatly reduced when CTL's were exposed to heat; 45 min of hyperthermic treatment decreased activity by greater than or equal to 99% while reducing the apparent cell viability (as indicated by trypan blue exclusion) by only 30%. When the P815 target cells rather than the CTL's were exposed to heat their susceptibility to immune lysis was not affected even after treatment times that were lethal to the tumor cells. Despite the dissimilar heat sensitivities of CTL and P815 cells, the dose-response curves for inhibition of protein synthesis by heat, as indicated by [3H]leucine incorporation, were similar for both cell types: neither the depression of protein synthesis in heated CTL's nor the decreased cytolytic ability of these cells was reversed within 3 hr. When irradiated or heated P815 cells were incubated with CTL's, the resulting survival curves were always additive, indicating that neither irradiation nor heat treatment affected the susceptibility of the tumor cells to immune attack. The extreme heat sensitivity of cytotoxic T-lymphocytes raises important questions about the possible effects of hyperthermic treatment on the immune competence of cancer patients.
Cancer Res 1976 Aug
PMID:Effects of Tumor-like assay conditions, lonizing radiation, and hyperthermia on immune lysis of tumor cells by cytotoxic T-lymphocytes. 0 45

In these experiments, we tested in various in vivo assays the immune responses of inbred C3H/HeN(MTV-) (C3H-) mice during carcinogenesis by chronic exposure to UV irradiation. Although the UV-treated mice were unable to reject syngeneic UV-induced tumor transplants, they rejected H-2-incompatible tumor allografts and H-2-compatible skin allografts. The primary hemagglutinin response to sheep red blood cells was normal in these mice, as were the induction of a local graft-versus-host reaction with lymphoid cells from UV-irradiated donors and the induction of an inflammatory response to dimethyl sulfoxide in the footpads of UV-treated mice. An early transient depression of two reactions in UV-irradiated mice occurred: delayed hypersensitivity to dinitrochlorobenzene measured by footpad swelling and the graft-versus-host reaction in UV-irradiated recipients measured by the use of the popliteal lymph node weight gain assay. Both of these reactions returned to a normal level before the development of primary tumors. We conclude that the inability of UV-irradiated mice to reject syngeneic and autochthonous UV-induced tumors was not due to a generalized immunosuppressive effect of chronic UV irradiation.
J Natl Cancer Inst 1977 Oct
PMID:In vivo immune responses of mice during carcinogenesis by ultraviolet irradiation. 2 May 14

Management of the chronic pain of cancer is a common and difficult problem. In addition to a medical examination of the patient, it is necessary to perform a psychological assessment of his premorbid personality, current mental status, and coping mechanisms to devise an individualized approach to his pain. The mainstay of cancer pain control are the narcotics, which differ primarily in potency and duration of action. Nonnarcotic analgesics are equianalgesic with the less potent narcotics. Antipsychotic drugs are useful as tranquilizers, antiemetics, and analgesic potentiators. Antidepressants and hypnotics permit the patient a more normal life-style. Stimulants such as cocaine and amphetamines both potentiate narcotic analgesia and reduce narcotic-induced somnolence and respiratory depression. Tetrahydrocannabinol offers no advantage over traditional analgesics. With care and patience, the physician can render practically any cancer patient pain-free.
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PMID:Medical management of chronic cancer pain. 3 26

Single-agent chemotherapy of advanced and recurrent squamous carcinoma of the female genital tract has been largely ineffective. Combination-drug therapy which has augmented the efficacy of chemotherapy in numerous solid and nonsolid human tumors is usually attended by a degree of toxicity that has discouraged its use against malignancies exhibiting a poor response to single agents. A seven-drug regimen consisting of cyclophosphamide, 5-fluorouracil, actinomycin D, vincristine, cytosine arabinoside, methotrexate, and bleomycin administered during a 24 hour period at 4 week intervals was selected for clinical trial against squamous malignancies of the female genitalia because of its proved broad-spectrum activity among solid tumors and its low incidence of serious toxicity. Severe bone marrow depression occurred during only two of 98 drug cycles involving 23 patients. An objective tumor response was observed in nine of 18 evaluable patients. This regimen appears to be useful in the palliative management of squamous carcinoma of the female genital tract.
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PMID:Seven-drug polychemotherapy in the treatment of advanced and recurrent squamous carcinoma of the female genital tract. 5

B and T lymphocytes have been measured in 100 women--71 patients with breast cancer and 29 controls--using sheep-erythrocyte rosetting techniques. Compared with controls (healthy women or patients with benign breast disease), there is a highly significant depression of T-cell percentage in all stages of breast cancer except locally advanced (stage 3) disease. These stage-3 cases seem to constitute a biologically distinct group. T-cell percentages in early (stage 1) patients overlap with those seen in stages 3 and 4, raising the possibility that there are in stage 1 two subpopulations of T-cell values that are associated with differences in subsequent tumour progression. B-lymphocyte levels are similar in all groups. Low T-cell levels return to normal after incubation with papain in virto but fall again after resuspending the treated lymphocytes in autologous (cancer) serum. The results suggest that T-cell depression is due to a masking factor on the surface of some T lymphocytes which is also present in the serum of cancer patients, and removable by enzyme digestion.
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PMID:T and B lymphocytes in breast cancer stage relationship and abrogation of T-lymphocyte depression by enzyme treatment in vitro. 5 39

The administration of 5-azacytidine to rats resulted in enhancement of thymidine incorporation into liver DNA. Repeated doses of the drug caused a greater than 10-fold increase of thymidine incorporation. In 5-azacytidine-treated intact rats no changes in the activity of thymidine and thymidylate kinases were observed, whereas a marked depression of thymidine phosphorylase activity occurred. In intact animals the mitotic activity in the drug-treated livers changed slightly; however, 5-azacytidine administration before partial hepatectomy resulted in a dramatic increase of mitotic activity in 24-hr regenerating livers. In this case the observed increase in incorporation of thymidine was paralleled both by increased activity of thymidine and thymidylate kinases and by a decline in thymidine phosphorylase activity. The higher incorporation of radioactivity into liver DNA in intact rats pretreated with the drug can be accounted for, at least partially, by the lower cellular degradation of the injected radioactive thymidine used for labeling. In addition, alterations in the labeling and in the mitotic activity of hepatocytes and nonparenchymal cells caused by 5-azacytidine should be taken into consideration.
Cancer Res 1976 Jan
PMID:Enhanced incorporation of thymidine into DNA in the liver of intact and partially hepatectomized rats pretreated with 5-azacytidine. 5 4

W/Fu rats inoculated s.c. with less than or equal to 5 x 10(7) syngeneic (C58NT)D (Gross virus-positive) lymphoma tumor cells normally develop a palpable tumor which reaches its maximum size (12 to 14 mm) at 6 to 8 days and is subsequently rejected by 10 to 12 days. However, rats previously sensitized with soluble tumor antigens from (C58NT)D cells prior to (C58NT)D tumor inoculation demonstrate a significant enhancement of tumor growth (the tumor reaches up to 26 mm and is rejected by 16 to 18 days). This enhancement persisted in antigen-treated rats that continued to receive soluble antigen after tumor inoculation. The in vivo enhancement coincided with a significant in vitro depression of cell-mediated cytotoxicity [assessed with 51Cr-labeled (C58NT)D target cells and peripheral blood leukocytes]. The observed tumor enhancement was specific, inasmuch as presensitization to either soluble tumor antigens from WR6 (Gross virus-negative) tumor, syngeneic to W/Fu rats, or to soluble antigen from W/Fu spleen cells had no enhancing effect on (C58NT)D tumor growth. Interestingly, sensitization to soluble tumor antigen alone did not elicit detectable cell-mediated immunity, cytotoxic antibody, or serum-blocking activity to the (C58NT)D tumor. We conclude that sensitization to soluble tumor antigens specifically impairs the immune apparatus normally acting in tumor rejection. This impairment appears to act primarily at the induction phase of the immune response.
Cancer Res 1976 Apr
PMID:Specific enhancement of tumor growth and depression of cell-mediated immunity following sensitization to soluble tumor antigens. 5 98

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.
Cancer 1977 Dec
PMID:Combination chemotherapy with bleomycin, cyclophosphamide and dactinomycin for the treatment of osteogenic sarcoma. 7 9

Three different doses of bleomycin (BLM) (2,1, and 0.01 mg/animal) were injected ip into groups of hairless mice. Cell kinetic alterations in the basal layer of the epidermis were studied up to 10 days after BLM administration. The two highest doses of BLM affected the epidermal cell kinetics in a similar way but with different time courses. Only a moderate depression of the labeling index was observed during the first 24 hours. The results indicate that cells affected by BLM in the middle of the G1 phase are arrested in their subsequent S phase, and that thereafter an increase in the rate of DNA synthesis may occur in the arrested cells without increasing the number of cells in S phase. The percentage of cell accumulated in S and G2 phases as determined by flow cytofluorometry never exceeded 130% of control values with any of the doses. Phase durations were determined from percentage of labeled mitoses curves after the highest dose of BLM and were not significantly different from normal values, indicating that the accumulated cels are probably out of cycle and unable to proliferate again. Calculations based on cell counts and mitotic rate showed that the cells had a prolonged lifespan. No block and subsequent release of cells specifically caused by BLM were observed. BLM has a complex effect on the epidermis, and therefore does not seem to be a promising agent for cell synchronization as a basis for combination chemotherapy in vivo.
Cancer Treat Rep 1978 Mar
PMID:Epidermla cell kinetics in hairless mice after bleomycin. I. Perturbations after different single doses. 7 87

Weanling male Sprague-Dawley rats were fed either a nutritionally complete synthetic diet (Diet 1) or a diet marginally deficient in choline and methionine, and lacking folacin (lipotrope deficient, Diet 2) to determine the role of hepatic mixed-function oxidase metabolism of aflatoxin B1 (AFB1) in the Diet 2-induced enhancement of AFB1 hepatocarcinogenesis previously reported. Hepatic microsomal mixed-function oxidase activities, as assayed by ethylmorphine N-demethylation, ethoxycoumarin O-dealkylation, cytochrome c reduction, AFB1 metabolism, and cytochrome P-450 content, were all depressed by Diet 2. Furthermore, the proportion of an i.p. dose of AFB (1 mg/kg) that became covalently bonded to DNA and RNA was similarly reduced when measured 6 hr after administration. The formation of AFB1-protein adducts was not influenced by dietary treatment. The depression of DNA and RNA adduct formation in the Diet 2 animals was probably related to the lower mixed-function oxidase activities and not to an alteration of glutathione levels, which remained unchanged by dietary treatment. These results suggest that the marginally lipotrope-deficient diet does not enhance tumor formation through an increased microsomal activation of AFB1. Alternative hypotheses without data are suggested.
Cancer Res 1978 Dec
PMID:Dietary lipotropes, hepatic microsomal mixed-function oxidase activities, and in vivo covalent binding of aflatoxin B1 in rats. 8 78


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