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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antigenic systems of oncornaviruses and particularly feline leukaemia virus (FeLV) are reviewed briefly. The use of immunological methods in studying the epidemiology of the disease is described. The incidence of FeLV infection as judged by a serological survey is at least 100 times greater than that of leukaemia in the cat population. Horizontal transmission, due to virus replication in respiratory and alimentary epithelial cells, is common. A method of producing high titres of antibody against membrane antigens of virus infected cells is described; the use of such vaccination is discussed in relation to several epidemiological facets of feline leukaemia virus infection. Leukaemia viruses are well known to cause immunodepression to heterologous antigens. The hypothesis is advanced that depression of the humoral antibody response to leukaemia virus antigens and cell membrane antigens may be an early event allowing establishment and replication of virus in haemic and the lymphatic tissues. Subsequent depression of cell mediated immunity through direct action of thymic cells is known to take place in the cat system. This may allow further spread of the virus with replication in epithelial cells which are not susceptible to cytotoxic action. Thus the primary events leading to leukaemogenesis may be an interplay between immunostimulation and immunodepression.
Br J Cancer Suppl 1975 Mar
PMID:The relation of immune response to pathogenesis, vaccination and epidemiology in virus induced leukaemia. 17 Sep 52

Cellular immune responses of patients with histologically confirmed lung carcinoma were assessed in vivo using cutaneous response and in vitro with a microlymphocyte blastogenic transformation (LBT) assay. In addition, correlation of the cutaneous response with the migration inhibitory factor (MIF) assay and LBT response was examined. The results indicated that cutaneous responses seen in patients with cancer of the lung were consistently lower than similar responses in normal controls (p less than 0.001). Similarily, the percentage of positive cutaneous responses seen with patients included in this study was lower than the frequencies reported by others. Stimulation of cells from lung cancer patients by PHA-M was also depressed when compared to similar lymphocytic responses in normal volunteers (p less than 0.001). The correlation between cutaneous response to tuberculin and the in vitro assays was high. The few instances of disparity demonstrate the need to utilize more than one assay in evaluating cellular immune functions. These data would support the work of others that indicate a depression of cellular immunity in advanced malignancy.
Cancer 1975 Dec
PMID:Cellular immunity in neoplasia. Antigen and mitogen responses in patients with bronchiogenic carcinoma. 17 58

Spleen cells removed from C57Bl/6J mice bearing a methylcholanthrene-induced fibrosarcoma (MC-16) demonstrate suppressed responsiveness of phytohemagglutinin (PHA) and bacterial lipopolysaccharide (LPS) induced mitogenesis as compared to non-tumorous mice. A similar depression of PHA-induced mitogenesis was observed with spleen cells from C3H/HeJ mice bearing syngeneic mammary adenocarcinomas (C3HBA). The administration of indomethacin, a non-competitive irreversible prostaglandin (Pg) synthesis inhibitor, (75 or 100 mug/mouse, IP) on an alternate day basis to groups of tumor-bearing mice of both strains, significantly enhanced immune cell responsiveness to mitogenic stimulation. The addition of indomethacin (10 mug/ml) to cultures of spleen cells from these tumor-bearing mice, as well as to DBA/1J mice bearing the Cloudman S-91 melanoma, enhanced spleen-cell responsiveness to mitogen-induced DNA synthesis by as much as 156%. Indomethacin administration in vivo or in vitro had no significant effect on mitogen-induced DNA synthesis of spleen cells from non-tumor-bearing animals. It is hypothesized that tumors, or tumor-cell antigens, increase Pg production of a population of spleen cells, and that the increased Pg content of the spleen may be important in controlling immune responsiveness in mice.
Int J Cancer 1976 Nov 15
PMID:Indomethacin enhancement of spleen-cell responsiveness to mitogen stimulation in tumorous mice. 18 13

A selective deficiency of uridine triphosphate (UTP) was induced in AS-30D rat ascites hepatoma cells by the synergistic action of D-galactosamine and 6-azauridine. The resistance of these hepatoma cells to low concentrations of D-galactosamine (less than 2 mM) was due to their active de novo pyrimidine synthesis which compensated the trapping of uridylate in the form of uridine diphosphate-amino sugars derived from D-galactosamine. The additional blockage of de novo pyrimidine synthesis led to noncompensated uridylate trapping with a UTP content of less than 0.05 mmole/kg of cell wet weight as compared to the control level of 0.66 mmole/kg. The induction of UTP deficiency by incubating the cells with low concentrations of D-galactosamine and 6-azauridine (0.5 mM each) was not accompanied by significant changes in the content of adenine and guanine nucleotides, uridine diphosphate glucose, and uridine diphosphate galactose. The depletion of UTP pools could be reversed within 10 min by the addition of uridine; orotate or uracil were completely ineffective in these hepatoma cells. A UTP content in the range of 0.1 to 0.4 mmole/kg, induced by either 6-azauridine or D-galactosamine, was associated with a reversible depression of cell growth in suspension culture. A UTP content below 0.05 mmole/kg led to irreversible growth inhibition and to necrocytosis in culture, as well as to a loss of transplantability in vivo. Uridine reversal studies indicated that the percentage of cells able to resume growth in culture decreased with an increasing time period of UTP deficiency. The deficiency period required for irreparable or lethal damage in these hepatoma cells ranged from 3 to 20 hr. The principle of noncompensated uridylate trapping can be extended to other inhibitors of nucleotide synthesis combined with various nucleotide-trapping sugar analogs. Noncompensated nucleotide trapping may be useful for an induction of selective nucleotide deficiencies in tumor cells.
Cancer Res 1977 Mar
PMID:Uridine triphosphate deficiency, growth inhibition, and death in ascites hepatoma cells induced by a combination of pyrimidine biosynthesis inhibition with uridylate trapping. 18 18

Twenty-four patients with small cell carcinoma of the lung were treated with a combination of vinblastine, 5 mg/m2 iv on Day 1; adriamycin, 40 mg/m2 iv on Day 1; and procarbazine, 100 mg/m2 orally on Days 1-7. The courses were repeated every 21 days. Tumor regression was noted in five of eight previously untreated patients, in two of six patients with previous chemotherapy, and in one of ten patients with previous chemotherapy and irradiation. The median duration of response was 130 days (range, 42-488+ days). The major toxic effects were bone marrow depression, gastrointestinal disturbances, and alopecia. This drug combination deserves consideration for inclusion into sequential combination chemotherapy regimens used in the treatment of this tumor type.
Cancer Treat Rep 1976 Sep
PMID:Phase II study of vinblastine, adriamycin, and procarbazine in small cell carcinoma of the lung. 18 21

Although elevated antibody levels to the Epstein-Barr virus (EBV) have been reported in a number of lympho-proliferative neoplasms, it has not been possible to determine whether these antibodies were the result of a specific response to an oncogenic agent (EBV), whether they were a non-specific humoral compensation for depressed cell-mediated immunity (CMI), or whether a different mechanism was responsible. We have previously shown in a group of lymphoma patients that depressed cellular immunity to a number of standard antigens (Candida, SKSD, etc.) is not associated with an increase in antibody to EBV. In this study, we tried to compare CMI to possible EBV and lymphoid cell line antigens with humoral antibody to EBV. The two basis CMI assays utilized were lymphocyte cytotoxicity (LC) and skin testing (ST) for delayed hypersensitivity. In the LC assay, an EBV-containing cell line (F265) was used as the target. Reactivity against F265 was stronger in normal individuals than in cancer patients, suggesting a relationship to general cellular immune competence. ST studies showed that membrane extracts from lymphoid cell lines derived from patients with Burkitt's lymphoma and nasopharyngeal carcinoma (NPC) were more likely to elicit a delayed hypersensitivity in lymphoma and NPC patients than cell lines derived from normal individuals. Patients with ST reactivity against the membrane preparations from the tumour-derived cell lines were as likely to have elevated EBV antibodies as patients without such reactivity. The data strongly indicated that the elevated EBV titres in lymphoma patients are not related to a specific or non-specific depression of CMI.
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PMID:Humoral and cellular immunity to EBV and lymphoid cell line antigens in human lymphoma. 19 66

Incubation of HeLa cells with the anticancer agent N-methyl-N-nitrosourea (MNU) results in: (a) depression of intracellular nicotinamide adenine dinucleotide levels; (b) stimulation of the chromatin-associated, chromosomal protein-modifying enzyme polyadenosine diphosphoribose [poly(ADP-ribose)] polymerase, which uses nicotinamide adenine dinucleotide as substrate; and (c) some fragmentation of cellular DNA. DNase treatment of HeLa nuclei in vitro also stimulates poly(ADP-ribose) polymerase activity, but not in nuclei derived from MNU-treated cells unless they have been subsequently incubated to allow for recovery from MNU damage. DNA polymerase activity is stimulated in vitro by poly(ADP) ribosylation of nuclear proteins. By using intact nuclei derived from MNU-treated HeLa cells, the repair via elongation of single-strand DNA breaks is demonstrated in vitro. This repair is dependent on DNA polymerase activity and is enhanced by adenosine diphosphate ribosylation of histones. Inhibition of poly(ADP-ribose) polymerase with nicotinamide results in extensive degradation of MNU-damaged DNA. Taken as a whole, these results suggest that poly(ADP-ribose) polymerase may play a role in the repair of alkylation damage to cellular DNA and that the inhibition of this enzyme in vivo might be exploited to potentiate the antitumor and carcinogenic activities of MNU.
Cancer Res 1977 Sep
PMID:A putative role for nicotinamide adenine dinucleotide-promoted nuclear protein modification in the antitumor activity of N-methyl-N-nitrosourea. 19 15

There is considerable evidence to suggest that macrophages participate in host resistance to the development and spread of cancer. We have, therefore, studied monocytemacrophage function in humans and animals with neoplasms. Approximately 60% of patients with various types of cancer were found to have abnormal monocyte chemotactic responsiveness in vitro, and abnormal chemotaxis was an indicator of poor prognosis in patients with melanoma. By studying patients before and after surgery, it was found that abnormal chemotactic responses normalized within weeks after removal of malignant tumors, indicating that a neoplasm itself might affect the host's monocyte chemotactic responsiveness. Subsequent studies using transplantable neoplasms in mice substantiated this hypothesis in that macrophage accumulation in vivo as well as macrophage chemotactic responsiveness in vitro was depressed in animals during the early phases of tumor growth. This depression of macrophage function could be attributed to a low-molecular-weight factor contained in murine neoplasms, which when given to normal mice was extremely potent in depressing peritoneal macrophage accumulation and chemotaxis but, paradoxically, enhanced phagocytosis. The serum of tumor-bearing mice also contained potent inhibitory activity for macrophage accumulation. In contrast to the effects on macrophages, granulocyte accumulation in vivo and chemotaxis in vitro was not depressed by the presence of a neoplasm or the administration of the factor from neoplasms. By releasing factors which depress macrophage migratory function, neoplasms may protect themselves from immunologically mediated host destruction during the early phases of tumor growth.
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PMID:Macrophage migratory dysfunction in cancer. A mechanism for subversion of surveillance. 19 6

The effect of serum from 12 cats with lymphosarcoma induced by feline leukemia virus (FeLV) on the response of normal cat peripheral blood lymphocytes to phytomitogen-induced blastogenesis was studied. The majority of FeLV sera, when tested at a concentration of 20% of the incubation medium, caused a 40 to 70% reduction in the mean blastogenic response to concanavalin A compared to the response obtained with a similar concentration of normal feline serum. Results with pokeweed mitogen were similar, but the depression in blastogenesis was less than with concanavalin A. Further studies showed that the blastogenic inhibitory activity of FeLV serum (a) was heat labile at 56 degrees for 30 min, (b) could not be overcome by greater concentrations of mitogens, (c) was proportional to the concentration of FeLV serum in the incubation medium, and (d) could not be demonstrated when lymphocytes were preincubated in FeLV serum followed by washing and reincubating in normal feline serum. The results suggested that a substance present in the serum of FeLV-infected cats contributes to altered immunological reactivity during leukemogenesis in the cat.
Cancer Res 1977 Nov
PMID:Inhibition of normal lymphocyte mitogenic reactivity by serum from feline leukemia virus-infected cats. 19 25

Eighteen patients with nasopharyngeal carcinoma (NPC) were compared to matched controls, before or after cobalt therapy, for the ability of their peripheral blood lymphocytes to: (1) form E and EAC rosettes and (2) mount a proliferative response with PHA, Con A and ALG. A slight decrease in the percentage of E rosettes and a moderate hyporesponsiveness to PHA and Con A were observed before treatment. The statistical significance of these alterations was borderline. Within the group of treated patients a much greater depression, including the response to ALG, was found, although a few long-term survivors responded to mitogens as well as the controls. These findings stress the difficulty of interpreting the results of a longitudinal study of cell-mediated immunity, specific or non-specific, in cancer patients. Finally, by comparing the proliferative response to the three mitogens before and after radiotherapy, it is suggested that their differential effect on these responses might be used in man, as it was in mice, to delineate lymphocyte subpopulations.
Int J Cancer 1977 Nov 15
PMID:Lymphocyte subpopulations and mitogenic responses in nasopharyngeal carcinoma, prior to and after radiotherapy. 20 May 72


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