Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven continuous cell lines of human malignant melanoma were studied in terms of their in vivo growth potential in the cheeck pouch of the cortisonized golden hamster. Progressive tumor growth was noted only among the melanoma lines which were grossly pigmented (10/32 transplants). None of the three amelanotic tumor lines showed progressive growth. The growing tumors could be identified as melanoma on morphological grounds and by histochemical demonstration of melanin granules. Histology of the tumor lesions revealed evidence of a host reaction to the tumor transplants. This was confirmed by demonstration of circulating antibodies directed against the implanted human cells. Correlations between in vivo heterotransplantability and in vitro saturation density of human melanoma cells were not found in the present study.
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PMID:Characterization of human malignant melanoma cell lines; V. Heterotransplantation in the hamster cheek pouch. 13 35

Mice have been immunosuppressed with cyclophosphamide, cortisone-acetate, irradiation, or Ehrlich ascitic fluid (EAF) and then grafted with Ehrlich tumor or with one of the following strain-specific tumors: thymoma, methylcholanthrene-induced fibrosarcoma, B-16 melanoma, lymphatic leukaemia, and myeloid leukaemia. Immunosuppression of the host influenced very differently the growth of transplanted malignancies. The growth of thymoma and of Ehrlich tumor was regularly enhanced. The growth of fibrosarcoma and of melanoma, on the other hand, was retarded in mice pretreated with EAF and X-rays, or remained unchanged in mice pretreated with drugs. Leukaemia growth was not influenced by any immunosuppressive treatment; the only exception was enhanced growth of lymphoid leukaemia in animals pretreated with EAF. Thus different tumors grew differently in animals immunosuppressed by the same immunosuppressive agent, while different immunosuppressive treatment changed the growth of one particular tumor always in the same way. From this we concluded: (1) there is no rule as to how immunosuppression of the host will influence tumor growth; and (2) the way in which the malignant growth will be changed depends mainly upon the type of the tumor and probably not very much upon the type of immunosuppressive treatment.
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PMID:Effect of immunosuppression on the growth of six murine tumors. 15 96

Recent studies suggested that 3',5'-cyclic AMP (CAMP) may be involved in the regulation of cell proliferation and differentiation. Theophylline, an inhibitor of cyclic nucleotide phosphodiesterase, elevated intracellular cAMP. A melanotic clone of the B16 melanoma was treated with theophylline and studied in vitro and in vivo. With 12 hours after 1.0 mM theophylline was added to growing cultures, the number of cells incorporating tritiated thymidine (3-H-TDR) and the rate of uptake of 3-H-TDR into DNA were significantly reduced. After 7 days, the number of cells in the control cultures increased twenty-four times, whereas theophylline-treated cells increased only sixfold. Compared to the controls, the theophylline-treated cells contained ten times the melanin and an elevated cAMP content. Stimulation of melanogenesis and inhibition of proliferation increased progressively with duration of exposure to theophylline. After 5 days of culture with theophylline, cells were assayed for plating efficiency in theophylline-free medium. Although the number of colony-forming cells was unaffected by previous exposure to theophylline, the colonies were composed of fewer cells inoculated into syngeneic hosts were less tumorigenic than untreated cells. However, theophylline treatment of hosts bearing B16 tumors failed to reduce the tumor growth rate, and theophylline did not potentiate the growth inhibition resulting from treatment with the synthetic polyribonucleotide, polyinosinic-polycytidylic acid.
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PMID:Maturation and differentiation of B16 melanoma cells induced by theophylline treatment. 16 92

The antitumor activity of three preparations of killed Bordetella pertussis (Bp) (Eli Lilly crude and fluid pertussis vaccines and Parke-Davis pertussis vaccine) was studied in the B16 melanoma and CaD2 mammary adenocarcinoma models. In these tumor systems; Bp had weak and variable tumor inhibitory activity and did not augment tumor rejection immunity. The intratumor injection of Bp did not affect the growth of the B16 tumor but significantly inhibited the growth of the CaD2 tumor. However, the established tumor did not regress. Admixture of Bp with B16 cells before inoculation inhibited tumor growth and prolonged survival of inoculated mice. Admixture of Bp with CaD2 cells completely suppressed tumor cell growth in 60% of inoculated mice. Intratumor injection of CaD2 with Bp combined with surgery provided no protection against subsequent development of metastases.
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PMID:Evaluation of antitumor activity of Bordetella pertussis in two murine tumor models. 16 59

Type-2 adenovirus was shown to inhibit the growth of transplantable hamster melanoma in 70% of Syrian hamsters without any injurious effect to the host. Greatest inhibition of tumor formation was seen when animals were injected with 10(6) TCD50 of adenovirus and 2.5 x 10(5) tumor cells, or 10(6) TCD50 of virus and 5.0 x 10(5) tumor cells followed either 1 or 7 days later by a second injection of a similar dose of virus. Significant inhibition in tumor growth was also noted when 2 injections of virus (10(6.2) TCD50/injection) were given on 2 separate occasions as late as 7 and 10 days after the inoculation of tumor cells. The mechanism of tumor inhibition is not known but it could be due to a combination of factors such as viral toxicity, viral oncolysis, and antitumor immunity.
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PMID:Inhibition of melanoma growth in hamsters by type-2 adenovirus. 17 Apr 80

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 systemic administration of 16,16-dimethyl prostaglandin E2-methyl ester (di-M-PGE2) on the growth of B-16 melanoma tumors has been studied in C57BL/6J mice. Daily i.p. injection of 5 mu of di-M-PGE2 commencing on the day of tumor inoculation with 10(5) and 10(6) viable cells delayed appearance of tumors; for the smaller tumor inoculum, it also increased median survival among treated mice from 23 to 33 days. Di-M-PGE2 treatment of mice with established tumors caused significant inhibition of tumor growth, as measured by a number of parameters including tumor diameters and volumes. At the time of sacrifice, di-M-PGE2-treated mice had tumors that were an average of 32% smaller (by weight), contained 60% fewer melanoma cells, and had higher concentrations of cyclic adenosine 3':5'-monophosphate and cyclic guanosine 3':5'-monophosphate (+225% and +100%, respectively).
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PMID:Inhibition of B-16 melanoma growth in vivo by a synthetic analog of prostaglandin E2. 19 22

Human malignant melanoma cell lines established in tissue culture were successfully transplanted sc into BALB/c nude mice. The growth rate of the resulting tumors was significantly suppressed when lymphocytes from the patient in whom the tumor arose were injected iv into BALB/c nude mice at the same time as sc tumor transplantation, but inoculation with lymphocytes from a person without a tumor was ineffective. Cell separation identified T-lymphocytes as the active subpopulation. Growth of the tumors was also significantly suppressed by reconstitution of the mice with normal BALB/c lymphocytes; lymphocytes from BALB/c mice previously immunized against the melanoma line were not more effective than nonimmune lymphocytes in preventing tumor growth. Sera from normal BALB/c mice or BALB/c mice immunized against a human melanoma cell line effectively suppressed growth of that cell line in BALB/c nude mice if given at the time of tumor transplant. The results suggested that, whereas murine lymphocytes reconstitute the ability of nude mice to react to xenogeneic antigens on the human tumor, human lymphocytes showed greater specificity to autologous human melanoma-associated antigens.
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PMID:Growth of human melanoma in nude mice: suppression by T-lymphocytes from the tumor donor: brief communication. 30 65

Sera from 134 selected patients with various types of cancer were tested for soluble antigen-antibody complexes by the C1q binding method. Sera from 85 healthy blood bank donors served as normal controls. C1q binding activity (C1q BA) values above the 95th percentile for healthy subjects were found in 83% of sera from patients with neoplastic diseases. The incidence of abnormal C1q BA values among patients with malignant melanoma was 83%, with breast cancer 74%, with colon cancer 75%, with lung cancer 88%, with leukemia and lymphoma 85%, and with miscellaneous tumors 94%. High C1q BA values were found most frequently in sera of patients who had been diagnosed relatively recently (within 5 mo) and who had evident residual disease after surgical treatment. Recurrence or progression of tumor growth occurred significantly more frequently in lung cancer patients with high C1q BA. DNA was not detected in cancer patients' sera and treatment with DNase did not decrease in C1q BA. C1q BA in sera could not be explained by the presence of antiglobulin antibodies. Sucrose density gradient ultracentrifugation studies of the serum C1q BA in 4 cancer patients showed that the major binding activity was found between 19S and 7S.
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PMID:The C1q binding test for soluble immune complexes: clinical correlations obtained in patients with cancer. 32 5

An immunopotentiating factor associated with spleen cells of C57BL/6J mice bearing the 3LL tumor is described. Supernatants of cultured spleen cells from tumor-bearing mice (TBM) augmented the generation of both 19S and 7S antibody-producing cells, when injected with sheep erythrocytes into syngeneic C57BL/6J mice. The enhancing supernatant acted both as a polyclonal activator, when injected in the absence of antigen, and as a potentiator of specific antigen-dependent humoral immune responses, when injected in the presence of antigen. It was found to augment induction of specific memory, but not memory expression. Concomitantly with their influence on humoral immune responses, TBM spleen cell supernatants enhanced tumor growth when injected, mixed with 3LL tumor cells, into syngeneic recipients. The secretion of a factor which augments antibody production was not confined to the 3LL tumor system. Spleen supernatants of C47BL mice carrying the B16 melanoma and those of C3H mice carrying the KHT sarcoma had a similar effect on antibody production. These findings suggest that an immunoregulatory factor(s) appears in spleen cells of TBM as a result of their interaction with the neoplastic tissue. This factor can potentiate production of antibodies, possibly also against tumor-associated antigens. The relevance of the immunopotentiating effects of such factor(s) to tumor growth is discussed.
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PMID:An immunoregulatory factor associated with spleen cells from tumor-bearing animals. I. Effect on tumor growth and antibody production. 35 90


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