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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tyrosinase activity in two sucrose gradient isolated melanosome fractions from a melanotic hamster melanoma was found to increase after alpha-chymotrypsin treatment. The enhancement in tyrosinase activity had its maximum at a concentration of 1 mg/ml alpha-chymotrypsin after 120 min incubation at 37 degrees C. No direct activating effect of alpha-chymotrypsin was found either on the soluble tyrosinase fraction from freshly prepared untreaed whole-tumor homogenate or on purified mushroom tyrosinase. The activating effect of alpha-chymotrypsin upon the melanosome tyrosinase is believed to be due to the endopeptidic hydrolysis of the--CO--NH--bound existing between tyrosinase and tyrosine and phenylalanine residues in the melanin molecule. Although alternative interpretations are not excluded, the observed enhancement in tyrosinase activity after alpha-chymotrypsin treatment of melanosomes might indicate the existence of an "enzyme liberating" mechanism in the melanosomes.
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PMID:Chymotrypsin activation of melanosome tyrosinase in hamster melanotic melanoma. 11 73

The mitogens concanavalin A (Con A) and bacterial lipopolysaccharide (LPS) stimulated normal spleen cells of DBA/2J, CBA/J, and BALB/c mice about equally in the presence of either isologous or homologous serum. This system revealed that sera from mice with five different methylcholanthrene-induced rhabdomyosarcomas inhibited mitogen stimulation of normal spleen cells. Sera from mice with a mammaryadenocarcinoma and spontaneous rhabdomyosarcoma were similarly suppressive. In contrast, sera from mice with melanoma were not inhibitory and often enhanced stimulation. Sera from tumor-bearing animals had the same effects both qualitatively and quantitatively on cells from the strain carrying the tumor and on cells from the other two strains. The mixed lymphocyte response of CBA/J times BALB/c spleen cells was affected exactly as were the responses to mitogen by the various sera. Stimulation by mitogen of mouse lymph-node cells and spleen cells with macrophages removed, as well as that of guinea pig spleen cells, was also inhibited by sera from mice with rhabdomyosarcoma and mammary adenocarcinoma.
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PMID:Effects of sera from tumor-bearing mice on mitogen and allogeneic cell stimulation of normal lymphoid cells. 12 99

A rapid microcytotoxicity assay for the detection of HL-A antigens on tissue culture cells derived from human solid tumors is described. Tumor cells were prelabeled with 125Iododeoxyuridine. Isotopically labeled tumor cells were reacted with up to 37 highly selected HL-A antisera and diluted rabbit complement. Results of the HL-A typing of nine human tumor cell lines are reported. Three melanoma cell lines showed individually distinct HL-A profiles at the first HL-A locus which agreed with the antigenic pattern of the tumor donor's autologous lymphocytes. Less reactivity was noted with HL-A antisera defining second locus specificities on the three melanoma cell lines, whereas some other cell lines showed more HL-A reactions than required to present a "full house". This method obviates the necessity for visually enumerating residual tumor target cells.
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PMID:A new micromethod for the detection of HL-A antigens on cultured human tumor cells. 12 40

Testing of delayed hypersensitivity responses to recall antigens, newly encountered antigens and tumor antigens has contributed to the understanding of several immunologic factors in human neoplasia. Patients with Hodgkin's disease tend to have depressed responses to both newly encountered and recall antigens. Patients with solid tumors are more likely to be deficient only in the response to newly encountered antigens. In patients who have intact response to recall antigens, reactivity to antigen preparations from tumor and control tissue may be studied. Tumor-associated or organ-associated antigens have been demonstrated by delayed hypersensitivity responses in leukemia, Burkitt's lymphoma, malignant melanoma and carcinoma of the lung, breast, cervix uteri and intestine. Approaches to a definition of the specificity of these reactions are described. The results with these tumor antigen tests correlate strongly with the clinical course. This is a promising technique for monitoring immunotherapy. The results from tests with recall and newly encountered antigens also correlate with the clinical status and perhaps with prognosis. Various possible interpretations of these changes are discussed. Further work should be directed toward an exact definition of immunologic defects in patients with cancer and toward the use of this understanding for a rational program of immunotherapy.
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PMID:Immunologic evaluation of patients with cancer by delayed hypersensitivity reactions. 12 44

Spontaneous cell-mediated cytotoxicity (SCMC) and antibody-dependent cellular cytotoxicity (ADCC) against 51Cr labeled allogeneic target cells of a human melanoma cell line (IGR3) were determined with purified effector lymphocytes and defibrinated whole blood from 14 melanoma patients and 13 healthy control persons. Peripheral blood lymphocytes were isolated by Ficoll gradient centrifugation (fraction F); subsequently the phagocytic and adherent cells were removed and the supernating cell population (fraction fff) was passaged through IgG anti-IgG columns to obtain a B cell free lymphocyte suspension (fraction fff-c). cells from the 3 lymphocyte fractions and from defibrinated whole blood were simultaneously tested for cytotoxic activity against unsensitized IGR3 target cells (SCMC assay) and IGR3 cells perviously sensitized with a rabbit anti-melanoma IgG (ADCC assay). Dose-response curves were established with all lymphocyte fractions and with whole blood. The following results were obtained. 1. With all lymphocyte fractions tested, ADCC was approximately 15 time higher than SCMC, whereas with whole blood, the difference tended to be less pronounced. 2. Elimination of phagoctic and adherent cells had no significant effect on SCMC and ADCC. 3. Passage over IgG anti-IgG columns drastically reduced cytotoxicity in both assays without, however, completely abolishing it. 4. The only difference seen between lymphocyte cytotoxicity of melanoma patients and control persons was a slight, but non-significant depression of SCMC and ADCC in melanoma patients. The results confirm and extend our previous report that SCMC against an allogeneic tumor cell-line is due to not-specific "Null" or "K" cell-activity rather than to specific T cell cytotoxicity. In one experiment freshly explanted melanoma cells were labeled with 51Cr and reacted wiht autologous blood and purified lymphocyte fractions. It was found that cellular cytotoxicity depending on serum factors (ADCC) was an effective lytic mechanism, whereas T cell-mediated cytotoxicity could not be demonstrated.
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PMID:Spontaneous and antibody-dependent cellular cytotoxicity in melanoma patients and healthy control presons. 13 45

The ultrastructural morphology of the tumour cycle which has as one of its features the blood-borne tumour embolus associated with thrombosis is illustrated by examples of four phases. (1) The intrinsic vasculature of tumours influences the process of intravasation of tumour cells to form bloodborne emboli. Scanning electron microscopy of melanoma tumours reveals channels containing erythrocytes which are sinusoidal in appearance. (2) The reaction of the circulating blood to the villi and folds of tumour cells is to coat the surface with plasma proteins and platelets. Walker 256 carcinoma cells become encrusted with platelets following agitation with rat platelet rich plasma. (3) Damaged endothelium appears to provide a more secure adhesional site for the tumour embolus. Platelets on a damaged site may provide an active adhesional region for the platelets on the passing embolus. (4) Tumour cells migrate through the endothelial layer from the adherent embolus and can be held up at the level of the basement membrane of the endothelium.
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PMID:Some aspects of blood borne tumour emboli associated with thrombosis. 13 7

A series of 42 patients with malignant melanoma treated with BCG adjuvant immunotherapy were studied for sequential changes in cellular immune reactivity to non-specific mitogens. Lymphocyte preparations were made monthly and stored in a viable condition in liquid nitrogen. After 6 months of treatment, all lymphocyte samples from an individual were recovered and tested for DNA synthesis after stimulation with PHA, PWM, Con A, PPD and MLC. The responses to the mitogens in the blastogenesis test were stable during the course of therapy. The MLC response did not increase significantly in patients treated with tumor-cell vaccines, and declined sharply in the six patients who subsequently relapsed and died. The in vitro PPD response increased 1 to 3 months after initiation of BCG in patients who were initially unresponsive to PPD in vitro. However, PPD-positive patients did not show any significant alteration of the PPD response. The PPD response did increase less sharply in patients whose disease eventually recurred than in those who remained without evidence of clinical disease. BCG therapy does not appear to correct lymphocyte proliferative defects in melanoma patients. Of the assays employed, the MLC and PPD tests appear to be the most useful as monitors of clinical status and response to therapy.
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PMID:Sequential examination of lymphocyte proliferative capacity in patients with malignant melanoma receiving BCG immunotherapy. 13 80

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

Twenty-four patients with far advanced malignant tumors, resistent to established chemotherapy,, were treated with the combination of MNU and Cyclophosphamide. The drugs were administered in six-day cycles sequentially. MNU in doses of 4 mg/kg body weight and Cyclophosphamide in doses of 8 mg/kg body weight were given. Results of treatment showed response (greater than 50% tumor regression) in 10 (42%) of the 24 treated patients. Seven remissions were complete and three partial. Patients with Hodgkin's disease, malignant melanoma and breast cancer responded to this combination chemotherapy. Objective remissions were obtained also in five of thirteen patients with primary or metastatic brain tumors and in five of nine patients with pulmonary metastases. Nausea and vomiting were the main toxic effects, especially after injections of MNU. Myelosuppression was noted in about 50% of treated patients. Since this combination of cytostatics showed significant antitumor activity, further investigations are necessary on a larger number of patients and in other types of malignant tumors.
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PMID:Combination chemotherapy with 1-methyl-1-nitrosourea (MNU) and cyclophosphamide in solid tumors. 14 13

A nearly fatal allergic reaction to intratumor BCG injections was associated with a complete remission of recurrent malignant melanoma. Clinical course and histologic sections suggested both anaphylactic and Arthus reactions. The occurrence of reactions at BCG injection sites as well as at uninjected sites of tumor suggests common BCG and melanoma antigens. The management of events involved in this often fatal postimmunotherapy complication involves the early administration of parenteral fluids, antituberculous therapy, antihistamines, and possible steroids. The prophylactic use of antihistamines and an in-hospital administration of intralesional BCG immunotherapy are strongly suggested. In the future, prophylactic INH may prove to be both therapeutically efficacious and protective against infectious complications.
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PMID:Risks of BCG intralesional therapy: an experience with melanoma. 14 18


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