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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The majority of melanoma tumor antigen activity present in melanoma extracts derived from fresh tumor tissue binds to a Sepharose-anti-beta2-microglobulin adsorbent. Removal of HLA antigens from the extracts of melanoma tissue by using a KBr flotation technique did not reduce either the tumor antigen activity of the extracts or the binding of melanoma tumor antigen (MTA) activity to the Sepharose-anti-beta2-microglobulin adsorbent. The complete blocking of MTA activity by pretreating the anti-beta2-microglobulin adsorbent with beta2-microglobulin and the lack of detectable MTA binding to a Sepharose anti-normal human serum adsorbent demonstrated the specificity of the binding of MTA to the anti-beta2-microglobulin adsorbent.
Cancer Res 1979 Feb
PMID:Association of melanoma tumor antigen activity with beta2-microglobulin. 8 15

The hemocytometer leukocyte adherence inhibition technique was employed in a criss-cross experimental design with two cancer patients (melanoma and colon carcinoma) and the corresponding tumor extracts. These extracts had been repeatedly tested for specific reactivity and lyophilized before transport to the workshop. The patients' leukocytes were mixed singly with each extract in the presence of normal serum, and the adherences of the cells were determined in hemocytometer chambers. Actual cell counts (total cells before washing and adherent cells after washing) are given in detail for the first time. Blood samples and reaction mixtures were coded by an independent observer. Determination of mean % adherence (+/- S.E.) showed that the melanoma patient's leukocytes (original adherence 70.8 +/- 2.8) reached with the melanoma extract (40.7 +/- 2.9; p less than 0.001) but not significantly with the colon carcinoma extract (61.5 +/- 4.1; p greater than 0.05). Similarly, the colon carcinoma patient's leukocytes (original adherence 68.6 +/- 2.7) reacted with the colon carcinoma extract (43.2 +/- 2.3; p less than 0.001) but adherence was not inhibited by the melanoma extract (76.9 +/- 2.6). The cancer patients were thus correctly identified with regard to tumor type in a simple blind trial.
Cancer Res 1979 Feb
PMID:Hemocytometer leukocyte adherence inhibition technique. 8 16

Heparinized samples of blood from three different patients were coded by impartial observers. The buffy coat leukocytes from the coded samples of blood were isolated and incubated separately with extracts of colon and pancreatic cancer in the tube leukocyte adherence inhibition assay. At the completion of the assay, the leukocytes from Patient 1 were equally nonadherent to both cancer extracts with a nonadherence index value of 8. By contrast, leukocytes from Patient 2 exhibited increased nonadherence to the extract of colon cancer (p = 0.02) with a nonadherence index value to colon cancer antigen of 89. Leukocytes from Patient 3 displayed increased nonadherence to the extract of pancreatic cancer (p less than 0.05) with a nonadherence index value to pancreatic cancer antigen of 39. When the code was broken, patients 1, 2, and 3 had diagnoses of malignant melanoma, colon cancer, and pancreatic cancer, respectively. Hence, this was a classical criss-cross experiment; the patient with malignant melanoma reacted to neither of the antigens, whereas the patients with colon and pancreatic cancer reacted to the sensitizing cancers which had unique organ-type specific neoantigens.
Cancer Res 1979 Feb
PMID:Demonstration of tube leukocyte adherence inhibition assay with coded samples of blood. 8 17

The leukocyte adherence inhibition assay was used to measure cell-mediated immunity in 26 patients with malignant glial neoplasms and 41 control subjects. A significant inhibition of leukocyte adherence was observed in 21 of 26 (80%) glioma patients in the presence of a 3 M KCl extract of glioma tissue, as compared to that of normal brain extract. Among the control group, no significant difference in the percentage of nonadherent leukocytes was noted in the presence of either antigen. To study the specificity of the reaction, a 3 M KCl extract of meningioma, pituitary tumor, carcinomas of breast, and lung, melanoma, brain, and heart tissues were used as nonspecific antigens. Such studies revealed significantly lower values of nonadherent leukocytes. These data indicate that patients with malignant glial neoplasms manifest a cellular immune response to glioma-associated antigens which can be measured by the tube leukocyte adherence inhibition assay and that leukocyte adherence inhibition assay may render additional useful information in diagnostic and prognostic evaluation of malignant glial neoplasms.
Cancer Res 1979 May
PMID:Specific cellular immune responses in patients with malignant gliomas. 8 87

Using radioiodinated Staphylococcus aureus protein A [125I]SPA to measure syngeneic, allogeneic and heterogeneic IgG bound to murine tumor cells, we performed a serological analysis of surface antigens of 8 solid tumors and 2 leukemias of BALB/c mice (3 chemically-induced colon carcinomas, 3 chemically-induced sarcomas, 1 murine leukemia virus (MuLV) induced leukemia, 1 irradiation induced leukemia, 1 spontaneous melanoma and 1 spontaneous sarcoma). We were able to detect and distinguish between at least five separate antigenic specificities on these tumors. Unique tumor-associated antigens were found on 3 of the tumors, MuLV related antigens on 8 tumors, fetal antigens on 7 tumors and two distinct common antigens on 7 tumors (common antigen 1 (CA-1) on 5 tumors and common antigen 2 (CA-2) on 2 tumors). Neither of the common antigens was found to be sarcoma, carcinoma or tissue-tupe specific. A number of tumors which did not originally express either MuLV or fetal antigens in primary cultures expressed these antigens after several serial passages in vitro.
Int J Cancer 1979 Mar 15
PMID:Tumor-associated antigens of chemically-induced murine tumors; the emergence of MuLV and fetal antigens after serial passage in culture. 8 20

Antisera to human renal cell carcinomas were produced by the immunization of goats and rabbits with dissociated tumor cells and/or tumor homogenates from single donors. After absorptions with human red blood cells and homogenates of human liver, lung, spleen, and heart, all the immune sera reacted on immunofluorescence with the brush border of the proximal convoluted tubules of adult and fetal human kidneys and with the proximal convoluted tubular epithelia of rabbits, guinea pigs, rats, and mice. After further absorption with pooled normal human kidney homogenates, the immune sera on immunofluorescence showed cytoplasmic staining of smears and sections of 21 of the 22 human renal cell carcinomas tested. These sera did not show any staining of normal adult human tissues including normal kidney adjacent to the carcinomas, perirenal fibroblasts and peripheral blood leukocytes from the patients, human fetal kidneys, transplanted renal adenocarcinoma of BALB/c mice, and several human tumors tested, i.e., transitional cell carcinoma of the bladder, adenocarcinomas of the breast and colon, squamous cell carcinoma of the lungs, malignant lymphoma, and melanoma. Autoradiography of tissue sections with 131I-labeled antitumor globulins revealed greater localization of radioactivity in tumors than in adjacent normal kidney. Membrane immunofluorescence with the immune sera rendered tumor-specific after appropriate absorptions revealed tumor-associated antigens on the surfaces of all 5 human renal carcinoma cell lines tested.
J Natl Cancer Inst 1979 Aug
PMID:Production and characterization of xenogeneic antisera to a human renal cell carcinoma-associated antigen. 8 35

Oncofetal antigen (OFA) has been defined with the use of human natural antibodies as a membrane antigen of human cancer cells that cross-reacts with human fetal brain tissues. The immunogen that elicits the antibody is unknown. The present study was undertaken to examine the immunogenicity of the OFA found on tumor cells. Postoperative melanoma patients were immunized with OFA-positive melanoma cells. Anti-OFA reactivities in the immunized sera were titrated by the immune adherence assay with the use of a known OFA-positive cultured melanoma cell line, M14, as target cell. Alloantibodies were excluded by absorption with lymphoblastoid cells autologous to M14. Anti-OFA antibody then was identified by absorption with fetal brain. In 6 months of immunization, 19 of 23 patients produced increased anti-OFA antibodies. The peak titers ranged from 1:16 to 1:2,048. Sera from 18 patients who were not immunized also were tested for 6 months postoperatively, and none had significant increases in antibody titers. The increase of anti-OFA antibody titer in response to the immunization with OFA-positive tumor cells suggests the immunogenic capability of tumor-related OFA in man.
J Natl Cancer Inst 1979 Aug
PMID:Oncofetal antigen: a tumor-associated fetal antigen immunogenic in man. 8 39

Biochemical characterization of serologically detected human melanoma antigens was undertaken for the development of immunodiagnostic assays in melanoma. An antiserum from a human melanoma patient, which detected melanoma antigens expressed on a large proportion of different melanoma cells, was used in leucocyte-dependent cytotoxic antibody (LDA) 51Cr-release assays to monitor the purification of melanoma antigens in urea/acetate extracts of lactoperoxidase 125I-labelled melanoma cell membranes. The separation procedures included affinity chromatography on Concanavalin A, gel filtration on porous polyacrylamide beads and preparative isoelectric focusing. The fractions were also monitored by polyacrylamide electrophoresis in sodium dodecyl sulphate and by measurement of beta 2 microglobulin and carcinoembryonic antigen content. The antigens detected by this antiserum appeared to be acidic (pI 3.5) low-mol.-wt glycoproteins of approximately 15,000 daltons which were resistant to heating at 56 degrees C and digestion with neuraminidase, but susceptible to repeated freeze-thawing and trypsin digestion. They did not appear to be related to HLA antigens, beta 2 microglobulin or known foetal antigens. The nature of the antigens detected in these studies is as yet unknown, but they appear similar to those described in the sera and urine of melanoma patients in previous reports. Thes combined results and the frequent expression of these antigens on melanoma cells from different patients suggest that assays to detect this antigen may provide a valuable immunodiagnostic aid in the management of melanoma.
Br J Cancer 1979 Oct
PMID:Detection of a low-molecular-weight antigen on melanoma cells by a human antiserum in leukocyte-dependent antibody assays. 9 79

Nine established human melanoma tissue-cultured cell lines heterotransplanted in C57BL/6 "nude" mice were exposed to each of 4 chemotherapeutic agents of known clinical activity against human melanoma. Two of the therapeutic agents, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and 5-(3,3-dimethyl-1-triazino) imidazole-4-carboxamide (DTIC), are known to be active against human melanoma; the other two, adriamycin and 5-azacytidine, are known to be inactive. Sterile saline served as a control agent. In 2 cell line heterotransplants, the control tumor spontaneously regressed. Of the 7 cell lines that remained for evaluation, 4 were sensitive to DTIC, 1 was sensitive to BCNU, and none was sensitive to adriamycin or 5-azacytidine. These data indicate that the nude mouse-human tumor model may be a predictive secondary screen for cancer chemotherapeutic agents.
J Natl Cancer Inst 1979 Nov
PMID:Evaluation of a "nude" mouse-human tumor panel as a predictive secondary screen for cancer chemotherapeutic agents. 9 97

A number of previous studies have shown that the level of natural killer (NK) cell activity in humans is relatively constant for a given individual but varies widely between individuals. The factors which determine this variability are largely unknown, but genetic factors appear to be involved. In the present study it was found that Rh- normal subjects and melanoma patients had significantly higher natural cytotoxicity to target cells than Rh+ patients. This difference did not appear to be due to sensitization against Rh antigens on the target cell and may indicate that genes determining NK-cell activity are associated with those determining the expression of Rh antigens. Analysis of the survival data for Rh- and Rh+ patients did not reveal any increase in survival attributable to the higher natural cytotoxicity in Rh- patients.
Br J Cancer 1979 Mar
PMID:Relationship of natural killer-cell activity to rhesus antigens in man. 11 95


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