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)

Membrane antigens of a cultured human melanoma line, UCLASO-M14, were studied using immune adherence techniques. Allogeneic sera from melanoma patients that were reactive with the M14 but nonreactive with lymphoid cells of the M14 donor were used as antibodies. The antigen responsible for the reaction between M14 and the antibodies was searched for in other cancer, normal, and fetal tissues using antibody absorption techniques. The antigen was found in a variety of different histological types of biopsied and cultured cancer cells as well as in melanomas. The antigen did not exist in biopsied normal tissues, but it appeared in cultured normal skin and muscle. Neither normal lymphocytes nor cultured lymphoid cells showed any antigenicity. The antigen was present in human fetal tissues and was the strongest in fetal brain tissues at 22 weeks of development. Liver, spleen, thymus, and small intestine from the same fetus were negative for antigen.
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PMID:A membrane antigen common to human cancer and fetal brain tissues. 6 13

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.
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PMID:Oncofetal antigen: a tumor-associated fetal antigen immunogenic in man. 8 39

Peripheral blood lymphoid cells (PBL) from cancer patients and normal donors were tested against three melanoma cell lines grown in either 10% fetal calf serum (FCS) or 2.5-5% human AB serum in order to determine if the heterologous membrane (HM) antigen or other FCS antigens acquired from the bovine serum supplement could influence lymphoid cell-mediated cytotoxicity in vitro. FCS-grown melanoma cells were more susceptible than the AB serum-grown subline to lymphocyte cytotoxic effects. Arming effects by autologous sera on normal donor lymphocytes and to a lesser extent on lymphocytes of cancer patients were more pronounced on the FCS-grown M12 melanoma cells. This effect was abrogated when the cells were grown in human AB serum for at least 8 weeks. The non-HM tumor-associated antigen remained at the same original low level. Blocking effects were more evident on the AB-grown M14 melanoma line. These data suggest that the FCS antigens on the cell surface may have been responsible for the augmented PBL cytotoxicity. The anti-FCS antibody present in normal and cancer patients' blood induced an antibody-dependent cellular cytotoxicity (ADCC). Elimination of arming activity against HM or other FCS antigens from AB-grown cells may have made the serum blocking factors more apparent. However, cytotoxicity against tumor cells by PBL from normal donors was still apparent even on the human serum-grown cells, suggesting that a different antigen-antibody system was also responsible for this "non-specific" activity.
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PMID:Human tumor cells grown in fetal calf serum and human serum: influences on the tests for lymphocyte cytotoxicity, serum blocking and serum arming effects. 94 29

A human malignant melanoma cell strain, UCLA-SO-M14 (M14), was adapted to grow in serum-free, chemically defined medium (CDM). The 3 M KCl extract prepared from the CDM-grown cells (M-14-CDM) was assayed against leukocytes from melanoma patients, patients with other cancers, and normal donors by leukocyte migration inhibition (LMI). The leukocytes from 15 to 27 (56%) melanoma patients tested were LMI positive. In contrast, 4 of 18 (22%) other cancer patients and 5 of 30 (17%) normal donors leukocytes were LMI positive. One of 14 melanoma patients' leukocytes were LMI positive for a control 3 M KCI extract from autologous muscle. Comparative studies were performed with the M14-CDM extract and a 3 M KCI extract from a freshly biopsied tumor specimen from the donor of the M14 cell strain. Seven of 12 (58%) melanoma patients' leukocytes were LMI positive to the M14-CDM extract, but only 2 of 12 (17%) were LMI positive to the autologous melanoma tissue extract. Furthermore, only 100 to 300 mug protein of M14-CDM extract were required to educe delayed cutaneous hypersensitivity response in 6 of 8 (75%) melanoma patients and 0 of 5 lung cancer patients, but 500 mug protein from biopsied autologous melanoma tissue extract were needed to produce delayed cutaneous hypersensitivity response in 24 of 42 (57%) melanoma patients and 7 of 28 (25%) nonmelanoma cancer patients. These data suggest: (a) the M14-CDM cells synthesized melanoma-associated antigen(s) (MAA) in CDM; (B) the 3 M KCI extraction procedure effectively removed the MAA from the M14-CDM cells; (c) the M14-CDM cells were a more potent source of MAA than the surgical autologous melanoma specimen; and (d) the M14-CDM cells provided a continuous source of standard MAA.
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PMID:Production of melanoma-associated antigen(s) by a defined malignant melanoma cell strain grown in chemically defined medium. 126 Jul 67

Lonidamine (LND), a dichlorinated derivative of indazole-3-carboxylic acid, has proved to exert a powerful antiproliferative effect and to impair the energy metabolism of normal and neoplastic cells. A target effect of the drug on the cell membrane structure was hypothesized. Thus, in order to elucidate better the mechanism of action of LND, the drug effects on the cell surface as well as on main cytoskeletal elements, i.e. actin microfilaments, microtubules and intermediate filaments, were investigated. In particular, an immunocytochemical and ultrastructural study was performed using two different cell lines: epithelial squamous carcinoma (A431) and melanoma (M14) cells. Treatment with 0.8 mM LND for 8 hr induced a remarkable rearrangement of the F-actin molecules with the disappearance of the stress fibers. As far as microtubules are concerned, formation of perinuclear patches of tubulin were detected after LND treatment. Intermediate filaments appeared to be differently affected by LND in the two cell types. Such changes were detected as an early phenomenon and the extent of the effects observed was positively related to the cell surface alterations and to the loss of cell viability, suggesting that the cytoskeletal elements might represent an additional target in the mechanisms of cytotoxic action of LND.
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PMID:The cytoskeleton as a subcellular target of the antineoplastic drug lonidamine. 129 47

In vivo and in vitro studies performed on the polar solvent N-methylformamide (NMF), as well as on its association with chemotherapeutic agents or X rays, have clearly demonstrated that this compound is capable of inducing changes in biological characteristics of tumor cells, e.g., cell differentiation. However, the mechanism of action of NMF is far from being elucidated. Hence, in order to better clarify such a mechanism an in vitro study was carried out by using mouse fibroblasts in primary culture (MEF) and human melanoma cultured cells (M14). Results obtained by immunocytochemical and ultrastructural methods with doses of NMF ranging from 0.1 to 7% are reported here. As a general rule, a different sensitivity (in terms of cytopathologic changes induced by NMF) was found between the cell types considered. In fact, melanoma cells appeared to be highly susceptible to the action of the drug, undergoing severe morphological modifications represented mainly by a reversible dose and time-dependent cell rounding and surface blebbing. In contrast, NMF-induced injury in MEF cells was characterized mainly by a simple retraction of the cell body. A cytochemical analysis of the expression of certain membrane antigens (e.g., glycoproteins, epidermal growth factor receptor, B2 microglobulin) in NMF-treated M14 cells undergoing blebbing was also carried out. A randomly distributed labeling of such molecules was observed. Accordingly, freeze-fracturing electron microscopic analysis also displayed a random distribution of intramembrane particles over the plasma membrane. When subcellular changes induced by the drug were investigated, a remarkable modification of cytoskeletal components was detected in both cell types. In particular, cross-linked actin microfilament bundles were easily observed in NMF-exposed MEF cells. Finally, when different experimental conditions which perturb calcium ion homeostasis or restore protein thiol group reduced state were analyzed, a noticeable impairment of the blebbing phenomenon was observed. Thus, a target effect of NMF on the microfilament system, probably leading, in turn, to several subcellular changes and cell surface blebbing, can be hypothesized. Such a cytoskeletal element-dependent cytopathology appears to be related to changes of the oxidized state of such molecules as well as to calcium ion perturbations.
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PMID:Cytoskeleton-dependent surface blebbing induced by the polar solvent N-methylformamide. 142 60

We developed a high-titer polyclonal antiserum to a glycoprotein tumor-associated antigen (TAA) by immunization of a baboon with the purified glycoprotein antigen. The baboon serum was fractionated into IgG and IgM components by DEAE Affi-Gel blue chromatography. The ability of the baboon IgM anti-TAA antibody to effect tumor cell lysis in the presence of complement was tested using a chromium-release assay. The baboon antibody was able to lyse melanoma target cells (20.8%-71.4% cytolysis), breast carcinoma cells (36.5%-38.9% cytolysis), and a neuroblastoma cell line (35.5% cytolysis) in the presence of complement but did not effect significant lysis of autologous lymphoblastoid cell lines (4.9% cytolysis) or peripheral blood lymphocytes from healthy volunteers (12.6% cytolysis). Cytolysis of melanoma target cells was completely inhibited by preabsorption of the IgM anti-TAA antibody with UCLA-SO-M14 (M14) cells and partially inhibited by preabsorption with several other melanoma cell lines. There was no significant inhibition of tumor cell lysis after preabsorption of the antibody with lymphoblastoid cell lines. Complement-dependent lysis of M14 targets could be blocked by addition of the purified antigen to the antibody prior to incubation with the tumor cells. Our results suggest that the glycoprotein TAA resides on the tumor cell surface and that the baboon IgM anti-TAA antibody recognizes the antigen on the cell surface and is able to fix complement and effect the lysis of the tumor cells.
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PMID:Complement-dependent lysis of tumor cells by a baboon IgM antibody to a tumor-associated antigen. 156 14

The effects of purified protein A from Staphylococcus aureus Cowan I stain on induction of lymphokine (IL-2) activated killer (LAK) activity were studied in normal as well as melanoma patient's lymphocyte. The coculture of peripheral blood mononuclear cells (PBMC) with various doses of protein A (0.001, 0.01 and 0.1 microgram/ml) and IL-2 (100 U/ml) for 4 days produced synergistic effect on the LAK cells mediated cytotoxicity. The potentiation of cytotoxicity and lytic ability of LAK cells against NK sensitive (K-562) and NK-resistant (M14) tumor cells were observed. Further there was potentiation of DNA synthesis in PBMC after 4 days culture. Similar results were found when PBMC from melanoma patients were cultured with PA and IL-2. The potentiation of LAK cell induction associated with its cytotoxic and lytic potential by low doses of IL-2/PA regiment may be helpful in the development of LAK immunotherapy of the cancer patients.
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PMID:Protein A potentiates lymphokine-activated killer cell induction in normal and melanoma patient lymphocytes. 159 62

L-Canavanine, like other aminoacid analogs, induces the synthesis of heat shock proteins (HPSs) but, unlike heat or other stressing agents, it fails to induce thermotolerance. We have studied the synthesis and the intracellular distribution of HSPs induced by canavanine, the effects of this analog on the viability and thermal sensitivity of a human melanoma cell line (M14) and the capacity of canavanine-induced HSPs to self regulate their own synthesis. Evidence indicates that the HSP induction is time--and dose--dependent and, also in the presence of arginine, is not associated with the development of thermotolerance. On the contrary, cells become more heat sensitive and are less efficient in the control of the feed-back mechanism that regulates HSP synthesis. The possible utilization of this substance as a potential aid for the treatment of tumors, in association with heat, was examined.
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PMID:Stress response, survival and enhancement of heat sensitivity in a human melanoma cell line treated with L-canavanine. 162 35

Different results have been reported on the expression of epidermal growth factor receptor (EGFR) in human melanocytic lesions, which may be due to different methodologic approaches. Therefore, we compared EGFR expression in six human melanoma cell lines by utilizing the monoclonal antibodies 2E9, 425, and 225, applying four immunocytochemical staining procedures. The results were compared with those obtained by a multiple point ligand binding assay. In addition, Northern blot analysis was performed. A three-step immunoperoxidase method using the monoclonal antibody 2E9 proved most sensitive. Staining intensities, estimated semiquantitatively, correlated well with the quantitative data obtained by the ligand-binding assay. Expression on the mRNA level was also in agreement with these results. Immunohistochemical staining of a large series of human cutaneous melanocytic lesions using the method selected showed differential EGFR expression in various stages of melanocytic tumor progression: 19% of common nevocellular nevi; 61% of dysplastic nevi, 89% of primary cutaneous melanomas, and 91% of melanoma metastases showed staining of the melanocytic cells. Intralesional heterogeneity of EGFR expression was present. Although the mean percentage of positive melanocytic cells in positive lesions did not increase with progression, mean staining intensity was stronger in malignant lesions compared to benign lesions. Ligand binding assays showed that EGFR expression in the highly metastasizing cell lines MV3 and BLM was at least 40 times higher than in the cell lines IF6, 530, M14, and Mel57, which do not or only sporadically metastasize after subcutaneous inoculation in nude mice. Although the differences between the various stages of progression are not absolute, we provide further evidence that EGFR expression increases in human melanocytic tumor progression.
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PMID:Increasing epidermal growth factor receptor expression in human melanocytic tumor progression. 162 28


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