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)

Antibodies to formalin-fixed, syngeneic melanoma cells were prepared in mice, purified by immunoaffinity chromatography, and tested for binding activity to viable melanoma cells. The radiolabeled antibodies detected congruent to 9 X 10(6) melanoma antigenic sites/cell. The calculated average association constant (Ka) for the antibody population was 7 to 10 X 10(7) M-1. The antibody was shown to block the binding of melanocyte-stimulating hormone in competitive cell surface binding studies. Results are discussed conceptually in terms of the potentially important role that the humoral immune response may play in the phenomenon of tumor progression.
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PMID:Immunological block to synthetic alpha-melanocyte-stimulating hormone: melanocyte interaction by antibodies isolated from cell-column immunoadsorbents. 45 90

The cytotoxic index was studied in 38 patients with melanoma. The cytotoxic effect would not be observed in tumor progression or in the persistent absence (1.5 years) of the signs of metastasization and recurrences in case of the previously removed tumor. The positive effect of the cytotoxic test in some cases was gained in the presence only of the primary focus or after the latter and metastases being removed, and in the long-term absence of metastases and recurrences in the period to come. In other cases the positive effect was gained during a short period of time before the appearance of metastases or in progressing of the disease. To fully estimate the results of the study the cytotoxic test should be methodically associated with studying of the blocking effect of patient's serum. The blood groups A. B. O compatibility or incompatibility of patient's and donor tumor cells did not influence the results of the cytotoxic test.
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PMID:[Cytotoxic index in melanoma patients]. 59 9

This study assess the effects of oral BCG, as a single agent, on tumor progression and on cell-mediated immune function in patients with metastatic malignant melanoma. Thirty patients were studied including 22 with measurable metastatic lesions and 8 with no detectable disease, following treatment of metastases by surgery, radiotherapy, or 5-(3, 3-dimethyl-1 -triazeno)-imidazole-4-carboxamide (DTIC; DIC). Oral BCG was given in doses of 120--240 mg, 1--3 times per week for periods ranging from 9 to 80 weeks and to total doses of from 1.2 to 20.1 gm. Patients were assessed by direct measurements of tumor mass, PPD skin test and in vitro blastogenic responses to PPD PHA. Of the 22 patient with measureable disease, 19 showed tumor progression and none showed regression of any lesion. Of the 8 without apparent disease, 5 remained stable and 3 had tumor recurrence. Of the total group of 30 patients, 8 showed some increased sensitivity to skin testing with PPD. Of 19 tested, 3 showed an increased PPD response in vitro, while 3 showed a decreased response. Six of 20 tested showed an increased PHA response in vitro. Oral BCG alone was not effective as an antitumor agent in patients with metastatic malignant melanoma.
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PMID:The use of oral BCG in the treatment or metastatic malignant melanoma. 78 99

Six intracarotid artery infusions of DTIC were performed in 4 patients with invasive malignant melanoma of the maxillo-facial region. A total dose of 3.5 to 7 g was well tolerated. Only 1 patient who received 9.5 g in 25 days developed a reversible bone marrow depletion. Two out of the 4 patients presented a transient 50% tumor surface regression, but no response was seen after the second infusion. Of the 2 remaining patients, 1 had no measurable effect and 1 experienced tumor progression.
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PMID:Regional chemotherapy of maxillofacial malignant melanoma with intracarotid artery infusion of DTIC. 89 97

CCNU (1-[2-chloroethyl]-3-cyclohexyl-1-nitrosourea, NSC-79037) was used to treat advanced malignancies in 329 evaluable patients. The treatment dosage was 130 mg/m2 for patients with adequate bone marrow reserve and 100 mg/m2 for those with compromised bone marrow. Oral treatment was repeated at 6-week intervals unless hematologic toxicity intervened. There were four complete responses: two in ovarian cancer, one with small cell carcinoma of the lung, and one with melanoma. Tumor response greater than 50% reduction in tumor size occurred in 39 patients (11.9%) while stable disease (no change or decrease or increase of less than 50% in tumor size) was noted in 152 patients (46.2%). Tumor progression occurred in 130 cases. Melanomas and ovarian and lung cancers had the highest response rates. Bone marrow depression was the major side effect of treatment; there was a significant positive correlation between the severity of leukopenia and thrombocytopenia and tumor response to treatment.
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PMID:Treatment of advanced malignancy with CCNU (NSC 79037): a phase II cooperative study with long-term follow up. 95 55

Melanoma cells carry membrane-bound antigens that induced both antibody production and cellular immunity. However, these antigens appear not to be tumor-specific, as the activity of human antisera can be absorbed out by fetal antigens. Nonetheless, the phenomenon of spontaneous regression, though mostly affecting only parts of a lesion, indicates that effective attack mechanisms do exist. Simultaneous tumor progression is due to heterogeneity of tumor cells, which vary widely in antigen expression. Cells that are not recognizable sneak through defense mechanisms and produce metastases.
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PMID:[Immunology of malignant melanoma (author's transl)]. 99 70

The neoplastic progression induced by intratracheal instillation of benzo[a]pyrene (BP) and magnesium oxide (MgO) was compared with that induced by intratracheal instillation of BP and ferric oxide (Fe2O3). BP and MgO produced squamous cell carcinomas and papillomas in the larynx with a latent period as shor as 9 weeks. They also induced many papillomas as well as squamous cell carcinomas and adenocarcinomas in the trachea and a papilloma, squamous cell carcinomas, adenocarcinomas, adenosquamous lesions, and peripheral adenomatoid lesions in the bronchi. They rarely caused tumors in other organs; only a few forestomach papillomas, one melanoma on the dorsal skin, and one ovarian carconoma were seen BP, with Fe2O3 as the carrier, induced a comparable number of histologically similar tumors; however, tumors developed more frequently in the main bronchi. Thus MgO strongly facilitated the tumor-inducing effects of BP, causing tumors in different areas of the respiratory tract, and was as effective as Fe2O3 as a carrier agent in the experimental induction of respiratory tumors.
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PMID:Magnesium oxide as carrier dust in benzo(a)pyrene-induced lung carcino-genesis in Syrian hamsters. 112 16

In vitro lymphocyte function was evaluated in 61 patients with different clinical stages of malignant melanoma. Thirty-one of these patients had localized disease, 13 regional metastases, 10 distant lymph node or skin metastases, and 7 visceral metastases. Following immunization, in vitro lymphocyte reactivity to three antigens (diphtheria toxoid, tetanus toxoid and alpha-hemocyanin of Helix pomatia) was studied in the presence of autologous serum, in addition to lymphocyte reactivity to phytohemagglutinin (PHA). The relationship of these tests with the clinical stage and the subsequent course of the disease in a 6 months' observation period was determined. The patients with visceral metastases (7) had a lowered lymphocyte reactivity to PHA compared with controls and the patients with other stages, while they also had a low reactivity to the test antigens (only significantly lowered compared with patients with localized disease). All these patients showed tumor progression or died from metastatic disease. Between the other stages (54 patients) there was no difference in lymphocyte reactivity to the test antigens or PHA. No correlation between lymphocyte reactivity to PHA and the subsequent course of the disease could be demonstrated in these 54 patients. However, lymphocyte reactivity to the test antigens following immunization showed a definite correlation with the subsequent course. Sixty-four percent (9/14) of patients without any lymphocyte reactivity to the three antigens showed tumor recurrence or progression, against 3% (1/40) of patients with positive lymphocyte reactivity to one, two, or three antigens. A suppressive effect of autologous serum on lymphocyte reactivity could be found only in 1 of 20 patients with a low reactivity to PHA or antigens. It is concluded that defects in lymphocyte function are related to subsequent tumor growth in patients with malignant melanoma.
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PMID:Humoral and cell-mediated immune response in patients with malignant melanoma. I. In vitro lymphocyte reactivity to PHA and antigens following immunization. 117 27

Expression of the endothelial adhesion molecule VCAM-1 was studied in human malignant melanoma lines by flow cytometry. Clones 2/4 and 2/14 (derived from the same lesion) had appreciable levels of VCAM-1 expression, whereas clone 2/21 and the lines A2058, Mel24, and A375 were negative. Clone 2/14 was selected for further analysis. Exposure to tumor necrosis factor (TNF) markedly augmented VCAM-1 on melanoma cells. Surface VCAM-1 was associated with expression of specific transcripts that were augmented by TNF. Analysis by reverse transcriptase and polymerase chain reaction using appropriate primers revealed that TNF-stimulated melanoma cells expressed both 7 and 6 immunoglobulin domain transcripts with predominance of the longer species. Tumor necrosis factor--stimulated melanoma cells bound more VLA-4-expressing cells (melanoma and monocytes) than resting tumor cells and anti-VCAM-1 monoclonal antibodies significantly inhibited binding, thus suggesting that surface VCAM-1 on melanoma is functional. Analysis of melanoma tissue sections demonstrated that VCAM-1 is not a marker of transformation of melanocytes because it can be detected in benign nevi. Although, unlike ICAM-1, VCAM-1 is not correlated with tumor progression, its expression in a fraction of primary melanomas indicates that it may play a role in regulating host immune response and homotypic interactions in some malignant melanomas.
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PMID:Regulated expression of vascular cell adhesion molecule-1 in human malignant melanoma. 128 17

We have recently described marked differences in cell migration rates and organization of actin in human melanoma cell lines isolated from various stages of tumor progression. Metastatic lines derived from lymph node metastases organized actin into stress fiber arrays and had high mean migration rates in vitro when compared to lines from other stages. Melanoma cells also reveal marked differences in localization of alpha-actinin and beta 1 integrins at stress fiber termination sites (focal contacts). Disruption of this organization is induced by antibodies against beta 1 integrins, alpha-actinin, recently postulated as having a role in linkage of actin to beta 1 integrins, is differentially expressed in melanoma cells by Northern blot analysis and a relatively high alpha-actinin to actin ratio is associated with stress fiber formation and increased cell migration. Furthermore, actin-binding protein, which cross-links actin filaments, is also significantly increased in lines exhibiting high migration rates. Control of migration and actin organization may be mediated by extracellular matrices and/or modulation of actin-associated proteins including alpha-actinin and actin binding protein. These findings provide evidence that an interaction of transmembrane adhesion molecules and elements of the cytoskeleton in melanoma cells may be responsible for differences in migration rates and capacity for metastasis.
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PMID:Actin organization and cell migration of melanoma cells relate to differential expression of integrins and actin-associated proteins. 129 73


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