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)

In the present study, the growth features and metastatic capacity of human primary and metastatic melanomas transplanted by different routes in nude mice was examined. Eight different human melanoma early cell cultures derived from 3 primary tumors, 1 local recurrence and 4 metastatic lesions of 6 melanoma patients were characterized for cell surface HLA (class I and II) and melanoma-associated antigens and karyotype. These tumors were then transplanted in CD-1 outbred nude mice by subcutaneous, intraperitoneal and intrasplenic routes. It was found that 7 out of 8 melanomas were tumorigenic after subcutaneous implantation without giving rise to metastases; 5 out of 7 melanomas grew when injected intraperitoneally and 3 of them disseminated to peritoneal organs and infiltrated intraperitoneal lymph nodes, liver and pancreas; of 8 melanomas implanted intrasplenically 4 grew in the spleen or invaded intraperitoneal lymph nodes, liver, pancreas, ovaries or lungs. Primary and metastatic melanomas did not differ in the pattern of dissemination. In fact, 2 out of 4 metastases and 1 of 3 primary tumors and 1 recurrence disseminated after intrasplenic or intraperitoneal inoculation. Heterogeneity in the growth pattern of different metastases of the same melanoma patient was also found. No correlation could be detected between the metastatic ability of melanoma cells studied and clinical stage of patients, tumor cell karyotype abnormalities, modal number or with the antigenic phenotype.
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PMID:Tumorigenicity and dissemination of primary and metastatic human melanomas implanted into different sites in athymic nude mice. 322 46

One hundred and twenty-four subjects belonging to 25 families, 51 with familial malignant melanoma (FMM), and 186 subjects belonging to 41 families, 41 with sporadic malignant melanoma, were typed for the HLA A, B, C and DR loci of the HLA system. There was the same statistically significant difference in the frequency of the haplotype A9, B35, Cw4 between each group of patients and the respective healthy relatives (p = 0.01, p = 0.01 and p = 4 x 10(-3), respectively). Moreover, the higher frequency of the haplotype A9, B35, Cw4 in the healthy members of the FMM families (42.46%) compared with the healthy members of the SMM families (23.44%) indicates that in the latter group other individuals are at risk for the disease. Furthermore, the different frequency of haplotypes B5, DR5 and B5, Cw1 suggest that differences exist between the two groups of healthy relatives. These observations confirm that the HLA region is involved in the etiology of malignant melanoma.
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PMID:HLA antigens in familial and sporadic cutaneous melanoma. 323 10

To investigate whether human melanoma cells intrinsically resistant to autologous LAKs do exist, and whether a relationship between the level of lysis of LAKs and spontaneous drug resistance can be identified at the clonal level, we studied 44 clones obtained from a metastatic melanoma lesion. The antigenic phenotype of clones revealed a marked heterogeneity in the expression of HLA antigens of classes I and II. The clones were subsequently tested for sensitivity to autologous LAK and for spontaneous resistance to Dx. No clone resistant to autologous LAK was found, although a considerable range of lysis was noted with a normal frequency distribution. Growth in agar of the 2 clones in which lysis was least pronounced (6 and 26) was completely inhibited after co-culture with LAKs, indicating a lack of absolute resistance to these effectors. Spontaneous resistance to Dx, evaluated as ID50, revealed instead that the majority of clones had a low ID50. The frequency distribution of clones showed a left-skewed curve. The percentage of specific 51Cr-release and the ID50 for Dx could be correlated in 25 clones by linear regression. Sensitivity to LAK did not correlate with HLA classes I or II or melanoma-associated antigen expression. These results support the contention that increased LAK sensitivity of tumor cells is associated with drug resistance.
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PMID:Differential lysis of melanoma clones by autologous recombinant interleukin 2-activated lymphocytes. Relationship with spontaneous resistance to doxorubicin (Dx). 326 90

The expression of 4 melanoma-associated antigens and of class I and II HLA antigens was investigated in 12 superficial spreading melanomas (SSM) and in 8 SSM with a vertical growth pattern portion (SS + NM) by the use of monoclonal antibodies and an indirect immunoperoxidase procedure. Monoclonal antibodies 225.28, 763.74, CL.203, VF19-LL217, Q5-13, W6-32 and anti-HLA-DR, were used. Each antigen was more frequently expressed by SS + NM on the whole than by SSM and also by the radial growth pattern portions of SS + NM than by SSM. Vertical growth pattern portions of SS + NM were not antigenically similar to radial growth pattern portions in the same tumors. The high frequency of antigen expression in radial growth pattern melanomas seems to be associated with the appearance of a more invasive cell population.
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PMID:Antigenic phenotype of radial growth phase melanomas with or without a vertical growth phase portion. 328 54

Immunohistochemical staining with monoclonal antibodies showed marked variations in the percentage of melanoma cells stained by anti-HLA Class I and anti-HLA Class II monoclonal antibodies among 48 locoregional metastases removed from 39 patients with malignant melanoma. On the other hand there was limited variation in the percentage of melanoma cells stained by anti-HLA antibodies in autologous locoregional metastases removed from 8 of 9 patients. In the remaining patient marked differences were found in the percentage of melanoma cells stained by anti-HLA Class I antibodies in the two parts of the lymph node metastasis analyzed. Therefore this patient was not included in additional analyses to correlate the level of expression of HLA antigens with the clinical course of the disease. In all the lesions tested the percentage of melanoma cells stained by anti-HLA Class II antibodies was lower than or equal to but never higher than that stained by anti-HLA Class I antibodies. According to the level of expression of HLA Class I and Class II antigens the 38 patients could be divided into three groups: Pattern A included lesions with more than 50% of tumor cells stained by anti-HLA Class I antibodies (mean, 86.1; median, 85) and 50% or less by anti-HLA Class II antibodies (mean, 10.5; median, 5); Pattern B included lesions with 50% or less tumor cells stained by anti-HLA Class I antibodies (mean, 14.9; median, 5) and by anti-HLA Class II antibodies (mean, 4.1; median, 1); Pattern C included lesions with more than 50% tumor cells stained by anti-HLA Class I antibodies (mean, 88.8; median, 92) and by anti-HLA Class II antibodies (mean, 70.0; median, 70). The survival of 21 patients with Pattern A was significantly longer than those of 13 and 4 patients with Patterns B and C, respectively. No difference in the survival of patients in the latter two groups was found. These results suggest that HLA antigens play a role in the biology of melanoma and that analysis of the level of HLA antigens in locoregional metastases of patients with melanoma may provide clinically useful information.
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PMID:Level of HLA antigens in locoregional metastases and clinical course of the disease in patients with melanoma. 333 74

Expression of class I HLA antigen has been shown to be reduced in a number of human tumours. Here we show that in a panel of 11 melanoma cell lines with variable class I HLA expression an inverse correlation exists between the mRNA levels of c-myc and class I HLA. This suggests that high expression of the c-myc oncogene might inhibit the class I HLA expression. To test this hypothesis a melanoma cell line with a low c-myc and high class I HLA mRNA expression was transfected with a c-myc expression vector. All clones expressing the transfected c-myc gene show reduced class I HLA mRNA and beta 2-microglobulin mRNA expression. Reduced class I HLA mRNA levels result in a lowered class I protein expression on the cell surface. Treatment with gamma-interferon fully restores the class I HLA and beta 2-microglobulin expression in these cells. This effect is preceded by a transient decrease of the c-myc mRNA level. These results show that the class I HLA expression is modulated by the level of c-myc expression, thus opening up the possibility that high expression of this oncogene influences the interaction of melanoma cells with the immune system.
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PMID:c-myc down-regulates class I HLA expression in human melanomas. 340 30

In a family including patients suffering from autoimmune disease (2 propositi: pernicious anemia and Graves' disease, pernicious anemia and autoimmune thyroiditis), we have determined common autoantibodies and tissue antigens (HLA) in 47 patients (26 males and 21 females) from 2 generations. In this family, we have found 4 cases of pernicious anemia, 5 cases of thyroid disease (2 Graves' disease), 3 women with repetitive abortions and 2 cases of melanoma. Patients with autoantibodies, often asymptomatic, are abnormally numerous (44% in generation II, 16% in generation III). A correlation with haplotype A1B8DR3 was found only for Graves' disease. Likelihood of forming autoantibodies appears to be of multifactorial origin. Its mode of transmission remains unknown.
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PMID:[Genetic factors predisposing to autoimmune diseases. Study of HLA antigens in a family with pernicious anemia and thyroid diseases]. 343 88

The expression of class I and class II HLA antigens has been studied on primary and metastatic human melanomas, and on cell clones derived from the latter. A panel of monoclonal antibodies and flow cytofluorometric analysis were used to evaluate the presence of HLA-A, B, C and -DR, DQ antigens on freshly isolated tumour cells. HLA class I antigens were present on 91% and 93% of primary and metastatic tumours, respectively. Sixty per cent of primary and 50% of metastatic melanomas expressed HLA-DR antigens, whereas 38% and 21% of cases were positive for HLA-DQ. A marked heterogeneity was evident among primary and metastatic lesions for expression of class I and II antigens. Similar findings were obtained by analysing the phenotype of melanoma clones which indicates that a marked antigenic heterogeneity for class I and II HLA antigens occurs even among clones isolated from short-term cultures of metastatic melanomas.
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PMID:Phenotypic heterogeneity of HLA products on human melanoma cells. 346 77

TCA (T Cell system A) is a di-allelic system of HLA-like antigens encoded by genes located about 15 cM telomeric to HLA-A. In normal individuals, TCA antigens are only expressed on a subpopulation of T cells, the TG lymphocytes. We now report on the expression of TCA on leukemias and other malignancies. An increased proportion of cells carrying the TCA phenotype was encountered in testing peripheral blood lymphocytes from patients with acute lymphoblastic T-cell leukemia (T-ALL), acute myeloid leukemia (AML), and chronic myeloid leukemia (CML). In contrast, patients with B-cell malignancies such as chronic lymphatic leukemia (CLL) and hairy cell leukemia (HCL) or non-T/non-B common acute lymphoblastic leukemia (common ALL) had normal proportions of TCA-positive lymphocytes. Quantitatively different levels of TCA expression are found on some melanoma cell lines and others are TCA negative. These variations are independent of the expression of HLA Class I antigens by the same cells. The expression of TCA antigens by malignant nonlymphoid cells suggests that this system may code for differentiation markers, important in the biology of neoplastic transformation.
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PMID:TCA: a polymorphic genetic marker in leukemias and melanoma cell lines. 348 57

In 1977, Dr. Mark Greene and Dr. Wallace Clark examined members of the B. and K. families, in which several individuals had developed cutaneous malignant melanoma. They recognized that both families had nevi that were unusual in morphology, pattern, distribution, size, and number. These dysplastic nevi identify the individuals in melanoma-prone families who are at increased risk of melanoma; the cumulative risk of melanoma approaches 100% in affected members. Formal genetic analyses have revealed that the dysplastic nevus and melanoma traits appear to be pleiotropic effects of a single, highly penetrant, autosomal dominant gene. Linkage studies have revealed weak linkage with Rh on the short arm of chromosome 1 (1p), and excluded linkage with the HLA region on chromosome 6p, transferrin on 3q, H-ras on 11p, and Gm on 14q. The most promising location for the melanoma/dysplastic nevus susceptibility locus remains chromosome 1p. Future studies will focus on the localization of the melanoma gene, and then the characterization of the gene product to elucidate the etiology of melanoma.
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PMID:Where have dysplastic nevi led us? 350 42


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