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)

Nevus cell components have been observed in up to 40% of melanomas, but little is known of the pathobiology of these components in relation to their malignant potential. We studied 44 nevi of the typical, dysplastic, congenital, and Spitz types with a battery of monoclonal and polyclonal antibodies that react on formalin-fixed, paraffin-embedded tissues (HMB.45, S-100 protein, RAP-5, epithelial membrane antigen [EMA], and neuron-specific enolase [NSE]) by avidin-biotin immunohistochemical methods. EMA and RAP-5 (which detects the ras oncogene-associated P21 protein) were negative in all cases. Melanoma-specific HMB.45 was strongly reactive with the epidermal component and had a weak to negative reaction with the dermal component in the typical nevi. However, the reaction seen with HMB.45 in the junctional component of dysplastic nevi, congenital nevi, and some Spitz nevi was heterogeneous. One Spitz nevi showed HMB.45 staining in a pattern near to that of melanoma. In contrast to HMB.45, S-100 protein labeled nevomelanocytes, regardless of whether they were within the epidermis or dermis, although, in half of the dysplastic nevi, the reaction was heterogeneous, with some atypical cells failing to stain. But, with cytologically atypical junctional component (dysplastic-appearing), congenital nevi also stained heterogeneously for S-100 protein compared with the dermal component. NSE stained the central component of some Spitz nevi more intensely than the lateral component. Junctional nevomelanocytic subsets of some congenital nevi revealed HMB.45 and S-100 reactivity similar to dysplastic nevi.
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PMID:Typical, dysplastic, congenital, and Spitz nevi: a comparative immunohistochemical study. 229 3

In white populations living at moderate or low latitudes, melanoma has become one of the most common tumors in young adults. Epidemiologic studies show a complex association with sun exposure. Risk is related positively to the levels of exposure typical of the place of residence, and also to personally controlled exposure, with the maximum risk being related to acute intermittent exposure. Risk also varies with pigmentation, family history of melanoma, and the presence of benign and of dysplastic nevi. The following methods of control of melanoma in such populations are discussed: the most effective methods depend on early diagnosis; primary prevention appears difficult and requires evaluation; identification of very high-risk subjects on the basis of family history and dysplastic nevi will affect only a very small proportion of melanomas; the use of simpler methods to identify high-risk subjects is explored. In Japan, melanoma is comparatively rare, but increasing as rapidly as elsewhere. The incidence rate of acral lentiginous melanoma appears similar to that in whites, comprising a large proportion of melanoma in Japan. Control programs cannot be designed rationally, since basic information on the occurrence, presentation, and survival of melanoma in Japan is lacking. Some specific research questions are suggested.
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PMID:Epidemiology and control of melanoma in white populations and in Japan. 271 53

A 37 year-old woman presented with type D2 familial dysplastic nevus syndrome with melanoma. A melanoma was excised of her back and more than one hundred pigmented lesions, four of which presented histologic characteristics of dysplastic nevus were observed. Several relatives of her presented multiple nevi and a sister of her mother and a brother of the patient had been diagnosed of melanoma. It is well established that such kind of nevi are precursor for melanomas, particularly familial forms. The clinical identification of such lesions is very simple and facilitates the diagnosis and early treatment of melanoma.
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PMID:[Dysplastic nevus syndrome with familial melanoma (type D2)]. 271 87

We used molecular genetic techniques and multipoint linkage analyses to locate the gene responsible for cutaneous malignant melanoma-dysplastic nevus. We evaluated 99 relatives and 26 spouses in six families with a predisposition to melanoma. Thirty-four family members had cutaneous malignant melanoma, and 31 of these 34 also had histologically confirmed dysplastic nevi. Twenty-four family members had dysplastic nevi alone. An analysis of the cosegregation of the cutaneous malignant melanoma-dysplastic nevus trait with 26 polymorphic DNA markers on the short arm of chromosome 1 demonstrated the presence of a gene for susceptibility to melanoma. The gene was located between an anonymous DNA marker (D1S47) and the gene locus for pronatrodilatin, a commonly used reference gene (PND), in chromosome band 1p36. The odds were greater than 260,000:1 in favor of linkage at this location.
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PMID:Mapping the gene for hereditary cutaneous malignant melanoma-dysplastic nevus to chromosome 1p. 230 22

Nuclei of melanocytes in 10 common acquired melanocytic nevi, 10 malignant melanomas and 10 dysplastic melanocytic nevi (melanocytic dysplasia) (MD) were morphometrically analyzed. MD group consisted of 6 lesions with (MD 1) and 4 without (MD 2) the clinical features of dysplastic nevi. The considered parameters were area, perimeter and form Ar. In the MD group, the results showed that median values of each considered parameter of MD 1 were close to those of MD 2. For each evaluated parameter, median values of MD turned out to be intermediate between those of common acquired melanocytic nevi and of malignant melanomas. Confirming the histologic evidence of a double - nonatypical and atypical - melanocytic population in melanocytic dysplasia, our data showed that nonatypical melanocytes were indistinguishable from melanocytes of common acquired nevi, while the atypical melanocytes were close to melanoma cells. The importance of atypical melanocytes is stressed in the diagnosis of melanocytic dysplasia.
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PMID:Common acquired melanocytic nevi, melanocytic dysplasia and malignant melanoma. A morphometric study. 273 Jul 99

The gene for familial malignant melanoma and its precursor lesion, the dysplastic nevus, has been assigned to a region of the distal short arm of chromosome 1, which is frequently involved in karyotypic abnormalities in melanoma cells. We have examined loci on chromosome 1p for loss-of-constitutional heterozygosity in 35 melanomas and 21 melanoma cell lines to analyze the role of these abnormalities in melanocyte transformation. Loss-of-heterozygosity at loci on chromosome 1p was identified in 15/35 (43%) melanomas and 11/21 (52%) melanoma cell lines. Analysis of multiple metastases derived from the same patient and of melanoma and lymphoblastoid samples from a family with hereditary melanoma showed that the loss-of-heterozygosity at loci on distal 1p is a late event in tumor progression, rather than the second mutation that would occur if melanoma were due to a cellular recessive mechanism. Comparisons with neuroblastoma and multiple endocrine neoplasia (MEN2) suggest that the frequent 1p loss-of-heterozygosity in these malignancies is a common late event of neuroectodermal tumor progression.
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PMID:Loss of alleles from the distal short arm of chromosome 1 occurs late in melanoma tumor progression. 273 11

This report describes the efficacy of skin examination for the early detection of second primary cutaneous melanomas among patients with nonfamilial melanoma. A series of 121 patients with newly diagnosed first primary cutaneous melanomas participated in a study of melanoma and dysplastic nevi. Of the 121 study participants, six patients were subsequently diagnosed with a second primary melanoma. For five of these patients, frequent skin examinations resulted in the detection of second primaries that were shallower in depth than was the first primary melanoma. In four cases, the second primaries were identified in low-risk growth phases (less than 0.76 mm); three of these low-risk tumors were melanoma in situ.
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PMID:Usefulness of frequent skin examination for the early detection of second primary cutaneous melanoma. 274 53

Of 92 pigmented macular lesions on the soles of Japanese, 88 lesions were histologically confirmed to be melanocytic: 65 ordinary acquired melanocytic nevi, 9 congenital melanocytic nevi, 5 dysplastic nevi, and 5 possible and 4 definite lesions of early malignant melanomas. None of the ordinary acquired melanocytic nevi were more than 7 mm in maximum diameter. Excluding congenital melanocytic nevi, there were 8 lesions whose greatest diameters were more than 7 mm: 2 dysplastic nevi, and 2 possible and 4 definite lesions of early malignant melanoma. Judging from the data obtained in this study, we propose the following clinical guideline for the detection of early lesions of malignant melanoma on the sole. If the pigmented lesions have no possibility of being congenital melanocytic nevus, black heel, lesions of Peutz-Jeghers syndrome, or 5-FU induced lesions, measure the maximum diameters. 1) Lesions with a diameter of more than 7 mm should be excised for histological evaluation. 2) Lesions with a diameter between 6 and 7 mm should be examined histologically when they show conspicuous irregularity in shape, color and/or border or are observed on the soles of a patient older than 50.
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PMID:[Clinical and histopathologic analyses of pigmented macular lesions on the soles of Japanese--proposal of a clinical guideline for detection of early malignant melanoma on the sole]. 274 66

The hereditary dysplastic nevus syndrome (DNS) is an autosomal dominant disorder in which affected individuals have increased numbers of dysplastic (premalignant) nevi and a greater than 100-fold increased risk of developing cutaneous melanoma. Epstein-Barr virus-transformed lymphoblastoid cell lines from patients with hereditary DNS have been shown to be hypermutable to UV radiation (M.I.R. Perera et al., Cancer Res., 46: 1005-1009, 1986). To examine the mechanism involved in this UV hypermutability, we used a shuttle vector plasmid, pZ189, which carries a 160-base pair marker gene, supF, and can replicate in human cells. pZ189 was treated with UV radiation and transfected into DNS6BE, a lymphoblastoid cell line from a patient with hereditary DNS. Plasmid survival after UV was similar with the DNS6BE line and with a lymphoblastoid cell line from a normal donor. Plasmid mutation frequency was greater with the DNS line in accord with the DNS cellular hypermutability. Base sequence analysis was performed on 69 mutated plasmids recovered from the DNS line. There were significantly more plasmids with single base substitution mutations (P less than 0.01) in comparison to UV-treated plasmids passed through normal fibroblasts. pZ189 hypermutability and an increased frequency of single base substitutions was previously found with a cell line from a melanoma-prone xeroderma pigmentosum patient. These differences may be related to the increased melanoma susceptibility in both DNS and xeroderma pigmentosum.
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PMID:Ultraviolet mutagenesis in a plasmid vector replicated in lymphoid cells from patient with the melanoma-prone disorder dysplastic nevus syndrome. 279 Aug 6

In 280 melanoma patients all data concerning familial and personal history, histology, and therapy were verified. All patients underwent total-body skin examination to check for the presence of dysplastic nevus syndrome (DNS). In 257/280 patients (91.8%) solitary melanomas were found, while in 23/280 patients (8.2%) multiple melanomas occurring simultaneously or consecutively were ascertained. Surprisingly, among the 12/280 patients (4.2%) with familial variants of melanoma, multiple melanomas were not found in a increased frequency. In patients with DNS (regardless of whether sporadic or familial) the frequency of multiple melanomas is higher: in patients with solitary melanomas DNS was found in 27/257 (10.5%), while in patients with multiple melanomas DNS was diagnosed in 11/23 (47.8%) (P less than 0.0005). In both groups (solitary and multiple melanomas) the mean age of patients with DNS was around 10 years lower. The frequency of additional primary malignancies in patients with cutaneous melanomas was 8.6%, and did not vary according as whether patients had solitary or multiple melanomas with or without DNS.
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PMID:[Increased incidence of multiple melanoma in sporadic and familial dysplastic nevus cell syndrome]. 280 14


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