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)

The reactivity of four monoclonal antibodies (MAbs) directed against IFN-gamma inducible antigens with melanocytic cells was investigated in the course of local and systemic tumor progression of human malignant melanoma. Frozen sections of histologically defined melanocytic tissues at different stages of progression were stained with these MAbs using an indirect immunoperoxidase technique. The reactivity of MAbs Me15/B3 and Me15/F9, directed against two different epitopes of a 90-kDa molecule, was found to correlate with melanoma progression. Indeed, a significantly lower percentage of small than of advanced primary melanomas or metastases stained positively. A differential staining of nevocytic and dysplastic nevi was further observed for these two MAbs, which were also non-reactive with normal skin melanocytes. The reactivity of MAb Me14/D12, which identifies the intercellular adhesion molecule ICAM-1 and MAb Mel14/F12, directed against a 40-kDa molecule, was found to be independent of the Breslow thickness of primary melanomas. Both the latter MAbs stained a high proportion of nevocytic and dysplastic nevi. The co-expression of the surface molecules defined by MAbs Me14/D12, Me15/B3 and Me15/F9 in the course of melanoma progression was also analyzed. The frequency of this co-expression increased according to the Breslow thickness of primary melanomas. In addition, up to 100% of metastases, as opposed to 20% of dysplastic nevi, were found to be simultaneously stained by these three MAbs. It is therefore conceivable that high-risk melanocytic lesions might be identified by the use of a combination of MAbs directed against IFN-gamma regulated antigens.
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PMID:The differential reactivity of cells of the melanocytic lineage with four monoclonal antibodies against IFN-gamma inducible molecules. 134 19

Regardless of subsequent clinical courses of patients with dysplastic nevi (DN), substantial evidence supporting DN as one of the melanoma-prone diseases is not yet available, especially in sporadic DN, due to the lack of genetic information other than retrospective studies in clinical observation. This study aimed at the immunohistological characterization of sporadic DN distinct from common nevi (CN) and at the evaluation of the potentially of sporadic DN for malignant transformation. We considered our results together with previous immunological and epidemiological reports. We noted the following three immunohistological characteristics. 1) Proliferating cell nuclear antigen (PCNA), one of the markers for active cell division, could be detected on DN cells in junctional nests of only one among ten DN examined but not on CN cells at all. 2) The altered expression of alpha-smooth muscle actin (alpha-Sma), often observed in melanoma cells, could not be detected in DN cells. However, anti-alpha-Sma monoclonal antibody (MoAb) clearly demonstrated distinctive hypervascularity in the stroma surrounding DN when compared with CN. 3) ME491 antigen, which is known to be expressed mainly in the radial growth phase of melanoma, was detected with similar intensity on both DN and CN. These data indicate that DN has a somewhat higher potentiality than CN for cell division and secretion of some cytokines which can induce hypervascularity in the surrounding stroma, but that DN has not yet undergone the significant phenotypic changes observed in melanoma cells. Further advancements in understanding molecular events in DN cells will be of great benefit in setting DN in the multiple oncogenic spectrum from pigment cells to melanoma.
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PMID:Dysplastic nevus syndrome: melanoma-prone disease. 136 25

Seven members of a family with dysplastic nevus syndrome (DNS) were examined clinically; skin biopsies of unaffected skin from 6 were taken. Biopsy-derived cultivated fibroblasts were examined by cytogenetic methods, i.e. by measuring the spontaneous and the UVB- and UVC-driven increase in sister chromatid exchange (SCE). A male patient with malignant melanoma, his son and his nephew, both with multiple dysplastic nevi, showed a distinctive elevation of UV-induced SCE, whereas the other, unaffected members of the family showed normal values. These results give evidence that in siblings with DNS the affected members can be identified not only on clinicopathological grounds but also by UV-induced elevated SCE at the cytogenetic level.
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PMID:Dysplastic nevus syndrome: intrafamilial identification of carriers by cytogenetics. 139 19

Melanoma cells have surface markers that are expressed differently than in normal melanocytes and nevus cells. Monoclonal antibodies may define a phenotypic map of the various melanocytic lesions and can be used in immunohistopathology and immunoscintigraphy. Monoclonal antibodies directed against melanoma-associated glycoproteins and glycolipids are being tested for therapy. Rearrangements or deletions on chromosome 1, 6, and 7 are the most frequently observed cytogenetic abnormalities. Molecular studies have not given a clear picture. A subset of HRAS alleles has been reported to be associated with melanoma. NRAS activation by point mutation has been found in one fourth of the cases. Allele losses at different loci have been reported. Genetic linkage studies have given conflicting results on the presence of a gene for the melanoma-dysplastic nevus syndrome on the short arm of chromosome 1.
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PMID:Cellular and molecular biology of melanoma. 143 44

There are a number of heritable disorders that have some association with skin cancer. Xeroderma pigmentosum, nevoid basal cell carcinoma syndrome, and familial melanoma and dysplastic nevi are three disorders associated with an extremely high rate of cutaneous malignancy. There is no known cure for these disorders, thus, patients and families need information about the disease process, treatment options, and guidelines aimed at prevention and early detection of skin cancer.
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PMID:Genodermatoses with profound malignant potential. 148 Aug 58

Three Japanese families with dysplastic nevus syndrome (DNS) are reported. Each family had at least two members with multiple dysplastic nevi (DN). Family members with DN or multiple moles had paler skin than average Japanese, usually sunburned, and tanned less than average, whereas members with darker skin almost never had DN. Each of two families had one cutaneous malignant melanoma (CMM) patient associated with multiple DN. Both CMMs were on the leg. In Japanese DNS, skin color and sun sensitivity seem to be closely related to DN. The locations of CMMs associated with DNS were unique: No CMMs were found on acral areas where they most frequently occur in Japanese.
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PMID:Dysplastic nevus syndrome among Japanese. A case study and review of the Japanese literature. 151 Feb 12

The National Institutes of Health Consensus Development Conference on Diagnosis and Treatment of Early Melanoma brought together experts in dermatology, pathology, epidemiology, public education, surveillance techniques, and potential new technologies as well as other health care professionals and the public to address (1) the clinical and histological characteristics of early melanoma; (2) the appropriate diagnosis, management, and followup of patients with early melanoma; (3) the role of dysplastic nevi and their significance; and (4) the role of education and screening in preventing melanoma morbidity and mortality. Following 2 days of presentations by experts and discussion by the audience, a consensus panel weighted the scientific evidence and prepared their consensus statement. Among their findings, the panel recommended that (1) melanoma in situ is a distinct entity effectively treated surgically with 0.5 centimeter margins; (2) thin invasive melanoma, less than 1 millimeter thick has the potential for long-term survival in more than 90 percent of patients after surgical excision with a 1 centimeter margin; (3) elective lymph node dissections and extensive staging evaluations are not recommended in early melanoma; (4) patients with early melanoma are at low risk for relapse but may be at high risk for development of subsequent melanomas and should be followed closely; (5) some family members of patients with melanoma are at increased risk for melanoma and should be enrolled in surveillance programs; and (6) education and screening programs have the potential to decrease morbidity and mortality from melanoma. The full text of the consensus panel's statement follows.
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PMID:Diagnosis and treatment of early melanoma. NIH Consensus Development Conference. January 27-29, 1992. 151 16

The frequency of malignant melanoma is rising at an alarming rate. Familial dysplastic nevi have been shown to be markers for and perhaps even precursors of malignant melanoma. This paper addresses the clinical and histologic features of these lesions, the structural and functional abnormalities of the melanocytes present in dysplastic nevi, the systemic and genetic abnormalities seen in patients with the dysplastic nevus syndrome, and the risk of melanoma in persons with dysplastic nevi. Management of persons with dysplastic nevi should include stressing sunlight avoidance and self-examination, deciding which lesion(s) to surgically excise, a schedule of visits to the physician, the possible use of photography, and the need to individualize patient management.
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PMID:Dysplastic (atypical) nevi: significance and management. 152 45

The paper presents a literature review of the last 10 years and original data. Dysplastic nevus is a category of pigmented skin lesions determined clinically and histologically. It presents a marker of melanoma and other tumours risk. To diagnose dysplastic nevi morphologically, two main (central complex nevus of ordinary type, melanocytic dysplasia in the nevus "shoulders") and 4 additional criteria should be recognized. The combination of the main and at least two additional criteria allows the diagnosis of dysplastic nevus.
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PMID:[Dysplastic nevus]. 152 2

Familial melanoma (MLM) is sometimes found associated with the dysplastic nevus syndrome (DNS). Considerable controversy exists over the possible assignment of a cutaneous malignant melanoma/dysplastic nevus gene, designated CMM, to the distal short arm of chromosome 1, linked to the PND and D1S47 loci. To date, no support for linkage of MLM alone to these markers has been found; likewise no study has been able to exclude the entire region between PND and D1S47 from linkage to MLM. We have carried out linkage studies between markers on 1p and MLM in seven Australian kindreds; three of these are the largest reported worldwide. We have been able to exclude localization of an MLM gene from a 40-cM region that spans the interval between D1S47 and PND and extends approximately 15 cM on either side of these markers. In addition, we can exclude a region of about 20 cM around the MYCL1/D1S57 loci.
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PMID:Exclusion of the familial melanoma locus (MLM) from the PND/D1S47 and MYCL1 regions of chromosome arm 1p in 7 Australian pedigrees. 153 Nov 37


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