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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Certain cutaneous lesions serve as both precursors of skin cancer and markers for increased risk. The solar or actinic keratosis serves such a role for the nonmelanoma (NMSC) forms of skin cancer (basal cell carcinoma and squamous cell carcinoma). Clinically, these keratoses manifest as rough, scaly, erythematous patches on chronically sun-exposed surfaces. Conversion to squamous cell carcinoma in an individual lesion is uncommon and has been estimated at 1 per 1000 per year. Individuals with actinic keratoses have had sufficient chronic photodamage to produce skin cancer, and regular surveillance is recommended. The second precursor for invasive NMSC is Bowen's disease (squamous cell carcinoma in situ). Invasion of the dermis results in frank squamous cell carcinoma. Some types of viral warts may develop into squamous cell carcinoma. The most important precursor/marker for melanoma is the clinically atypical mole (CAM) or dysplastic nevus. CAMs occur in 5-10% of the U.S. population. CAMs, under photographic follow-up, have been observed to evolve into cutaneous melanoma. The frequency of conversion to melanoma of any single CAM is quite low; however, in melanoma-prone families, prospectively diagnosed melanomas arise in association with a histopathologically observed dysplastic nevus in more than 80% of the cases. Giant congenital melanocytic nevi have an approximately 6% lifetime risk of melanoma development. The risk associated with small congenital nevi is uncertain. Lentigo maligna develop into invasive melanoma with a frequency reported in the literature ranging from 5-50%.
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PMID:Precursors to skin cancer. 780 89

Both digital imaging and epiluminescence microscopy hold promise for improved early detection of cutaneous melanoma. Several centers have been actively working in these areas during the past decade. These experiences and preliminary work based on the image capture of 83 pigmented lesions at our center using a prototype digital imaging system (SKINVIEW) are described. This system is based, in part, on the analysis of lesional morphologic features, such as shape, border, and radii. Histopathologic correlation was matched against these features to assess the efficacy of diagnosis. At our center, these parameters alone were not sufficient to discriminate between benign and malignant lesions, in part, because the melanomas were, in general, early lesions and many of the nevi were sufficiently clinically atypical to require removal for discrimination from melanoma. In addition, technical improvements in the image capturing and processing mechanism are needed. Rapid progress in this area is anticipated.
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PMID:Computerized digital image analysis: an aid for melanoma diagnosis--preliminary investigations and brief review. 785 52

A case-control study was set up to assess the risk of eye melanoma in relation to the number and type of cutaneous melanocytic naevi and pigmented lesions of the iris. Cases comprised 211 unselected ocular melanoma patients attending the Ocular Oncology Clinic at Moorfields Eye Hospital, London, during November 1990 to October 1991 and diagnosed after August 1986. Hospital and general practice controls (416) were recruited in the North East Thames Region of the UK. Cutaneous naevi greater than or equal to 2 mm in diameter were counted on the skin. Clinically atypical and congenital naevi were recorded separately. Pigmented lesions of the iris were counted. The relative risk for ocular melanoma increased with numbers of atypical naevi and numbers of common naevi. Ten percent of cases but 3% of controls had at least 100 naevi of 2 mm or greater diameter. Seven percent of cases and 0.4% of controls had 4 or more atypical naevi. Pigmented lesions of the iris were significantly more common in cases than controls. Nine percent of cases had the Atypical Mole syndrome (AMS) phenotype compared with 1% of controls. Six cases had concurrent cutaneous melanoma primaries. We conclude that atypical and iris naevi are important risk factors for eye melanoma and that patients with eye melanoma are at increased risk of cutaneous melanoma. Dermatological examination for the AMS phenotype and cutaneous melanoma should be recommended in eye melanoma patients with large numbers of pigmented lesions of the skin or family history of melanoma.
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PMID:Risk of ocular melanoma in relation to cutaneous and iris naevi. 786 Jan 35

The BCL-2 gene is the prototype of a newly described family of oncogenes involved in tumorigenesis by blocking apoptosis, or programmed cell death. Overexpression of BCL-2 protein was originally described in follicular B-cell lymphomas bearing the 14;18 translocation. BCL-2 overexpression has also been described in other lymphomas and more rarely in neoplasms outside the lymphoid tissue. The aim of this paper is to determine the immunohistochemical expression of BCL-2 in intradermal nevi and primary invasive and metastatic melanoma. Formalin-fixed and paraffin-embedded tissues from 4 cutaneous melanoma metastases, 10 primary invasive melanomas, and 10 intradermal melanocytic nevi were immunolabeled with monoclonal antibodies directed against BCL-2 protein (Dako, clone 124) and Ki-67 antigen (Amac, clone MIB-1), after antigen retrieval techniques. Morphologically normal epidermal melanocytes expressed BCL-2, as did nevi and melanomas in virtually all cells. However, whereas the labeling in normal melanocytes and nevus cells showed a uniformly strong reactivity, melanoma cells showed a variable but mainly weak reactivity. Ki-67 antigen expression was restricted to melanomas. The widespread expression of BCL-2 suggests that this oncoprotein cannot be involved in the malignant transformation of melanocytic cells. It seems likely that the decreased BCL-2 expression detected in melanomas may reflect one further step of tumor progression in melanocytic neoplasms.
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PMID:Immunohistochemical expression of BCL-2 in melanomas and intradermal nevi. 786 49

Over-expression of the HER-2 oncogene correlates with poor prognosis in breast and ovarian carcinomas. Using a sensitive immunohistochemical assay, we have detected low levels of gp185HER-2 in intradermal nevi (78%) and in primary (75%) and metastatic melanomas (58%). The HER-2 gene product expressed by cultured melanoma cells had the expected molecular weight, but no levels of tyrosine phosphorylation could be detected. Consistently, we were unable to inhibit in vitro growth of melanoma cells with an anti-gp 185HER-2 MAb, in conditions in which the growth of SKBr-3 breast-carcinoma cells was severely impaired. However, immunotoxins to gp 185HER-2 were able to kill gp185HER-2-positive melanoma cells. These data indicate that low levels of gp185HER-2 are expressed by the melanocyte lineage, with no correlation with transformation or tumor progression. Nevertheless, gp185HER-2 appears a suitable target for immunotherapy of cutaneous melanoma.
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PMID:Expression of gp185HER-2 in human cutaneous melanoma: implications for experimental immunotherapeutics. 790 52

Hereditary dysplastic naevus syndrome (DNS) is a familial disorder characterized by dysplastic naevi and an approximately 85-fold increased risk of developing malignant cutaneous melanoma. Cell lines from individuals with DNS have shown hypermutability following exposure to UV irradiation. The cause of this hypermutability is unknown, and no DNA repair defect has been identified. We have studied the capacity of lymphocytes from individuals with DNS to reactivate the chloramphenicol acetyltransferase gene in transfected plasmids that had been inactivated by UV irradiation. We found no difference in plasmid reactivation between lymphocytes from individuals with DNS and those obtained from healthy control persons matched for sex, age and smoking habits. This finding indicates that DNS is not associated with a significant quantitative defect in nucleotide excision repair of DNA.
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PMID:Normal reactivation of plasmid DNA inactivated by UV irradiation by lymphocytes from individuals with hereditary dysplastic naevus syndrome. 791 61

Mutations in N-ras exon 2 codon 61 were studied in formalin-fixed human melanoma metastases. DNA fragments including codon 61 were amplified by polymerase chain reaction (PCR) and mutational analysis was performed by oligonucleotide hybridization (ODN), allele specific PCR and PCR combined with single strand conformation polymorphism analysis (SSCP). Thirty metastases from 25 patients with 'spontaneous' cutaneous melanoma were compared with 35 metastases from 17 patients with 'hereditary' cutaneous melanoma. The frequency of mutations as measured by PCR/ODN was significantly higher in patients with hereditary melanoma (mutations in 24% versus 59%, p < 0.05). The most frequent mutations were C/A transversions to lysine (AAA). The occurrence of lysine mutations was, in addition, studied by allele specific polymerase chain reaction. Again, the mutation frequency was significantly higher in metastases from patients with hereditary melanoma. PCR/SSCP finally enabled the isolation of lysine mutant alleles and nucleotide sequence analysis which confirmed the presence of the mutated codon 61. The relatively higher frequency of N-ras mutations in tumours from patients with hereditary melanoma may be related to the hypermutability described in hereditary melanoma and dysplastic naevus syndrome. The results support an involvement of N-ras mutations in the molecular pathogenesis of melanoma.
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PMID:Melanoma metastases from patients with hereditary cutaneous malignant melanoma contain a high frequency of N-ras activating mutations. 791 62

Thirteen families have been studied clinically as the basis for a linkage study of susceptibility to cutaneous melanoma. Previous studies have shown that a number of families with predisposition to melanoma have abnormal naevi, now known as the atypical mole syndrome (AMS) phenotype. Many groups performing linkage studies using families selected from geographical areas with higher rates of melanoma have concentrated on the diagnosis of melanoma to identify presumptive gene carriers. In the UK, in the absence of extended families with multiple cases of melanoma, we have attempted to identify gene carriers through the presence of the AMS phenotype. Previously the AMS phenotype has been poorly defined and so we have developed a scoring system to define the AMS in an attempt to allow for variation in expression among gene carriers. In this report, we document the clinical characteristics of all 13 families and the use of our scoring system. The pattern of inheritance within these selected families of the AMS phenotype with or without melanoma is consistent with a dominant gene.
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PMID:Family studies in melanoma: identification of the atypical mole syndrome (AMS) phenotype. 795 Mar 55

While it is recognized that relatives of melanoma patients are at increased risk for this disease, the source and extent of variation in melanoma risk between families of melanoma cases is unknown. Heterogeneity of familial melanoma risk was assessed among the families (comprising 7,666 first-degree relatives) of 1,149 cutaneous melanoma cases diagnosed in Queensland, Australia, between 1982 and 1987. The measure of familial melanoma risk was based on the number of cases of melanoma in the family in excess of those predicted from the age-, sex-, and birth cohort-specific cumulative incidences of melanoma among all relatives in the sample. Probands over-reported melanoma occurrence among their relatives, with a false positive reporting rate of 44.5% (216 false reports out of 485). Only medically verified cases among relatives were included in the analysis. There was statistically significant heterogeneity in family risk, with 53 (4.7%) of the total 1,116 unrelated families containing significantly more melanoma cases than expected considering the size of the family, and the age, sex, and birth cohort distributions of family members. In univariate analyses, members of the high-risk families were significantly more likely to have poor ability to tan, a propensity to sunburn, fair skin color, red hair, and many melanocytic nevi. When all variables were included simultaneously in a multiple logistic regression model, only the associations with tanning ability, skin color, and number of nevi remained significant. There were no significant differences overall between high-risk and other families in the sites and ages at diagnosis of melanoma, although melanomas on variably sun-exposed sites (trunk and legs) were diagnosed earlier in the high-risk families, independent of the stage at diagnosis.
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PMID:Heterogeneity of melanoma risk in families of melanoma patients. 798 58

Evidence from several countries suggests that the long-continued increase in melanoma-related mortality is slowing or has ceased. In some countries, decreasing rates are now seen particularly in women. These trends are probably due to successful primary prevention and early diagnosis. However, incidence continues to increase, even in areas of already high incidence such as Australia. Sun exposure has been established as the major cause of cutaneous melanoma in white patients, and no other environmental factors show a consistent association. Links to occupation, diet, and hormonal factors are still not clearly established. The frequency of nevi is likely to be both a good indicator of future melanoma risk and a short-term biologic marker of the effects of sun exposure; valuable new studies on the latitude gradient and natural history of nevi have been published. Primary prevention of skin cancers is now a priority in high-risk countries, and studies in Australia are clarifying the effect of education on sun exposure behavior. Although surveillance of particularly high-risk persons is valuable, the benefits of more widespread targeting or screening of high-risk persons remains unclear. Useful studies on the reliability of diagnostic and screening examinations have been produced, along with preliminary data on the value of diagnostic aids such as epiluminescence microscopy.
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PMID:Etiology, epidemiology, risk factors, and public health issues of melanoma. 801 96


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