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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Melanins, pigments of photoprotection and camouflage, are very photoreactive and can both absorb and emit active oxygen species. Nevertheless, black skinned individuals rarely develop skin cancer and melanin is assumed to act as a solar screen. Since DNA is the target for solar carcinogenesis, the effect of melanin on Ultraviolet (UV)-induced thymine lesions was examined in mouse melanoma and carcinoma cells that varied in melanin content. Cells prelabeled with 14C-dThd were irradiated with UVC; DNA was isolated, purified, degraded to bases by acid hydrolysis and analyzed by HPLC. Thymine dimers were detected in all of the extracts of irradiated cells. Melanotic and hypomelanotic but not mammary carcinoma cell DNA from irradiated cells contained hydrophilic thymine derivatives. The quantity of these damaged bases was a function of both the UVC dose and the cellular melanin content. One such derivative was identified by gas chromatography-mass spectroscopy as thymine glycol. The other appears to be derived from thymine glycol by further oxidation during acid hydrolysis of the DNA. The finding of oxidative DNA damage in melanin-containing cells suggests that melanin may be implicated in the etiology of caucasian skin cancer, particularly melanoma. Furthermore, the projected decrease in stratospheric ozone could impact in an unanticipated deleterious manner on dark-skinned individuals.
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PMID:Melanin photosensitizes ultraviolet light (UVC) DNA damage in pigmented cells. 237 74

The purpose of these studies was to determine whether ultraviolet radiation contributes to the induction of cutaneous melanocytic tumors in mice. At 4 days of age, C3H/HeNCr(MTV-) mice received an initiating dose of 7,12-dimethylbenz(a)anthracene, followed by twice weekly applications of croton oil. Of the mice treated with this protocol, 31% developed melanoma. The addition of chronic doses of ultraviolet radiation (UVR) to the carcinogen treated site dramatically accelerated the development of the melanomas. Substituting UVR for the initiator or the promoter in this two-stage carcinogenesis model resulted in the development of a few melanocytic tumors (less than 10%). These experiments demonstrate that UVR accelerated the development of cutaneous melanocytic tumors induced in mice by chemical carcinogens and participated in the induction of these tumors by serving as a weak initiator or promoter.
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PMID:The role of ultraviolet radiation in the induction of melanocytic skin tumors in inbred mice. 251 15

The incidence of malignant melanoma of the skin has increased rapidly among white people during the last decade. Although the pathogenesis of malignant melanoma is not clear, epidemiologic data and experimental work indicates that ultraviolet (UV) radiation plays a critical role in tumorigenesis. Recent data implicate peroxidative reactions in UV-carcinogenesis and clearly demonstrate that selenium (Se) confers protection, in part by inducing cellular-free radical scavenging systems and by enhancing peroxide breakdown, thus enhancing the capacity of the cell to cope with oxidant stress. With this in mind, we investigated the Se status of 101 patients with malignant melanoma. Our study revealed significantly lower Se levels in the sera of melanoma patients than of controls. Although patients in all clinical stages had lower Se levels than the controls, patients in stage III (disseminated melanoma) had the lowest levels. Separate analysis of histogenetic subtypes of melanoma revealed that lentigo maligna melanoma (LMM) and superficial spreading melanoma (SSM) had the strongest association with depressed Se serum levels. Our results, showing for the first time that malignant melanoma is associated with low Se concentrations, are consistent with results of epidemiologic studies showing an inverse correlation between serum Se levels and certain cancers.
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PMID:Serum selenium levels in patients with malignant melanoma. 256 30

In order to evaluate the relative significance of previous grenz-ray treatment for human non melanoma skin carcinogenesis, the files were studied of all patients treated for non melanoma skin cancer of the scalp (n = 82, male/female ratio 1.1) at the Department of Dermatology, the Finsen Institute, from 1976 to 1985. Fourteen patients, with a male/female ratio of 3.7, were treated for squamous cell cancer (SCC). Sixty-five patients, with a male/female ratio of 0.9, were treated for basal cell cancer (BCC). Twelve patients (15%, 11 with BCCs, 1 SCC), of which eight with psoriasis, were previously treated with grenz rays on the scalp, and two of them had not been exposed to additional skin carcinogens. Comparably, malignant conversion in sebaceous and verrucous nevi accounted for 9 cases or 11%. Characteristically, scalp cancers associated with previous grenz-ray treatment were BCCs, the male/female ratio were less than 0.1 and two-thirds occurred in patients with multiple skin cancer. That grenz-ray related scalp cancers more often develop in females than in males was further confirmed by comparison to the sex distribution among patients treated on the scalp with grenz rays in the years 1950, 1960 and 1970 (p less than 0.01). (Accepted August 10, 1988.)
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PMID:Non melanoma skin cancer of the scalp. On the etiology. 256 32

Southern blot analyses of the xiphophorine genome with probes specific for 15 viral and cellular oncogenes revealed that only three v-erbB related EcoRI fragments comprising 4.9 kb of a certain X, 11.5 kb of another X, and 6.7 kb of both a Y and a Z chromosome are inherited in parallel with the Tu complex and melanoma formation. They are accessory in the genome, and are highly homologous with each other and with an ubiquitous autosomal 7.5-kb fragment. The latter one is probably linked to the indispensable Tu complex that is postulated to be present in all individuals of Xiphophorus irrespective of whether they possess or lack the capacity to form melanoma in interspecific hybrids. Three restriction fragments, the X-chromosomal 4.9-kb, the Y-chromosomal 6.7-kb and the ubiquitous Tu-nonlinked 5.5-kb EcoRI fragments were cloned and sequenced. The X- and the Y-chromosomal fragments show perfect identity in the regions of the putative exons C and D of the EGF receptor gene and minor but significant differences to the putative exon C (exon D not identified) of the Tu-nonlinked fragment of 5.5 kb, indicating that at least two different types of x-erb B genes coding for slightly different EGF-receptors exist in the fish. Northern blot analyses revealed expression of the Tu-linked x-erbB genes (x-gfrB genes) in both transformed and nontransformed tissue, suggesting their essential role in regulation of normal cell proliferation and in carcinogenesis. We conclude that the indispensable x-egfrB genes remain unchanged and strictly regulated, while the sex chromosomal accessory x-egfrB genes possibly undergo dramatic changes in structure and/or function (e.g., unscheduled expression, ectopic expression, point mutations, truncation) leading to activation of the oncogenic potential of these genes, which in turn could induce several cellular events involved in the switch from the normal to the transformed state of the cell. In contrast, none of the x-erbA restriction fragments could be assigned to the Tu-complex or to any regulatory gene (R or S). These results, however, do not exclude the existence of a structural and/or functional relation between x-erbA genes and R and S genes. We therefore analyzed x-erbA genes by cloning, sequencing, and expression studies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Search for genes critical for the early and/or late events in carcinogenesis: studies in Xiphophorus (Pisces, Teleostei). 257 36

This review relates concepts derived from the study of chemically induced skin cancer in animal models to the pathogenesis of malignant melanoma in humans. Most chemically induced experimental cancers in animals, including melanomas in rodents, arise within a benign precursor lesion. The initiation-promotion-progression sequence is a central concept in animal models for carcinogenesis. Many human melanomas appear to arise from epidermal melanocytes, with no associated precursor lesion. This article considers why there is no apparent precursor in many human melanomas and the consequences of this absence. Melanocyte physiology and factors that govern escape from defenses such as DNA repair, local tissue environment, and immunity presumably influence melanocyte conversion to melanoma. These factors may determine the absence of a precursor lesion in primary melanomas. In addition, it is possible that some human melanomas arise by cellular mechanisms different from those causing cancer in rodent models. Both molecular and prospective clinical studies will be required to explain this apparent paradox in the pathogenesis of melanoma. A similar approach may help to explain the origin of basal cell carcinoma and perhaps other human cancers that appear to arise directly from normal cells. From a clinical point of view, the absence of an identifiable, benign precursor lesion requires even greater emphasis on melanoma prevention. Research on mechanisms of ultraviolet carcinogenesis indicates that appropriate postexposure treatments may be useful in preventing long-term consequences of sunburn, including melanoma.
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PMID:Apparent absence of a benign precursor lesion: implications for the pathogenesis of malignant melanoma. 267 14

Based on the two mutation hypothesis in the development of retinoblastoma, loss of heterozygosity (LOH) of specific chromosome has been implicated in the presence of tumor suppressor gene. Studies on the LOH in different types of tumors revealed that LOH of each chromosome might play a different role in the multistep process of carcinogenesis: LOH of some chromosomes may play an etiological role in the development of some tumors, while that of other chromosomes or the same chromosome in other tumors, may play a role in the progression of tumors. LOH of chromosome 13 is an example for the former cases, and the latter cases involve LOH of chromosome 17 in colorectal carcinoma and osteosarcoma, chromosome 10 in glioblastoma, chromosome 1 in neuroblastoma and malignant melanoma, and chromosome 11 in breast carcinoma. These studies indicates that the progressive or concerted LOH could be a measure of the highly malignant or metastatic potentiality. However, it should be borne in mind that, especially in polyploid tumors, LOH also occurs as a random event following the polyploidization-segregation process.
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PMID:[Loss of heterozygosity in the progression of tumors]. 267 92

Epidemiologic and etiological research about the pathogenesis of melanoma remains a controversial issue. The dominant cause appears to rest on the relation between the genetically determined susceptibility of the host and ultraviolet radiation (UVR). Basic to the understanding however is the knowledge about the clinical and histopathological, the genotypical and phenotypical heterogeneity of this tumor entity. In terms of the multistage concept of carcinogenesis, melanocytes, atypical or normal, are exposed to a mutagenic event, predominantly UVR, initiating malignant growth in a genetically altered and susceptible genome. The initiation could also occur spontaneously or as the result of other insults such as chemical carcinogens, viral infections, ionizing radiation etc. Promotion through the stage of melanocytic dysplasia or de novo from an altered skin, follows additional exposure to UVR or cocarcinogens and is likely to be modulated by ethnic, dietary, endocrine but also protective factors and concomitant disease. In terms of descriptive epidemiology, melanoma may be caused by exposure to intermittent and intense sunlight on unacclimatized skin. The mechanism of this association such as the wavelength responsible, effects of total dose, intensity of dose rate, latency period between exposure and the clinical incidence of disease finally the stage of carcinogenesis affected by UVR and other initiating factors and the impact of any specific modulation for the pathogenesis and clinical course of the disease remain to be elucidated.
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PMID:Etiology and risk factors of melanoma. 269 6

Malignant melanomas were found in 15.8% of xeroderma pigmentosum (XP) patients with skin cancer in Japan. When multiple cancers were scored separately depending on the histopathologic types, 12.1% of the skin cancers in XP patients was malignant malignant melanoma. The relative incidence of malignant melanoma in skin cancer in XP patients is similar to that in skin cancer in general (12.6%), reported previously. Most of the malignant melanoma in XP patients developed in skin exposed to sunlight, in contrast to the high incidence of malignant melanoma in general in the unexposed skin of Japanese people. A DNA repair defect of UV damage is strongly suggested to be responsible for the high incidence of skin cancer in XP patients. The onset of malignant melanoma in XP patients was about ten years old, and was as early as those of basal cell carcinoma and squamous cell carcinoma in the patients with very low DNA repair capacities. Among nine genetic complementation groups and a variant type, group A XP cells were found to be extremely hypermutable by ultraviolet light, while group C XP cells were also hypermutable, but at the same level as normal cells when adjusted for survival. Mutagenesis as a possible mechanism of carcinogenesis in XP is supported by these results, but evidence in other cancer-prone hereditary diseases is yet to be obtained.
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PMID:Melanoma and other skin cancers in xeroderma pigmentosum patients and mutation in their cells. 271 57

Transplanted tumours (melanoma B16 and breast cancer) were analysed in different phases of development histologically and electronmicroscopically. The described specific ultrastructural changes of tumours cells in the course of neoplastic transformation have confirmed the supposition that the process of carcinogenesis is multiphasal and continuous.
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PMID:[Histologic and electron microscopic analysis of experimentally transplanted CaM and MB16 tumors]. 281 29


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