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

An animal experiment is presented in which pigmented hairless mice were exposed once per fortnight to high doses of ultraviolet B (UVB) to study tumorigenesis. The aim of the study was to confirm a causal relationship between cutaneous melanoma and UV radiation, and to find an animal model to study it. The experiment was based on the hypothesis that the risk of developing a melanoma is increased by a history of severe sunburns. Pigmented hairless mice, Skh-hr2, were exposed once every fortnight to high doses of UVB radiation from fluorescent sunlamps, Westinghouse FS40 T12. Heavy actinic damage was observed for several days after each exposure. Seventeen of the 24 animals eventually developed tumors. Histopathologically, 80% of the tumors were squamous cell carcinomas. Depositions of melanophages were observed, but no melanomas. In this mouse experiment no causal relationship between cutaneous melanomas and UV radiation could be established.
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PMID:Ultraviolet B-induced tumors in pigmented hairless mice, with an unsuccessful attempt to induce cutaneous melanoma. 240 Jun 77

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

The recognition of recurring sites of chromosome change in human cancers has pinpointed the location in the genome of several important growth-regulatory sequences (e.g., cellular oncogenes). This report details the finding of a recurring translocation site involving the long arm of chromosome 6 (6q) in malignant melanoma. We have observed a translocation (t) between chromosomes 1 and 6 in five different cases of malignant metastatic melanoma. All five melanomas evidencing t(1;6) involved band regions 6q11-13, while two different regions of chromosome 1 (p22, q12-q21) were shown to be translocated to 6q. In reviewing previously published cases of melanoma, an additional two cases of t(1;6) and 13 cases of other translocations to 6q11-13 have been identified. Chromosome 6q contains several biologically important gene sequences including the proto-oncogenes ros, myb, and mas1. However, based on current mapping studies, the breakpoint of this translocation (6q11-13) is not within the region encoding these sequences. By analogy to other systems, molecular analysis of the translocation breakpoints may identify a gene(s) which plays a role in melanoma tumorigenesis.
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PMID:Identification of a recurring translocation site involving chromosome 6 in human malignant melanoma. 264 39

Genetic tumours of Xiphophorus are one of the classical experimental models that underline the concept that cancers develop as a result of abnormal gene expression. Formal genetics has indicated that cancer development in Xiphophorus starts when oncogenes are expressed abnormally due to elimination of tumour suppressor genes. The suppressor gene Diff seems to suppress malignancy by controlling terminal differentiation of cells. It appears now that control of terminal differentiation may also be one of the properties of human tumour suppressor loci, in particular the Rb gene. Although it is difficult at this point to envision which molecular or biochemical function of tumour suppressor genes we might be able to identify, research on tumour suppression will at least allow another glimpse at how basic mechanisms of cell differentiation and multiplication operate. It is not clear, however, if elimination of tumour suppressor genes alone is sufficient to elicit the fully malignant phenotype. Cytogenetic studies have shown various nonrandom chromosomal abnormalities in those human tumours in which elimination of a tumour suppressor gene seems to be a critical step in tumorigenesis. In Xiphophorus, it is obvious from our molecular studies that additional genetic events can contribute to the malignant phenotype. Of these, amplification of cellular DNA may have a role in malignant progression of melanomas. At this point, the exact contribution of amplification to genetic melanoma is unclear. Judging from the role of amplification in human and murine tumours, the significance of amplification, in addition to suppressor elimination, in melanomas of Xiphophorus is likely to be high.
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PMID:Genetic suppression of malignancy. 268 Sep 48

Hybrids between certain species of the teleost Xiphophorus predictably develop melanomas. Classical Mendelian crossing experiments have allowed us to identify genetic loci involved in eliciting and in suppressing tumorigenesis. The overall picture is that melanoma formation results from functional elimination of a suppressor locus allowing abnormal expression of a melanoma locus. Melanoma formation in Xiphophorus behaves like a recessive trait. The fish melanomas consist of incompletely differentiated pigment cells and in many aspects resemble their murine and human counterparts. Cytogenetic studies of cells of the genetic melanomas have provided evidence for chromosomal abnormalities. In particular, cytogenetic manifestations of amplified DNA were detected in a cell line derived from a malignant melanoma. Amplified DNA was isolated and was found to be amplified in a particular type of genetic melanoma. Our results suggest that genetic changes in addition to elimination of suppressor genes contribute to the malignant phenotype of melanoma in Xiphophorus. It is possible that a similar situation occurs in cancers of higher vertebrates, including humans.
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PMID:Suppression of genetic melanoma in the fish Xiphophorus. 274 31

In order to distinguish those chromosomal aberrations associated with tumorigenesis from those associated with tumor progression of malignant melanoma, chromosome analysis was performed on eight tumors derived from one patient. Three common marker chromosomes, a deletion of chromosome 1, a deletion of chromosome 9, and a translocation involving chromosomes 7 and 12, were identified in each tumor. The presence of common markers in these intrapatient tumors indicates the monoclonal origin of these tumors. Furthermore, the consistent and specific involvement of chromosome 9 in both interpatient and intrapatient studies suggests the crucial role that chromosome 9 plays during the development of human malignant melanoma. In addition to common markers, different overlapping markers including those involving chromosomes 2, 3, and 6, were also identified, suggesting that chromosomes 2, 3, and 6 are most likely associated with the progression, instead of the genesis, of the tumor. Finally, lesion-specific marker chromosomes were identified in each tumor indicating the nonrandom selection and modification of the metastatic process. The nature of chromosomal evolution among the eight tumors was clearly demonstrated by the retention and amplification of specific marker chromosomes, with the latter tumors containing more overlapping markers than the early tumors and the recurrence of identical markers in the different branches of evolution. One of the last three tumors obtained immediately before the death of the patient contained all the overlapping markers identified in other tumors, which may indicate that a plateau of chromosomal evolution of these tumors has been reached. These observations demonstrate a nonrandom or programmed chromosome evolution of human neoplasia that could be intrinsic to the aneuploid nature of neoplasia.
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PMID:Chromosomal evolution in the progression and metastasis of human malignant melanoma. A multiple lesion study. 277 22

Xeroderma pigmentosum is an autosomal recessive, precancerous dermatosis caused by defective repair of ultraviolet-damaged DNA. Characterized clinically by progressive cutaneous pigmentary alterations and tumorigenesis, it serves as a model for ultraviolet carcinogenesis. We describe the clinical and histopathologic findings in a 31-year-old woman with xeroderma pigmentosum and a massive iris melanoma of the left eye. Histologic examination following enucleation revealed diffuse iris replacement by spindle and epithelioid cells with extension into the trabecular meshwork. Evidence of direct extraocular extension was absent, and a metastatic evaluation showed no abnormalities. To our knowledge, this is the first reported case of xeroderma pigmentosum complicated by melanoma of the iris. It provides further evidence suggesting a role for sunlight exposure in the pathogenesis of uveal melanoma.
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PMID:Malignant melanoma of the iris in xeroderma pigmentosum. 292 65

Epidermal growth factor (EGF) receptor is expressed selectively by human melanoma cells which show the presence of an extra copy of chromosome 7. None of the cells of benign pigmented lesions (nevi) or radial growth phase (nonmetastatic) primary melanoma expressed EGF receptor and none of these cells showed an extra copy of chromosome 7. The results indicate that a single extra dose of a gene (for EGF receptor) may provide a selective advantage to cells in the late stages of tumorigenesis.
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PMID:Expression of the receptor for epidermal growth factor correlates with increased dosage of chromosome 7 in malignant melanoma. 298 38

The prevalence of non-melanoma skin cancer has been studied in a group of 85 patients who have undergone renal transplantation. We also investigated the relationship between the development of neoplastic lesions and the duration of immunosuppression, previous sun exposure and infection with human papilloma virus. The overall prevalence of neoplastic and pre-neoplastic epidermal lesions in the group was 25 per cent, higher than that previously reported in studies from the United Kingdom. In patients who had survived for more than 80 months after transplantation the prevalence of these lesions was 38 per cent. There was no apparent relationship between sun exposure or skin type and the development of cutaneous neoplasia, despite the fact that the majority of lesions were found on sun-exposed sites. Exposure to ultraviolet radiation (UVR) is probably important as an initiator or co-factor rather than as a precipitant. In both sexes, high sun exposure was associated with the presence of viral warts. In females, there was a strong association between the presence of viral warts and the occurrence of neoplastic lesions elsewhere, giving support to the hypothesis that ultraviolet radiation may be acting as a co-factor in virally-mediated oncogenesis. Epidermal cell kinetic studies in 39 patients using in-vitro exposure to 3H thymidine and autoradiographic techniques showed no difference between the patients with neoplastic lesions and unaffected patients, and is not therefore a useful method of identifying an 'at risk' group.
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PMID:Dysplastic epidermal change in immunosuppressed patients with renal transplants. 331 94

Generalized malnutrition results in inhibition of tumorigenesis and tumor growth in experimental animal models. Neither the specific nutrient deficiency nor the mechanism has been definitely elucidated. We have shown previously that dietary sodium deprivation in rapidly growing rats retards protoplasmic growth. This effect was correlated to the extracellular fluid (ECF) volume expansion which is dependent on sodium accumulation. Since solid tumors are composed of a large quantity of ECF (which includes plasma volume) it was postulated that preventing the accumulation of new ECF by means of sodium restriction would influence tumor growth. The present study was designed to determine the effects of salt restriction on tumor growth and to relate these effects to ECF volume. Approximately 10(6) viable B16 melanoma cells were injected into C57BL/6 x DBA/2 F1 and C57 mice. A salt restricted diet (sodium less than 3 microeq/g) was provided ad libitum. The drinking solution was distilled water for the experimental group and 0.45% saline solution for the controls. There was a significant decrease in tumor growth rates during sodium restriction. The total body ECF volume increased when dietary sodium was supplied but did not change during salt restriction. Therefore, the only source for the ECF in the tumor mass was from nontumorous tissue. We conclude that during dietary sodium restriction solid tumor growth is retarded and can proceed only to the extent that ECF is released from cachectic body tissues.
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PMID:Restriction of tumor growth in mice by sodium-deficient diet. 337 Jun 41


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