Cancer of the Skin

Gordon, Hugh

doi:10.1136/bmj.2.4727.348

BMJ

1951

DOI: 10.1136/bmj.2.4727.348

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Cancer of the Skin

Hugh Gordon¹

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1973

1989

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Cited by 2 publications

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“…The parental wild species are not susceptible to neoplasia, even after exposure to high doses of potential physical and chemical carcinogens. However, when these species are cross-bred in the laboratory, their hybrid offspring and succeeding backcross generations (to the parental swordtail) are sensitive to carcinogens, although to different degrees (16,17), presumably as a result of crossing out most of the antioncogenes or melanocyte differentiation genes.We explored the responses of different hybrids to UVirradiation and obtained two strains susceptible to UVinduced melanoma. The fish model is a legitimate one, since fish melanomas closely resemble the tumors that arise in human skin (18,19).…”

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confidence: 99%

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Animal model for ultraviolet radiation-induced melanoma: platyfish-swordtail hybrid.

Setlow

Woodhead

Grist

1989

Proc. Natl. Acad. Sci. U.S.A.

181

121

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Sunlight exposure is strongly indicated as one of the important etiologic agents in human cutaneous malignant melanoma. However, because of the absence of good animal models, it has not been possible to estimate the wavelengths or wavelength regions involved. We have developed a useful animal model from crosses and backcrosses of platyfish (Xiphophorus maculatus) and swordtails (Xiphophorus heUeri).Two strains of these fish are susceptible to invasive melanoma induction by exposure to filtered radiation from sunlamps in the wavelength ranges A > 290 nm and A > 304 nm. Multiple exposures on 5-20 consecutive days beginning on day 5 after birth or a single exposure of =200 J/(m2 day) of A > 304 nm result in a tumor prevalence of 20% to 40% at 4 months of age compared with a background rate of 12% in one strain and 2% in another. Exposure of the fish to visible light after UV exposure reduces the prevalence to background. The melanomas are similar in many respects to mammalian melanomas, as judged by light and electron microscopy. The genetics of the crosses determined by others and the high sensitivity of the hybrids to melanoma induction indicate that the UV radiation probably inactivates the one tumor repressor gene (or a small number of tumor repressor genes) in the hybrid fish. The small size of the animals and their high susceptibility to melanoma induction make them ideal for action spectroscopy.Agents that cause a decrease in stratospheric ozone would cause an increase in UV-B (A = 280-320 nm) intensities at the earth's surface without appreciably changing the longer UV or visible intensities of light. Melanoma among the white population of the United States and Europe is increasing dramatically as a function of time, probably as a result of changing lifestyles (1). The relation between latitude and melanoma mortality suggests that there is a correlation between the average solar radiation and mortality from malignant melanoma. However, it is not known which parts of the solar spectrum can plausibly be related to the increasing mortality because, although sunlight exposure seems to be an essential component in melanoma incidence, it is not the only one. Body areas most exposed to light are not the primary locations of melanomas as they are for basal and squamous cell carcinomas. There is good evidence that UV-B is tumorigenic in animals (2) and can cause neoplastic transformation in vitro (3). Four types of experiment indicate that light energy absorbed in DNA can cause cellular damage leading to tumors: (i) the tumorigenicity of fish cells as a result of UV-irradiation in vitro can be photoreactivated (4)-a process that monomerizes UV-induced cyclobutane pyrimidine dimers in DNA; (ii) the wavelengths effective in neoplastic transformation in vitro are those absorbed by DNA (5); (iii) transformation in vitro by UV is photoreactivable (6); and (iv) xeroderma pigmentosum individuals are defective in the ability to repair UV damages in their DNA and are extraordinarily sensitive to cancer induction, inc...

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mentioning

confidence: 99%

mentioning

confidence: 99%

Animal model for ultraviolet radiation-induced melanoma: platyfish-swordtail hybrid.

Setlow

Woodhead

Grist

1989

Proc. Natl. Acad. Sci. U.S.A.

181

121

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“…A different type of hereditary tumor is seen as a result of the production of hybrids between two different species. One of the best-studied examples is the high frequency of melanomas in the platyfish-swordtail hybrid (25,26). These tumors are due to the release of normal constraints on the growth of platyfish melanocytes.…”

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A General Theory of Carcinogenesis

Comings

1973

Proc. Natl. Acad. Sci. U.S.A.

397

113

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A general hypothesis of carcinogenesis is proposed consisting of the following features: ( 1 ) It is suggested that all cells possess multiple structural genes ( Tr ) capable of coding for transforming factors which can release the cell from its normal constraints on growth. ( 2 ) In adult cells they are suppressed by diploid pairs of regulatory genes and some of the transforming genes are tissue specific. ( 3 ) The Tr loci are temporarily activated at some stage of embryogenesis and possibly during some stage of the cell cycle in adult cells. ( 4 ) Spontaneous tumors, or tumors induced by chemicals or radiation, arise as the result of a double mutation of any set of regulatory genes releasing the suppression of the corresponding Tr genes and leading to transformation of the cell. ( 5 ) Autosomal dominant hereditary tumors, such as retinoblastoma, are the result of germ-line inheritance of one inactive regulatory gene. Subsequent somatic mutation of the other regulatory gene leads to tumor formation. ( 6 ) The Philadelphia chromosome produces inactivation of one regulatory gene by position effect. A somatic mutation of the other leads to chronic myelogenous leukemia. ( 7 ) Oncogenic viruses evolved by the extraction of host Tr genes with their conversion to viral transforming genes. As a result, in addition to the above mechanisms, tumors may also be produced by the reintroduction of these genes into susceptible host cells.

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Cancer of the Skin

Cited by 2 publications

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Animal model for ultraviolet radiation-induced melanoma: platyfish-swordtail hybrid.

Animal model for ultraviolet radiation-induced melanoma: platyfish-swordtail hybrid.

A General Theory of Carcinogenesis

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