Search for Genes Critical for the Early and/or Late Events in Carcinogenesis: Studies in Xiphophorus (Pisces, Teleostei)

Zechel, C; Schleenbecker, Uwe; Anders, A.; Pfütz, Marita; Anderš, F.

doi:10.1007/978-3-642-74621-5_64

Cited by 10 publications

(8 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The doses needed to abolish rejection of UV-induced tumors were also in the 100 kJ/m2 range of radiation of A > 280 nm (27). These comparisons indicate that the high susceptibility of the hybrid fish to melanoma induction by UV is not the result of the induction of a stimulatory factor nor the inhibition of an immunological rejection system for preexisting transformed cells in the hybrid fish but probably reflects the UV-inactivation of the small number of tumor suppressor or antioncogenes in the hybrid animals (28) as Anders and his colleagues found with chemical carcinogens (17).…”

Section: Discussionmentioning

confidence: 91%

“…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).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

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

Setlow

Woodhead

Grist

1989

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

181

121

View full text Add to dashboard Cite

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...

show abstract

Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

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

Setlow

Woodhead

Grist

1989

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

181

121

View full text Add to dashboard Cite

show abstract

“…Xmrk-2 has been mapped to the sex-chromosomal region harboring the macromelanophore locus (Schartl, 1990;Weis and Schartl, 1998). Both the macromelanophore locus and Xmrk-2 are considered`accessory' loci, as individual ®sh within a population can be found without either locus (Schartl, 1990;Weis and Schartl, 1998;Wittbrodt et al, 1989;Woolcock et al, 1994;Zechel et al, 1989). A structurally closely related gene known as Xmrk-1 also resides on the sex chromosomes, but its expression is not correlated to melanomagenesis; instead, it is expressed during embryogenesis, and in adult tissues as well (Adam et al, 1991;Woolcock et al, 1994;Zechel et al, 1992a,b).…”

Section: Introductionmentioning

confidence: 99%

Comparative structure and characterization of a CDKN2 gene in a Xiphophorus fish melanoma model

Kazianis

Coletta

et al. 1999

Oncogene

View full text Add to dashboard Cite

We have cloned, sequenced, and characterized the RNA expression properties of a ®sh CDKN2 gene from Xiphophorus helleri and X. maculatus. This gene, termed CDKN2X, shows a high degree of amino acid sequence similarity to members of the mammalian CDKN2 gene family, which includes the tumor suppressor loci CDKN2A (P16) and CDKN2B (P15). Comparative sequence analysis suggests that ®sh CDKN2X is similarly related to all four mammalian gene family members, and may represent a descendant of an ancestral prototypic CDKN2 gene. CDKN2X was mapped to a region on autosomal Xiphophorus linkage group V (LG V) known to contain the DIFF gene that acts as a tumor suppressor of melanoma formation in X. helleri/X. maculatus backcross hybrids. Thus, CDKN2X may be a candidate for the tumor suppressor DIFF gene. Here we have sequenced CDKN2X in both Xiphophorus species and have characterized its expression in normal and melanotic tissues within control and backcross hybrid ®sh. A simultaneous expressional analysis of the Xmrk-2 tyrosine kinase receptor gene, which is strongly implicated in melanomagenesis in this system, was also performed. RT ± PCR analyses revealed that both genes were highly expressed in melanomas. For CDKN2X, this result contrasts numerous ®ndings in human tumors including human melanoma in which either CDKN2A (P16) deactivation or LOH was observed.

show abstract

“…The widespread use of the classical melanoma cross stems from its simple two-gene inheritance that suggests the existence of an oncogene and an apparent tumor suppressor and to the reproducibility and relatively quick production of melanomas. The oncogene has been cloned and is referred to as the Xiphophorus melanoma receptor tyrosine kinase [Xmrk, although alternative naming schemes exist in the literature (Zechel et al 1988(Zechel et al , 1989Wittbrodt et al 1989;Woolcock et al 1994 (Morizot et al 1991(Morizot et al , 1993D. Morizot, unpubl.).…”

mentioning

confidence: 99%

Genetic mapping in Xiphophorus hybrid fish: assignment of 43 AP-PCR/RAPD and isozyme markers to multipoint linkage groups.

et al. 1996

View full text Add to dashboard Cite

The combined use of the arbitrarily primed polymerase chain reaction [AP-PCR, also known as random amplification of polymorphic DNA (RAPD)] and isozyme mapping resulted in the production of 87 potential marker loci, enabling an overall expansion within the genetic map of the fish genus Xiphophorus. Use of DNA sequencing-style acrylamide gels and carefully controlled conditions of amplification and silver staining allowed exceptional resolution and reproducibility of AP-PCR/RAPD generated markers. Linkage analysis of AP-PCR/RAPD and isozyme markers resulted in the addition of 16 new markers to Xiphophorus linkage groups (LGs) I, II, III, V, IX, X, XII, and XIV. Addition of 5 AP-PCR/RAPD markers to linkage group U6 containing the Tailspot pigment pattern locus (P) and designation of eight new unassigned linkage groups with 22 markers was also accomplished. Genetic linkage data allowed inference of the existence of a novel pigment pattern modifier locus. Expansion of the Xiphophorus gene map by linkage analysis of AP-PCR/RAPD markers in conjunction with isozyme polymorphisms should lead to the rapid saturation of genetic linkage groups such as LG V, which will probably be instrumental to cloning the Diff tumor suppressor gene locus.

show abstract

Search for Genes Critical for the Early and/or Late Events in Carcinogenesis: Studies in Xiphophorus (Pisces, Teleostei)

Cited by 10 publications

References 42 publications

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

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

Comparative structure and characterization of a CDKN2 gene in a Xiphophorus fish melanoma model

Genetic mapping in Xiphophorus hybrid fish: assignment of 43 AP-PCR/RAPD and isozyme markers to multipoint linkage groups.

Contact Info

Product

Resources

About