The Genes That Carcinogens Act Upon

Anderš, F.; Schartl, Manfred; Barnekow, Angelika; Schmidt, C. R.; Lüke, Wolfgang; Jaenel-Dess, G.; Anders, A.

doi:10.1007/978-3-642-70385-0_51

Cited by 7 publications

(3 citation statements)

References 38 publications

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“…In Drosophila recessive mutations at more than 20 different loci can result in a variety of tissue-specific tumours (Gateff, 1978;Gatef, 1982) (Anders, 1983;Anders et al, 1985). The affected genes have been referred to as anti-oncogenes (Green & Wyke, 1985;Knudson, 1985) although this term should not be taken to necessarily imply a direct interaction with oncogenes.…”

Section: Gene Loss or Inactivation In Tumoursmentioning

confidence: 99%

Recessive mechanisms of malignancy

Green

1988

Br J Cancer

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It is increasingly recognised that recessive mutations play an important role in the pathogenesis of many forms of malignancy. Some of the affected loci may prove to be recessively-activated proto-oncogenes, but others are now known to be tumorigenic solely by virtue of their loss or inactivation and therefore form a distinct and novel family of tumour genes. Preliminary evidence suggests that such genes are likely to be functionally heterogeneous and to encode molecules involved in the inhibition of cellular proliferation and/or the induction of differentiation. Their further study is likely to illuminate fundamental mechanisms of normal cellular growth and differentiation as well as having important implications for the pathogenesis and management of cancer.

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Section: Gene Loss or Inactivation In Tumoursmentioning

confidence: 99%

Recessive mechanisms of malignancy

Green

1988

Br J Cancer

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“…Anders et al 1980). A ®sh line-speci®c suppressor gene ensemble controlled by a principal suppressor gene governs an oncogene ensemble and thereby protects the cutaneous pigment cells from any experimentally stimulated or incidentally occurring change or outgrowth to melanoma (F. Anders et al 1985.…”

Section: Resultsmentioning

confidence: 99%

Paragenetic suppressors of suppressor genes - a new class of oncodeterminants

Roushdy

Michel

Petry

et al. 1999

Journal of Cancer Research and Clinical Oncology

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Impairment or loss of suppressor genes is a common event permitting the oncogene/suppressor gene machinery to develop neoplasia. Following prenatal treatment with X-rays and UV-B, we detected a new class of oncodeterminants that could not be specified as genes. This points to paragenetic elements that suppress suppressorgenes and thus provoke melanoma at earlier ages of onset as expected, with increased severity and increased number of incidences in successive generations, in the absence of further treatment. These elements were isolated from a xiphophorine DNA library by endogenously labeled long terminal repeats (LTR) of a xiphophorine retrovirus, and were characterized as retrotransposons by Southern and Northern blotting and reverse transcription/polymerase chain reaction and transient transfection studies, in situ hybridization, and sequencing. They appear in multiple copies in the telomeric chromosome regions, where they can extend. Three open reading frames (ORF) are flanked by LTR that contain genetically active regulatory elements, and are inducible by UV-B. ORF 3 shows nests of CG dinucleotides and CGG trinucleotides, which are reminiscent of CGG nests predisposing subjects to anticipation of certain human diseases involving tumor generation. Genetic anticipation as defined by Nettleship (1909) or Warren (1996) including an increase of neoplasia might represent an acquired genetic load in preceding generations, which might provide a lead to a molecular understanding of the worldwide increase of incidences of human tumor.

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“…In some cases, this situation leads to the spontaneous formation of melanomas (for review, see Anders 1991). In other cases, Xiphophorus melanomas can be induced by chemical or UV exposures (Anders et al 1985;Setlow et al 1989).…”

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confidence: 99%

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

et al. 1996

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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.

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The Genes That Carcinogens Act Upon

Cited by 7 publications

References 38 publications

Recessive mechanisms of malignancy

Recessive mechanisms of malignancy

Paragenetic suppressors of suppressor genes - a new class of oncodeterminants

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

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