Summary
The genetic information for neoplastic transformation is inherited as a normal part of the genome in all individuals of Xiphophorus. Neoplasia, however, was found only in hybrids between members of different populations and local races. It can be classified in (a) a large group that is triggered by mutagens, (b) a large group triggered by promoters, (c) a small group that develops “spontaneously”, and (d) a small group that is inherited according to Men-delian Laws. The process leading to susceptibility for neoplasia is represented by the disintegration of coa-dapted gene systems that normally protect the fish from neoplasia. Hybridization is the most effective process that leads to disintegration of the protection gene-systems. Environmental mutagens and promoters (i.e. carcinogens) may complete disintegration and thus may trigger neoplasia.
The phenomenon of introducing susceptibility to neoplasia by means of hybridization has been observed in a large variety of plants and animals (Table 2). While we have no data on the relation between hybridization and cancer in human beings comparable to those in plants and animals, we put the question whether the many facts on tumor incidence in humans, that do not agree with the concept of the primacy of environmental factors in carcinogenesis may be explained by interpopulational and interracial hybridization in preceding generations. Based on our studies on Xiphophorus we suppose that environmental factors represent only the peak of an iceberg in the multistep process of the causation of neoplasia. The most important steps leading to neoplasia, i.e. those that bring about susceptibility, are supposed to be hidden in our ancestry.
Zusammenfassung
Alle Individuen von Xiphophorus haben in ihrem Genom die genetische Information zur Tumorbildung. Neoplasmen wurden allerdings nur bei Bastarden von Angehörigen verschiedener Populationen oder Lokalrassen gefunden. Vier Neopla-sie-Typen verschiedener Ätiologie wurden nachgewiesen: (a) Eine große Gruppe mutagen-abhängiger, (b) eine ebenfalls große Gruppe promotor-abhängiger, (c) eine kleine Gruppe „spontan” entstehender und (d) eine ebenfalls kleine Gruppe dominant erblicher Neoplasmen. Der Prozeß, der zur Krebs-Suszeptibilität führt, beruht auf einem bastardierungsbedingten genetischen Abbau koadaptierter Gensysteme, die normalerweise vor Krebs schützen. Mutagene und Promotoren (Karzinogene im herkömmlichen Sinne) vervollständigen den Abbau dieser Gensysteme in Soma-zellen und lösen auf diese Weise die Krebsbildung aus.
Die Entstehung von Krebs-Suszeptibilität durch Bastardierung ist bei allen Gruppen der höheren Pflanzen und Tiere beobachtet worden (Tabelle 2). Es wird deshalb die Frage gestellt, ob und wie stark Bastardierung zwischen Angehörigen verschiedener menschlicher Populationen und Lokalrassen zur großen Krebshäufigkeit mancher hochentwickelter Nationen ursächlich beigetragen hat. Auf Grund unserer Studien an Xiphophorus vermuten wir, daß die Karzinogene aus der Umwelt im Ursachengefüge des neoplastischen Wachstums nur die Spitze eines Eisberges darstellen, während die wichtigste Komponente, die Suszeptibilität zur Krebsbildung, bei unseren Vorfahren im Verborgenen liegt.
Vortrag auf der 111. Versammlung der Gesellschaft Deutscher Naturforscher und Ärzte, Hamburg, 21.-25. September 1980.
Die Arbeiten wurden durch die Deutsche Forschungsgemeinschaft (SFB 103, Zellenergetik und Zelldifferenzierung, Marburg), die Stiftung Volkswagenwerk und die Justus-Liebig-Universität Gießen unterstützt. Sie basieren auf Arbeiten von Curt Kosswig und Myron Gordon, enthalten Ideen von Walter He-ston, und wären ohne die Hilfe meiner früheren und jetzigen Mitarbeiter, die die Daten 25 Jahre hindurch zusammengetragen haben, nicht möglich gewesen. - Bei der Anfertigung des Manuskriptes halfen Frau Dipl. Biol. A. Schartl, Frau Silomon-Pflug und Herr Dr. E. Scholl
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Anders, F. (1981). Erb- und Umweltfaktoren im Ursachengefiige des neoplastischen Wachstums nach Studien an Xiphophorus. In: Verhandlungen der Gesellschaft Deutscher Naturforscher und Ärzte. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-38057-4_20
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