The deranged growth pattern of the cancer cell can be triggered by endogenous and exogenous factors, but ultimately cellular genes appear to occupy a central position in triggering malignant growth. Today's terminology defines these genes as ‘oncogenes’ and ‘tumour suppressor genes’. Their identification stems from the merging of achievements made by different scientific disciplines – genetics, virology, molecular genetics and cytogenetics.
Get full access to this article
View all access options for this article.
References
1.
HestonW. E., Genetics of cancer. J. Hered. 65, 262–272 (1974).
2.
BoveriTh., Zur Frage der Entstehung maligner Tumoren. Verlag Gustav Fischer, Jena (1914).
3.
KosswigC., Über Bastarde der TeleostierPlatypoecilus und Xiphophorus. Z. indukt. Abbstamm. Vererbungsl. 44, 253–254 (1927).
4.
GordonM.. Pigment cell inheritance in the Mexican killfish, Platypoecilus. J. Hered. 19, 551–556 (1928).
5.
SchwabM., Oncogenes and tumor suppressor genes in Xiphophorus. Trends Genet. 3, 38–42 (1987).
6.
BauerK.-H., Mutationstheorie der Geschwulstentstehung: Übergang von Körperzellen in Geschwulstzellen durch Gen-Änderung. VerlagJulius Springer, Berlin (1928).
7.
VarmusH. E., Form and function of retroviral proviruses. Science216, 812–820 (1982).
8.
BishopJ. M., The molecular genetics of cancer. Science235, 305–311 (1987).
SchwabM., OehlmannR., BrüderleinS. and WakamatsuY., Amplified dna in cells of genetic melanoma ofXiphophorus. Oncogene4, 139–144 (1989).
11.
SchwabM., Amplification of NYMC in human neuroblastomas. Trends Genet. 1, 271–275 (1985).
12.
AmlerL. C. and SchwabM., Amplified NYMC in human neuroblastoma cells is often arranged in clustered tandem repeats of differently recombined dna. Molec. Cell Biol, (in press).
13.
BrodeurG., SeegerR. C., SchwabM., VarmusH. and BishopJ. M., Amplification of NYMC in untreated human neuroblastoma correlates with advanced disease stage. Science224, 1121–1124 (1984).
14.
SeegerR. C., BrodeurG. M., SatherH., DaltonA., SiegelS. E., WongK. Y. and HammondD., Association of multiple copies of the NYMC oncogene with rapid progression of neuroblastomas. N. Engl. J. Med. 313, 1111–1116 (1985).
15.
SlamonD. J., ClarkG. M., WongS. G., LevinW. J., UllrichA. and McGuireW. L., Human breast cancer: Correlation of relapse and survival with amplification of the her-2/neu oncogene. Science235, 117–182 (1987).
16.
SchwabM., SchlagP., BrüderleinS. and van der BoschK., Oncogene amplification in colorectal cancer, inHerreraL., (Ed.), Familial Adenomatous Polyposis, pp. 343–352. Alan Liss, New York (1989).
17.
SchwabM., Amplification of cellular oncogenes during evolution of tumor cells, inThe Role of dna Amplification in Carcinogenesis, zur HausenH. and SchlehoferJ. R.(Eds), pp. 178–185. Lipincott, Philadelphia (1987).
18.
MartinssonT., StahlF., PollweinP., WenzelA., LevanA., SchwabM. and LevanG., Tumorigenicity of sewa murine cells correlates with degree of MYC amplification. Oncogene3, 437–441 (1988).
19.
SchwabM. and BishopJ. M., Sustained expression of the human proto-oncogene NYMC rescues rat embryo cells from senescence. Proc. Nat. Acad. Sci. us85, 9585–9589 (1988).
20.
SchwabM., VarmusH. and BishopJ. M., Human NYMC gene contributes to neoplastic transformation of mammalian cells in culture. Nature316, 160–162 (1985).
21.
KnudsonA. G., Mutation and cancer: statistical study of retinoblastoma. Proc. Nat. Acad. Sci. us68, 820–823 (1971).
22.
HansenM. F. and CavaneeW. K., Genetics of cancer predisposition. Cancer Res. 47, 5518–5527 (1987).
23.
SchwabM., Genetic principles of tumor suppression. Biochim. Biophys. Acta– Rev Cancer (in press).
24.
GreenM. R., When the products of oncogenes and antioncogenes meet. Cell56, 1–3 (1989).
25.
RöslF., DürstM. and zur HausenH., Selective suppression of human papillomavirus transcription in non-tumorigenic cells by 5-azacytidine. emboJ. 7, 1321–1328 (1988).
