Oncogenes and malignant transformation

Abstract

A tumor stems from the derailment of a single cell. Not unreasonably, it has been assumed that such a dysfunction is caused by somatic mutations inactivating one or more of the finely tuned regulatory systems that govern cellular systems. In recent years, however, it has become evident that in some cases the cancerous state is not due to inactivation but to mutational activation of genes producing dominant cancer genes. This insight was gained from experiments in which DNA from tumor material was transferred (transfected) into cultured animal cells. In some instances transfer of tumor DNA led to the formation of colonies of oncogenic ceils, whereas the DNA from normal cells had no effect. With the recently developed recombinant-DNA techniques, it has been possible to isolate from the multitude of genes present in tumor cells those that were responsible for this transforming activity. Often, these genes have been found to be identical or related to the cellular homologues of the oncogenes identified in oncogenic retroviruses. Retroviruses derive their generic name because their reproductive cycle, involves the conversion of the ss-RNA genome to a ds-DNA copy, i.e. a reversal of the classical DNARNA-protein sequence. This DNA copy is integrated into the host cell genome where it functions as a template for progeny virus RNA molecules. On the basis of their oncogenicity, retroviruses are classified into two groups:

DOI: 10.1007/BF00255828

Cite this paper

@article{Ormondt1986OncogenesAM, title={Oncogenes and malignant transformation}, author={H. van Ormondt and A. J. van der Eb}, journal={Urological Research}, year={1986}, volume={14}, pages={119-122} }