Opposite Long-range Interactions Between Normal and Malignant Cells

Abstract

Discussion on the origin and development of cancer has rapidly increased since the detection of the existence of oncogenes (for review see Kurth, 1983; Ochoa, 1985). Although carcinogenesis is assumed to be a multistep process, molecular biology has made it clear that oncogenes can contribute greatly to the development of a tumor. Normal cells of very different animals, such as worms, flies, other insects, birds, mammals, and humans contain similar oncogenes (“c-genes”). This indicates a high conservation of this set of genes, and an important function for them in growth and development, particularly in embryogenesis. Some retroviruses have appropriated oncogenes by genetic recombination from normal cells, so that retrovirus infection, introducing additional viral (and modified) oncogenes (“v-genes”) into normal cells, as well as carcinogen-mediated activation of cellular oncogenes, may both lead to increased synthesis of oncogene-encoded informational proteins that convert normal cells to cancer cells. Some of these proteins are tyrosine kinases that catalyze the phosphorylation of the tyrosine residues of proteins. They find a location within the cell membrane and may alter the surface properties of the cell; others, evidently non-enzymatic in nature, are found in the cell nucleus and may influence gene activities in general. Further possible activities of oncogene are their mutation, their transposition, or their amplification (= extra replication, i.e. increase in number). The latter phenomenon is now commonly accepted as an important factor in drug resistance (e.g., Schimke, 1984).