Cancer: re-evolution of eucaryotic to procaryotic replication units--a result of genetic transposition?

Abstract

We have consistently tried to present our "procaryote-hypothesis" of oncogenesis in the light of evolution. It is suggested that the replication units are the essential starting points of oncogenesis, and cancer is the result of a short and compact re-evolution from eucaryotic to procaryotic replicons. In our view, the process of re-evolution or reactivation of procaryotic replication units and/or their precursors starts with the activity of a cancerogen and proceeds by genetic rearrangements, possibly by genetic transposition. Consequently, some remarks had to be made on: (a) the evolution of self-replicative species; (b) the evolvement of procaryotes to eucaryotes; and (c) the various mobile repeated genetic elements. Moreover, we have taken into consideration the important fact that most of the mammalian genome is reversibly repressed and "that there is in these modern genes still a memory of ancient sequences" ( Eigen et al., 1981). We can only speculate on the extent of the evolutionary conservation, particularly of certain ancient nucleotide sequences related to autonomous, indefinite self-replication. Nevertheless, no real argument can be made against the simple possibility that a re-evolution of eucaryotic to procaryotic replicons lead to cancer.