An Epigenetic Model for the Origin of Cancer

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Abstract
A unifying concept that appears to provide an understanding of cancer as a fundamental scientific problem is presented. This concept, which was initially developed on the basis of experiments using the relatively uncomplicated plant tumor systems, now appears applicable to animal and human tumors as well. Evidence is provided to show that the tumor problem is fundamentally a problem of anomalous cellular differentiation and that the heritable cellular change that underlies the tumorous state is similar to that which underlies cell specialization occurring during the normal course of development in all higher organisms. Both cellular differentiation and tumorigenesis depend for their expression on the persistent activation of select but, in part, different genes (whether normal, foreign, or both) present in the genome of a cell. Since heritable cellular changes of this kind may be induced by physical, chemical, and biological agents of the most diverse type, and since cells may remain totipotent during the time that they exhibit the tumor phenotype, the results reported here suggest that whether the normal or tumor phenotype is expressed is determined by how the genetic information present in a cell is regulated in the cell. Regulation leading to the establishment and maintenance of the tumorous state may be accomplished in different ways by the different types of oncogenic agents. Thus cancer and related neoplastic diseases appear to have a common underlying heritable cellular change in which the diverse manifestations of the tumorous state commonly observed would simply reflect different expressions of this heritable cellular change.

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