Dominant oncogenes and recessive tumor suppressor genes are widely imp
licated in the pathogenesis of human neoplasia. Several recent experim
ental findings suggested that an oncogene and a tumor suppressor gene
can share a similar ontogeny from the parental normal 'in vivo' gene.
At least three mechanisms have been demonstrated to be responsible for
this ambivalent expression: the mutations located in different region
s of the gene, transcriptional and post-transcriptional events (especi
ally alternative splicing) and cell- and/or time-dependent control of
gene expression. There are also evolutionary explanations for the exis
tence of such genes with ambivalent expression.