The association between aberrations of the human genome and the develo
pment of cancer is well established. Gene imprinting, defined as gene
expression based on the gamete of origin, has previously been shown to
be involved in this process by the loss of tumor suppressor gene regu
lation. We suggest that the activation of imprinted proto-oncogenes an
d growth factors may also play a vital role in tumorigenisis. Mechanis
tically, this can occur when the gene is removed from its imprinted se
quence area, thus escaping repression. Synteny between the human and m
ouse genome provides the opportunity for targeted studies of imprinted
genes suspected to be involved in cancer.