Towards an animal model for retinoblastoma

Abstract

Within the past decade a large repertoire of cellular oncogenes has been implicated in the genesis of many types of cancers. These oncogenes all function to promote the neoplastic growth of cells in which they act. Indeed, they all appear to derive from normal cell genes, proto-oncogenes, which act to stimulate normal cell proliferation. During this period, evidence has also been presented to suggest that elements that normally function to inhibit cell proliferation are also playing a role in the process of carcinogenesis. For instance, in a number of distinct types of tumors it was found that genetic material from specific chromosomal loci was absent in tumor DNAs, but present in the adjacent normal cell DNA. This indicates that loss of genetic material represents at least one step in the pathogenesis of these tumors. It seems likely that the normal function of the genes that are lost in these tumors is to restrain the growth of cells from which the tumors originate. For this reason such genes have been named recessive oncogenes or anti-oncogenes.