The role of the oncogene c‐myc in sporadic large bowel cancer and familial polyposis coli

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Abstract
The human myc gene is homologous to the v‐myc gene, which was discovered in the avian oncogenic retrovirus MC29. Abnormally high expression of the cellular oncogenes is suspected to be involved in nonviral carcinogenesis. This article reviews the evidence that elevated expression of the human myc gene is involved in sporadic colon carcinoma and familial polyposis coli. The abundance of myc RNA and protein is frequently higher in colorectal cancer than in normal mucosa. The mechanism of this altered expression is obscure because the structure and quantity of myc DNA are very rarely disturbed. The COL0320 cell line is discussed as one unusual example of myc DNA rearrangement and amplification. There is a correlation between tumor‐specific elevated myc RNA level and location in the bowel; tumors distal to the transverse colon are more likely to have elevated myc expression. The site distribution of unselected colorectal malignancies with an elevated myc RNA level is similar to the site distribution of familial polyposis coli tumors. With this observation it is suggested that elevated myc RNA may be a marker of a distinct type of colorectal cancer that involves the same genetic events as precede familial polyposis coli cancer.