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The incidence of metachronous colorectal cancer has most often been reported as a crude rate: second cancers/index cancers. The reported incidence varies between 0.5 percent and 3.6 percent. However, these calculations do not take into account factors such as length of survival and length of follow-up. The cumulative incidence more accurately reflects the risk for developing a metachronous cancer and was determined in a retrospective analysis of 5,476 patients who were diagnosed with colon or rectal cancer between 1965 and 1985. The cumulative probability was calculated by determining the number of patients developing a metachronous colon cancer vs. the number remaining at risk at that point in time. The calculated annual incidence for metachronous tumors was 0.35 percent per year. The cumulative incidence at 18 years was 6.3 percent. Analysis also demonstrated that metachronous cancers were diagnosed at earlier stages than were index cancers (P = 0.03). Subgroup analysis was performed on patients diagnosed with metachronous cancer before and after 1980. There was a difference in the incidence of metachronous cancers between these two groups (P = 0.04).

The presence of rectal cancer should not preclude the diagnosis of HNPCC, because the incidence of rectal cancer in MSH2 was comparable with that in the general population. Phenotypic variations, including the preponderance of extracolonic cancers in MSH2 patients, did not result in survival differences between genotypic subgroups. These phenotypic features of HNPCC genotypes may have clinical significance in the design of specific screening, surveillance, and follow-up for affected individuals.

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We report the first evidence of increased levels of the retinoblastoma (Rb) message in a majority of colorectal cancers when compared with normal mucosa. Southern blot analysis showed an increase in Rb gene copy number in at least 28% of colorectal carcinomas relative to normal mucosa. These results plus previous reports of nonrandom chromosome 13 gains in approximately 50% of colorectal cancers suggest that an increase in Rb gene copy number occurs frequently in these tumors. Possible mechanisms pertaining to overexpression of the Rb gene are discussed in relation to its role as a recessive cancer gene.