Telomerase activity is commonly detected in hereditary nonpolyposis colorectal cancers.

Telomerase activity can be detected in most human cancers. These findings are consistent with the telomere hypothesis, which predicts telomerase expression after a number of mitotic divisions to prevent the progressive and catastrophic loss of telomeres. However, telomerase is not detected in a minority of colorectal cancers suggesting either alternative mechanisms of immortalization or that their telomeres have not yet shortened sufficiently to require telomerase activity. Colorectal cancers arising in patients with hereditary nonpolyposis colorectal cancer (HNPCC) were examined for telomerase activity because compared to sporadic tumors, HNPCC tumors are less likely to pass a telomere threshold as they occur in younger patients and exhibit "accelerated" progression, perhaps because of their characteristic mutator phenotypes and losses of mismatch repair. Primary, colorectal cancers, 13 in HNPCC patients, and 37 sporadic tumors (17 with mutator phenotypes) were examined for telomerase activity by the TRAP (telomeric repeat amplification protocol) assay. The majority of colorectal cancers contained detectable telomerase activity regardless of underlying phenotype (77 percent of HNPCC; 81 percent of sporadic tumors, 88 percent with mutator phenotypes and 75 percent without mutator phenotypes). Therefore, telomerase expression appears to be commonly acquired in the progression of both mutator phenotype and sporadic colorectal cancers.