Replication error phenotype, clinicopathological variables, and patient outcome in Dukes' B stage II (T3,N0,M0) colorectal cancer

Aims--To examine the relation between the replication error (RER) phenotype and other genetic events, clinical features, Dukes' B stage II (T3,NO,MO) colorectal cancer. Methods--RER phenotype was investigated in 159 patients by PCR amplificatio n of microsatellite marker loci on chromoparaffin wax embedded tissue. Results--Of 159 colorectal cancers studied, 22 (14%) were RER+ while 137 (8 6%) were RER- for two or more loci. RER+ tumours were more commonly located in the right colon, tended to be larger than poorly differentiated than RE R- cancers. No significant associations were seen between RER status and th e presence of a long term survival and other genetic events, clinical featu res, and long term survival in patients with Dukes' B stage II (T3,N0,M0) c olorectal of microsatellite marker loci on chromosomes 5q, 17p, 17q, and 18 q from tumour DNA extracted from archival tissue. Data on activating c-Ki-r as mutations were available from a previous study. Immunohistochemical dete ction of p53 and c-erbB-2 expression was performed on paraffin wax embedded tissue, the right colon, tended to be larger than RER- tumours, and were m ore often poorly differentiated than RER- cancers, between RER status and t he presence of a mutant c-Ki-ras gene, or between RER status and p53, c-erb B-2, or c-myc gene expression. Univariate survival analysis showed that out come was similar in RER+ and RER- cases. Multivariate survival analysis sho wed that the relative risk of death for patients with RER+ cancers was 0.95 that of patients with RER- cancers. Conclusions--The results suggest that, while the RER phenotype may be assoc iated with some differences in tumour pathology (site, size, differentiatio n), it is not associated with the genetic alterations studied or with signi ficant differences in long term survival.