RT Journal Article SR Electronic T1 Replication error phenotype, clinicopathological variables, and patient outcome in Dukes' B stage II (T3,N0,M0) colorectal cancer JF Gut JO Gut FD BMJ Publishing Group Ltd and British Society of Gastroenterology SP 200 OP 204 DO 10.1136/gut.46.2.200 VO 46 IS 2 A1 B Curran A1 K Lenehan A1 H Mulcahy A1 O Tighe A1 M A Bennett A1 E W Kay A1 D P O'Donoghue A1 M Leader A1 D T Croke YR 2000 UL http://gut.bmj.com/content/46/2/200.abstract AB AIMS To examine the relation between the replication error (RER) phenotype and other genetic events, clinical features, and long term survival in patients with Dukes' B stage II (T3,N0,M0) colorectal cancer. METHODS RER phenotype was investigated in 159 patients by PCR amplification of microsatellite marker loci on chromosomes 5q, 17p, 17q, and 18q from tumour DNA extracted from archival tissue. Data on activating c-Ki-ras mutations were available from a previous study. Immunohistochemical detection of p53 and c-erbB-2 expression was performed on paraffin wax embedded tissue. RESULTS Of 159 colorectal cancers studied, 22 (14%) were RER+ while 137 (86%) were RER− for two or more loci. RER+ tumours were more commonly located in the right colon, tended to be larger than RER− tumours, and were more often poorly differentiated than RER− cancers. No significant associations were seen between RER status and the presence of a mutant c-Ki-ras gene, or between RER status and p53, c-erbB-2, or c-myc gene expression. Univariate survival analysis showed that outcome was similar in RER+ and RER− cases. Multivariate survival analysis showed 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 associated with some differences in tumour pathology (site, size, differentiation), it is not associated with the genetic alterations studied or with significant differences in long term survival.