Ki-ras mutation and p53 overexpression predict the clinical behavior of colorectal cancer: a Southwest Oncology Group study.

摘要: We assessed Ki-ras mutations by single-strand conformation polymorphism followed DNA sequencing, p53 expression immunohistochemistry, ploidy status, and S-phase fraction in 66 stage II 163 III colon cancer patients enrolled on a randomized trial of surgery observation or adjuvant levamisole 5-fluorouracil (5FU) plus (Intergroup Trial 0035) to see whether these factors were independently associated with survival differential effects therapy. A Cox proportional hazards model was used describe marker therapy interactions, adjustment for the clinical covariates affecting survival. Bonferroni account multiple testing. Mutation gene found 41% cancers poor prognosis but not III. In II, 7-year 86% versus 58% those wild type mutations. After treatment variables, hazard ratio (HR) death 4.5; 95% confidence interval (CI), 1.7-12.1 (P = 0.012). overexpression 63% favorable II. Seven-year 56% 43% no (HR, 2.2; CI, 1.3-3.6; P Aneuploidy more common than (66 47%; 0.009) related either group. The proliferative rate greater aneuploid diploid There benefit nor any subgroups defined mutational status. III, 5FU improved wild-type (76 44%; HR, 0.4; 0.2-0.8) without (64 26%; 0.3; 0.1-0.7). Adjuvant did overexpression. differ according status rate. mutation is significant risk factor absence after covariates. Exploratory analyses suggest that from levamisole, whereas do not. An independent study will be required determine response depends