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Smoking is a major risk factor for urothelial cell carcinoma of the bladder (UCC). Mutations in theFGFR3andTP53genes have been shown to define two distinct pathways in superficial papillary and invasive UCC disease, respectively. We investigated the relationship between smoking and these mutations by means of denaturing high performance liquid chromatography and sequencing for 110 primary UCC of the bladder. This study included 48 current smokers, 31 ex-smokers and 31 non-smokers. Thirty-five of the tumors were stage pTa, 40 pT1 and 35 ≥pT2. Fourteen of the tumors were grade 1, 37 were grade 2 and 59 grade 3. Smoking was associated with high stage (P= 0.03) and high grade tumors (P= 0.006). Twenty-two of the 110 tumors studied harboredTP53mutations (20%) and 43 harboredFGFR3mutations (39%). Odds ratios (OR) were higher forTP53mutations in current smokers [OR, 2.25; 95% confidence interval (95% CI), 0.65–7.75] and ex-smokers (OR, 1.62; 95% CI, 0.41–6.42) than in non-smokers. DoubleTP53mutations and the A:T→G:CTP53mutation pattern was found only in current smokers. Patients with theFGFR3  wild-type/TP53  mutatedgenotype had significantly higher levels of tobacco consumption, as measured in pack-years (P= 0.01). Smoking influenced neither the frequency nor the pattern ofFGFR3mutations. Our results suggest that smoking is associated with invasive and high grade UCCs, at initial presentation, and influencedTP53or the molecular pathway defined by these mutations. In contrast,FGFR3mutations are not affected by smoking and probably result from endogenous alterations. These data have potential implications for clinical management and prevention strategies.

carcinogenesis

Mutations in               TP53              , but not               FGFR3              , in urothelial cell carcinoma of the bladder are influenced by smoking: contribution of exogenous versus endogenous carcinogens