Summary of the materials and methods and patients sections of the various published and unpublished studies.

UP indicates a study unpublished as of March 2012. Data for individual patients are available for the unpublished data and for Lindgren et al. paper (Table S4).All cases: both newly diagnosed cases (incident cases) and cases of recurrence or progression were studied.All FGFR3 mutation analyses were performed on DNA, except for the study by Lindgren et al. (2006), in which mutations were assessed on RNA. For TP53 mutation analysis, DNA was analysed, except for the study by Lindgren et al. (2006) and functional assays in yeast (FASAY), which were based on RNA (Ishioka et al. 1993).‡FASAY results were highly concordant with those for the sequencing of TP53 (Camplejohn et al., 2000).*The FGFR3 mutations R248C, S249C, G372C, and Y375C studied account for 95% of all bladder tumours with FGFR3 mutations.**Mutations R248C, S249C, G372C, Y375C, A393E, K652E and K652Q, K652M, K652T account for 99.57% of all tumours with FGFR3 mutations.***Mutations of exons 7, 10 and 15 of FGFR3 account for 100% of all mutated tumors.†Mutations of exons 4 to 11 of TP53 account for 98% of all mutated tumors.††Mutations of exons 2 to 11 of TP53 account for 100% of all mutated tumors.†††Mutations of exons 4 to 9 of TP53account for 98% of all mutated tumors.††††Mutations of exons 5 to 8 of TP53 account for 90% of all mutated tumors.