{'fraction_non_alphanumeric': 0.017464424320827943, 'fraction_numerical': 0.00129366106080207, 'mean_word_length': 6.546341463414634, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Genetic susceptibility to bladder cancer with an emphasis on gene–gene and gene–environmental interactions

Purpose of review The present article reviews recent reports on molecular epidemiological studies for exploring susceptibility genes for bladder cancer, with particular focus on gene–gene and gene–environmental interactions. Recent findings Recent large case–control studies and meta-analyses have confirmed that N-acetyl transferase2 slow acetylator and glutathione S-transferase Mu null genotype were modest susceptibility factors for bladder cancer, with probable interactions between N-acetyl transferase2 slow acetylator and smoking. Several interesting studies using a multigenic pathway-based genotyping approach and novel statistical tools showed significant interactions among potential functional single nucleotide polymorphisms in DNA repair pathway genes and smoking and gene–diet interaction; however, the resultant interactions warrant validation. Summary Previous studies using a candidate gene approach have not only identified a few bladder cancer susceptibility loci but also produced a large number of false positive results. A multigenic pathway-based approach may identify gene–gene and gene–environment interactions and increase predictive power. Several statistical tools have been applied to identify gene–gene and gene–environment interactions, but future efforts should be directed toward integrating results obtained from different statistical tools and validating resultant interactions from different studies.