作者: Damiano Fantini , Roland Seiler , Joshua J. Meeks
DOI: 10.1016/J.UROLONC.2018.09.017
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摘要: Abstract Background Bladder cancer is the fifth most common in United States and smoking largest known risk factor. Tobacco-derived carcinogens may induce accumulation of somatic mutations urothelial cells, likely promote tumorigenesis. However, it still unknown whether smoking-induced bladder carcinogenesis results tumors with distinctive molecular features that can be therapeutically exploited. Methods We investigated genomic alterations human examined their association patient history. performed bioinformatic analyses looked at differences gene expression, mutations, DNA mutational signatures comparing nonsmokers, reformed smokers, current smokers. Results detected a limited set expression mutation between smokers nonsmokers. also identified specific signature enriched from This was described before has been linked to repair defects tumors, as well direct effect nitrosamine BBN murine model cancer. Conclusion showed associations status selected signatures, which could provide insights biology tumor progression.