Genetic Susceptibility to Bladder Cancer Risk and Outcome

Abstract

Bladder cancer is an excellent model for studying genetic susceptibility and gene–environment interaction in cancer etiology. The candidate gene approach found NAT2 slow acetylator and GSTM1-null genotypes to be bladder cancer susceptibility loci and also demonstrated interactions between these two genotypes and smoking in modulating bladder cancer risk. Recent genome-wide association studies identified at least eight novel genetic susceptibility loci for bladder cancer. Genetic determinants of clinical outcomes have been inconclusive. The future directions are to identify more genetic susceptibility loci for bladder cancer risk and outcome through a genome-wide association study approach, identify the causal genes and variants, study the biological mechanisms underlying the association between the causal variants and bladder cancer risk, detect gene–environment interactions and incorporate genetic knowledge into clinically applicable risk prediction models to benefit patients and public health.

KEYWORDS::

• BCG
• bladder cancer
• candidate gene approach
• genetic susceptibility
• genome-wide association study
• single-nucleotide polymorphism

Financial & competing interests disclosure

This work was partially supported by NIH grants U01 CA 127615 (Xifeng Wu), R01 CA 74880 (Xifeng Wu), P50 CA91846 (Xifeng Wu) and R01 CA CA131335 (Jian Gu) from the National Cancer Institute and funds from the University of Texas MD Anderson Cancer Center Research Trust (Xifeng Wu). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was partially supported by NIH grants U01 CA 127615 (Xifeng Wu), R01 CA 74880 (Xifeng Wu), P50 CA91846 (Xifeng Wu) and R01 CA CA131335 (Jian Gu) from the National Cancer Institute and funds from the University of Texas MD Anderson Cancer Center Research Trust (Xifeng Wu). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.