Purpose The genetic factors that influence bladder cancer risk remain largely unknown. Previous research has suggested that there is a strong genetic component underlying the risk of developing bladder cancer. The Wnt/β-catenin signaling pathway is a key modulator of cellular proliferation through its regulation of stem cell homeostasis. Furthermore, variants in the Wnt/β-catenin signaling pathway have been implicated in the development of other cancers leading us to believe this pathway may play a vital role in bladder cancer development. Materials and Methods A total of 230 SNPS in 40 genes in the Wnt/β-catenin signaling pathway were genotyped in 803 bladder cancer cases and 803 healthy controls. Results Twenty SNPs were nominally significant for risk. Individuals with two variants of LRP6: rs10743980 were associated with a decreased risk of bladder cancer (OR=0.76, 95% CI: 0.58–0.99, P=0.039) in the recessive model in the initial analysis and was also validated using the bladder GWAS chip (OR=0.51, 95% CI: 0.27–1.00, P=0.049) (P value for combined analysis: P=0.007). Conclusion Together, these findings implicate variants in the Wnt/β-catenin stem-cell pathway as playing a role in bladder cancer etiology.
Background Postprandial glucose (PPG) and insulin responses play a role in carcinogenesis. We evaluated the association between dietary glycemic index (GI) and glycemic load (GL), markers of carbohydrate intake and PPG, and lung cancer risk in non-Hispanic whites. Methods GL and GI were assessed among 1,905 newly diagnosed lung cancer cases recruited from the University of Texas MD Anderson Cancer Center in Houston, Texas and 2,413 healthy controls recruited at Kelsey-Seybold Clinics in Houston. We assessed associations between quintiles of GI/GL and lung cancer risk and effect modification by various risk factors. Odds ratios (ORs) and 95% confidence intervals (CI) were estimated using multivariable logistic regression. Results We observed a significant association between GI (5th vs 1st quintile (Q)) OR = 1.49, 95% CI: 1.21–1.83, P-trend <0.001) and lung cancer risk and GIac (5th vs 1st Q OR = 1.48, 95% CI: 1.20–1.81, P-trend =0.001) and lung cancer risk. We observed a more pronounced association between GI and lung cancer risk among never smokers, (5th vs 1st Q OR=2.25, 95% CI: 1.42–3.57), squamous cell carcinomas (SCCs) (5th vs 1st Q OR=1.92, 95% CI: 1.30–2.83) and those with less than 12 years of education (5th vs 1st Q OR=1.75, 95% CI: 1.19–2.58, P-interaction = 0.02). Conclusion This study suggests that dietary glycemic index and other lung cancer risk factors may jointly and independently influence lung cancer etiology. Impact Understanding the role of glycemic index in lung cancer could inform prevention strategies and elucidate biological pathways related to lung cancer risk.
QOL after diagnosis is a significant prognostic indicator for patients with PDAC. Multiple factors determine QOL, suggesting possible means of intervention to improve QOL and outcomes of PDAC patients.
Patient reported health-related quality of life (QOL) is a major component of the overall well-being of cancer patients, with links to prognosis. In 6,420 lung cancer patients, we identified patient characteristics and genetic determinants of QOL. Patient responses from the SF-12 questionnaire was used to calculate normalized Physical Component Summary (PCS) and Mental Component Summary (MCS) scores. Further, we analyzed 218 single nucleotide polymorphisms (SNPs) in the p38 MAPK signaling pathway, a key mediator of response to cellular and environmental stress, as genetic determinants of QOL in a subset of the study population (N = 641). Trends among demographic factors for mean PCS and MCS included smoking status (PCS Ptrend < 0.001, MCS Ptrend < 0.001) and education (PCS Ptrend < 0.001, MCS Ptrend < 0.001). Similar relationships were seen for MCS. The homozygous rare genotype of MEF2B: rs2040562 showed an increased risk of a poor MCS (OR: 3.06, 95% CI: 1.05–8.92, P = 0.041). Finally, survival analysis showed that a low PCS or a MCS was associated with increased risks of five-year mortality (HR = 1.63, 95% CI: 1.51–1.77, HR = 1.23, 95% CI: 1.16–1.32, respectively) and there was a significant reduction in median survival time (Plog-rank < 0.001). These findings suggest that multiple factors contribute to QOL in lung cancer patients, and baseline QOL can impact survival.
Reducing lung cancer risk by modifying diet is highly desirable. We investigated whether different U.S. dietary patterns were associated with lung cancer risk. Dietary patterns were derived using exploratory factor analysis for 2139 non-small cell lung cancer (NSCLC) cases and 2163 frequency-matched controls. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). Highest adherence (highest vs. lowest quintile) to the “Tex-Mex”, “fruits and vegetables”, and “American/Western” patterns was associated with a 55% reduced (OR = 0.45; 95% CI = 0.37–0.56; P < 0.001), 32% reduced (OR = 0.68; 95% CI = 0.55–0.85; P = 0.001), and 45% increased (OR = 1.45; 95% CI = 1.18–1.78; P < 0.001) risk of lung cancer, respectively. The effects were stronger for squamous cell carcinoma and ever smokers for the “fruits and vegetables” pattern, and stronger for other non-small cell lung cancer and never smokers for the “American/Western” pattern. Among six genome-wide association (GWA) studies-identified lung cancer susceptibility loci assessed, a variant (rs2808630) of the C-reactive protein gene modified the associations for the “fruits and vegetables” (P for interaction = 0.03) and “American/Western” (P for interaction = 0.02) patterns. Our study first showed that the “Tex-Mex” dietary pattern was associated with a reduced lung cancer risk. Also, the “fruits and vegetables” and “American/Western” patterns affected lung cancer risk, and the effects were further modified by host genetic background.
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