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Objective: The International Agency for Research on Cancer has classified 13 infectious agents as carcinogenic or probably carcinogenic to humans. We aimed to estimate the percentage (ie, population-attributable fraction) and number of incident cancer cases in Texas in 2015 that were attributable to oncogenic infections, overall and by race/ethnicity. Methods: We calculated population-attributable fractions for cancers attributable to human papillomavirus (HPV), Helicobacter pylori, hepatitis C virus (HCV), hepatitis B virus (HBV), and human herpesvirus 8 (HHV-8) infections using prevalence estimates from National Health and Nutrition Examination Survey laboratory data and relative risks associated with infection from previous epidemiological studies. The Texas Cancer Registry provided cancer incidence data. Results: We estimated that 3603 excess cancer cases, or 3.5% of all cancers diagnosed in 2015, among adults aged ≥25 in Texas were attributable to oncogenic infections. Hispanic adults had the highest proportion of cancer cases attributable to infections (5.6%), followed by non-Hispanic Black (5.4%) and non-Hispanic White (2.3%) adults. HPV infection caused the highest proportion of all cancer cases (1.8%) compared with other oncogenic infections (HCV, 0.8%; H pylori, 0.5%; HBV, 0.3%; HHV-8, 0.1%). Hispanic adults had the highest proportions of all cancers caused by HPV infection (2.6%) and H pylori (1.1%), and non-Hispanic Black adults had the highest proportions of all cancers caused by HCV infection (1.7%), HBV infection (0.7%), and HHV-8 (0.3%). Conclusion: Preventable oncogenic infections contribute to cancer incidence in Texas and may affect racial/ethnic minority groups disproportionately. Infection control and prevention should be stressed as an important component of cancer prevention. [ABSTRACT FROM AUTHOR]

Background: Acid-suppressant medications, including proton pump inhibitors (PPIs) and H2 receptor antagonists (H2RAs), are frequently prescribed and have been linked to increased risk of some gastrointestinal cancers.Aims: We examined whether post-diagnosis use of PPIs/H2RAs is associated with the risk of mortality in gastrointestinal cancer patients.Methods: We used data from patients with esophageal cancer, gastric cancer, or hepatocellular carcinomas (HCCs) in the national VA Central Cancer Registry diagnosed between 2002 and 2016. We identified PPI/H2RA prescriptions that were filled before and after cancer diagnosis and used time-dependent Cox regression models to calculate adjusted hazard ratios (HRs) and 95% CIs for mortality risk. We used a time-varying exposure to avoid immortal-time bias and a 3-month lag to reduce reverse causation. A sensitivity analysis was conducted varying the lag duration between the date of cancer diagnosis and the start of follow-up.Results: PPIs were used by the majority (54% post-diagnosis use) of patients. We found no association between post-diagnosis PPI use and cancer-specific mortality in esophageal adenocarcinoma (HR 0.93; 95% CI 0.84-1.02), esophageal squamous cell carcinoma (HR 0.99; 95% CI 0.87-1.12), or gastric cardia cancer (HR 1.04; 95% CI 0.89-1.22) patients. Post-diagnosis PPI use was, however, associated with the increased risk of cancer-specific mortality for patients with gastric non-cardia cancer (HR 1.50; 95% CI 1.29-1.74) and HCC (HR 1.31; 95% CI 1.23-1.40). The results were similar for associations with post-diagnosis use of H2RAs. There was no association with pre-diagnosis PPI/H2RA use.Conclusion: Post-diagnosis PPI/H2RA use was associated with the increased mortality in gastric non-cardia cancer and HCC patients. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori infection is an established causal factor for non-cardia gastric cancer. H. pylori negative gastric cancer prevalence among US patients is unclear.Methods: This retrospective cohort study examined H. pylori prevalence among consecutive patients with incident non-cardia gastric adenocarcinoma at the Houston VA Hospital (11/2007-10/2018). H. pylori positivity was defined by H. pylori on histopathology, positive antibody serology, stool antigen, or urea breath testing. We examined for trends in H. pylori negative gastric cancer based on year of diagnosis. Associations between histopathologic and cancer-related outcomes with H. pylori positivity were determined using regression models.Results: Of 91 patients with gastric adenocarcinoma, most were men (N = 87, 95.6%), black (N = 47, 51.6%), with mean age at diagnosis of 68.0 years (SD 10.8). In addition to gastric cancer biopsy histopathology, 74 patients (81.3%) had ≥ 1 testing for H. pylori, including antibody serology (n = 34), non-cancer gastric biopsy histopathology (n = 63), or stool antigen (n = 1). The overall prevalence of H. pylori infection was 38.5% and 45.9% among patients with ≥ 2 H. pylori tests. The proportions of H. pylori positive gastric cancer decreased from 50.0% (2007-2010) to 43.4% (2011-2014) and 29.3% (2015-2018) (p = 0.096). Active/acute gastritis (adjOR 3.74), atrophic gastritis (adjOR 15.30), and gastric intestinal metaplasia (adjOR 3.65) were associated with H. pylori positive gastric cancer.Discussion: The prevalence of H. pylori infection among patients with non-cardia gastric adenocarcinoma is relatively low (38.5-45.9%) and decreasing over time. This finding suggests there may be other important causal factors apart from H. pylori for gastric adenocarcinoma. [ABSTRACT FROM AUTHOR]

Background Pancreatic ductal adenocarcinoma is a major contributor to cancer-related mortality in the United States. We aimed to investigate trends in incidence rates from all 50 states from 2001 to 2016, overall and by race, sex, and state and using age-period-cohort analyses. Methods Age-adjusted incidence rates and trends in adults aged 35 years and older were calculated using data from the US Cancer Statistics registry. We used joinpoint regression to compute annual percent changes (APC) and average annual percent changes. We also analyzed incidence trends by age groups and birth cohorts through age-period-cohort modeling. Results Age-standardized incidence rates increased by 1.23% (95% confidence interval [CI] = 0.92% to 1.54%) annually between 2001 and 2008 but were stable between 2008 and 2016 (APC = 0.11%, 95% CI = -0.13% to 0.35%). APCs and inflection points were no different for men and women. Rates increased statistically significantly among non-Hispanic whites (NHW) and non-Hispanic blacks between 2001 and 2007 and between 2001 and 2008, respectively, but, in later years, rates increased slowly among NHWs (APC = 0.36%, 95% CI = 0.12% to 0.60%), and were stable among non-Hispanic blacks (APC = -0.40%, 95% CI = -0.89% to 0.10%). The number of states with age-standardized incidence rates no less than 20.4 per 100 000 increased from 16 in 2001–2003 to 40 by 2015–2016. We found a strong birth cohort effect in both men and women and increasing rates among successive birth cohorts of NHWs. Conclusions The incidence of pancreatic ductal adenocarcinoma has consistently increased in the United States, albeit at slower rates recently. We observed notable increases among NHWs and in some states in the central and southern part of the country. [ABSTRACT FROM AUTHOR]

Background: The United States has large regional variation in primary prevention campaigns for skin cancer. We collected data from all 50 states to examine changes in melanoma incidence and performed age-period-cohort analyses to describe the simultaneous effects of age, period, and cohort on incidence rates.Methods: Annual melanoma incidence rates for non-Hispanic whites from 2001 to 2015 were extracted from the US Cancer Statistics registry. Secular trends were examined overall and by sex and state. We used joinpoint regression to compute annual percent change and average annual percent change and corresponding 95% confidence intervals (CIs). We also analyzed incidence trends by 5-year age group and birth cohort using incidence rate ratios and age-period-cohort modeling.Results: Melanoma incidence increased from 20.7 per 100 000 (95% CI = 20.5 to 20.9) in 2001 to 28.2 per 100 000 (95% CI = 28.0 to 28.5) in 2015, increasing by 3.90% (95% CI = 2.36% to 5.48%) annually between 2001 and 2005 and 1.68% (95% CI = 1.37% to 1.99%) annually from 2005 through 2015. The average annual percent change in melanoma incidence rates were similar for men (2.34%, 95% CI = 1.91 to 2.78) and women (2.25%, 95% CI = 1.60 to 2.91). Age-specific relative risk by birth cohort increased from circa 1921 to 1981 before decreasing. Compared with adults born circa 1956, those born circa 1991 had lower melanoma risk (incidence rate ratio  = 0.85; 95% CI = 0.77 to 0.94). Geographic variation was observed; some states still have melanoma rates trending upwards in all birth cohorts.Conclusions: The continued increase in melanoma incidence among non-Hispanic whites, particularly in states where rates continue to rise among recent and current birth cohorts, underscores the need for increased public health campaigns aimed at reducing sun exposure. [ABSTRACT FROM AUTHOR]

Epidemiological studies of statin use and liver cancer risk have produced conflicting results. We examined the association between statin use and risk of primary liver cancer in two large independent study populations taking account of important covariates and main indications of statins such as high cholesterol and chronic liver disease. We performed a nested case–control study within the Scottish Primary Care Clinical Informatics Unit (PCCIU) database. Five controls were matched to cases with primary liver cancer and we used conditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with statin use. We also conducted a prospective cohort study within the UK Biobank using self‐reported statin use and cancer‐registry recorded primary liver cancer outcomes. Cox regression was used to calculate hazard ratios (HRs) and 95% CIs. In the PCCIU case–control analysis, 434 liver cancer cases were matched to 2,103 controls. In the UK Biobank cohort, 182 out of 475,768 participants developed incident liver cancer. Statin use was associated with 39% lower risk of liver cancer in the PCCIU (adjusted OR 0.61, 95% CI 0.43–0.87). When we examined specific subtypes of liver cancer in the UK Biobank, statin use was associated with lower risk of hepatocellular carcinoma (HCC; adjusted HR, 0.48; 95% CI, 0.24–0.94) but not intrahepatic bile duct carcinoma (IBDC; adjusted HR, 1.09; 95% CI, 0.45–2.64). In conclusion, we found a consistent inverse relationship between statin use and risk of primary liver cancer which was only seen for HCC but not IBDC. What's new? Does statin use affect the risk of liver cancer? Previous studies have been contradictory, perhaps due to their failure to adjust for covariates such as high cholesterol and chronic liver disease. In this analysis of two large, independent studies, the authors found that the risk of hepatocellular carcinoma was cut by almost half with statin use. The same did not hold true for intrahepatic bile duct carcinoma. With liver‐cancer incidence and mortality rising worldwide, these results may offer one avenue for improved prevention. [ABSTRACT FROM AUTHOR]

Background: Incidence rates for hepatocellular carcinoma (HCC) vary considerably by age, sex, and race/ethnicity. We assessed whether the underlying reasons for variations in HCC among subgroups of the population by age, sex, race/ethnicity, and birth cohort are uniform or whether they interact with one another or have changed over time. Methods: Data were from the U.S. Cancer Statistics registry. We assessed annual trends within population subgroups and examined for secular trends in the male-to-female ratio for HCC incidence. We used joinpoint regression to compute annual percent change and average annual percent change (AAPC) and corresponding 95% confidence intervals (CI). We also used age-period-cohort models to disentangle period and cohort effects. Results: Between 2001 and 2015, HCC rates increased in men and women =50 years, remained stable among women ages 40 to 49 years, but decreased among males ages 40 to 44 years (AAPC = -2.47%; 95% CI, -3.15% to -1.80%) and 45 to 49 years (AAPC = -3.49%; 95% CI, -4.78% to -2.17%). As a result, the male-to-female incidence rate ratio (IRR) among persons aged <50 years decreased from 4.63 in 2001 to 2.42 in 2015 but remained stable over time among persons aged =50 years. HCC rates were lower among successive cohorts of males born after circa 1956, whereas HCC rates among females born circa 1991 were higher than those among females born circa 1956 (IRR = 1.67; 95% CI, 1.05-2.65). Conclusions: As a result of decreasing incidence among males aged <50 years and strong cohort effect, the epidemiology of HCC is changing from a disease with striking male predominance to one with less male predominance. [ABSTRACT FROM AUTHOR]

Texas has the highest rates of hepatocellular carcinoma (HCC) in the United States. Exposure to toxicants may play a role in liver disease. Several mechanisms of arsenic carcinogenesis have been proposed, however, the evidence in human populations is limited to associations between HCC and ingestion of arsenic-contaminated drinking water. Through an ecological study, we examined associations between ambient arsenic and HCC incidence rates. Primary outcome was HCC incidence rates based on Texas Cancer Registry (TCR) data. Primary exposure of interest was the simulated census-tract level estimate of arsenic exposure concentration (EC) from the U.S. Environmental Protection Agency 2011 National Air Toxics Assessment (NATA). We analyzed the association between the arsenic EC and HCC using the negative binomial Poisson regression model separately for six study groups that were based on race/ethnicity and sex. We adjusted the main analyses for selected characteristics. Texas has 5265 census tracts and TCR reported 18,235 new ≥20 years old HCC diagnoses between 2007 and 2015. We observed significant differences along racial-ethnic and sex groups while accounting for socioeconomic deprivation, urban/rural residency, and senior residents' health insurance status. Census tracts with the highest arsenic EC had elevated rates of HCC among NH black men (Quintile 5 vs. Quintile 1: IRR = 2.18, 95% CI: 1.66–2.86), NH black women (Quintile 5 vs. Quintile 1: IRR = 1.72, 95% CI: 1.33–2.22) and NH white men (Quintile 5 vs. Quintile 1: IRR = 1.38, 95% CI: 1.24–1.54). The associations in the remaining study groups were either inconsistent or attenuated. Our finding suggests a potential inhalation pathway for the Arsenic-HCC association; however, the ecological nature of our study precludes the interpretation of a causal link between exposure to aerial arsenic and HCC. This finding needs to be further examined in cohort studies. • Arsenic in the air may contribute to increase in liver cancer diagnosis. • Neighborhood concentration of arsenic in air varies across racial-ethnic groups. • Neighborhoods with highest arsenic concentration had elevated rates of HCC. • Disparity along racial-ethnic and sex lines for the arsenic-HCC association. • A potential inhalation pathway for the Arsenic-HCC association. [ABSTRACT FROM AUTHOR]

The available risk stratification indices for hepatocellular cancer (HCC) have limited applicability. We developed and externally validated an HCC risk stratification index in U.S. cohorts of patients with cirrhosis. We used data from 2 prospective U.S. cohorts to develop the risk index. Patients with cirrhosis were enrolled from 8 centers and followed until development of HCC, death, or December 31, 2021. We identified an optimal set of predictors with the highest discriminatory ability (C-index) for HCC. The predictors were refit using competing risk regression and its predictive performance was evaluated using the area under the receiver-operating characteristic curve (AUROC). External validation was performed in a cohort of 21,550 patients with cirrhosis seen in the U.S Veterans Affairs system between 2018 and 2019 with follow-up through 2021. We developed the model in 2431 patients (mean age 60 years, 31% women, 24% cured hepatitis C, 16% alcoholic liver disease, and 29% nonalcoholic fatty liver disease). The selected model had a C-index of 0.77 (95% confidence interval [CI], 0.73–0.81), and the predictors were age, sex, smoking, alcohol use, body mass index, etiology, α-fetoprotein, albumin, alanine aminotransferase, and platelet levels. The AUROCs were 0.75 (95% CI, 0.65–0.85) at 1 year and 0.77 (95% CI, 0.71–0.83) at 2 years, and the model was well calibrated. In the external validation cohort, the AUROC at 2 years was 0.70 with excellent calibration. The risk index, including objective and routinely available risk factors, can differentiate patients with cirrhosis who will develop HCC and help guide discussions regarding HCC surveillance and prevention. Future studies are needed for additional external validation and refinement of risk stratification. [ABSTRACT FROM AUTHOR]