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Background: Mortality from cervical cancer has declined steadily in the United States over the past several decades due to widespread screening for precancerous and early-stage cervical cancer (ECC), which are significantly easier to treat compared with late-stage cervical cancer (LCC). Unequal screening access continues to cause significant racial/ethnic disparities in cervical cancer diagnosis stage. This study examined the underlying role of neighborhood-level socioeconomic disadvantage as a potential mediator of the association between race/ethnicity and cervical cancer diagnosis stage. Methods: We analyzed Texas Cancer Registry data for cervical cancer cases diagnosed among women ages 18 or older from 2010 to 2018. We performed causal mediation analyses of the association between race/ethnicity and cervical cancer stage at diagnosis mediated by neighborhood-level socioeconomic disadvantage. Results: Of the 9,192 women with cervical cancer, 4,720 (51.3%) had LCC at diagnosis. Compared with non-Hispanic white (NHW) women (106.13, standard deviation (SD) = 13.32), non-Hispanic Black (NHB; 111.46, SD = 9.55) and Hispanic (112.32, SD = 9.42) women had higher area deprivation index (ADI) and had greater odds of LCC diagnosis [total effects: adjusted odds ratios (AOR) = 1.29 (95% CI, 1.11–1.46) and AOR 1.14 (95% CI, 1.03–1.25), respectively]. Approximately 34.7% and 71.6% of the disparity in LCC diagnosis were attributable to higher neighborhood socioeconomic disadvantage among NHB and Hispanic women, respectively. Conclusions: LCC disparity varied by race/ethnicity and was partly attributable to neighborhood disadvantage. The disparity among Hispanic women due to neighborhood deprivation was twice as high among NHB women. Impact: Findings may be used to develop targeted race- and place-specific interventions to improve cancer care equity.

It is unclear whether obesity confers increased risk of non-cardia gastric adenocarcinoma and its precursor, gastric intestinal metaplasia. Here, we examined whether various dimensions of adiposity independently predispose to the development of non-cardia gastric intestinal metaplasia.We compared data from 409 non-cardia gastric intestinal metaplasia cases and 1748 controls without any gastric intestinal metaplasia from a cross-sectional study at the VA Medical Center in Houston, Texas. Participants completed standardized questionnaires, underwent anthropometric measurements, and underwent a study endoscopy with gastric mapping biopsies. Non-cardia gastric intestinal metaplasia cases included participants with intestinal metaplasia on any non-cardia gastric biopsy. We calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) using logistic regression models.Increasing body mass index (BMI) was not associated with risk of non-cardia gastric intestinal metaplasia (per unit BMI adjusted OR, 0.98; 95% CI, 0.96-1.00). Similarly, we found no associations with increase in waist circumference (per 10-cm increase adjusted OR, 0.94; 95% CI, 0.87-1.03) and waist-to-hip ratio (WHR) (per unit WHR adjusted OR, 2.34; 95% CI, 0.37-14.7). However, there was a significant inverse association with gastric intestinal metaplasia and increasing hip circumference, reflecting gluteofemoral obesity (per 10-cm increase adjusted OR, 0.89; 95% CI, 0.80-0.98). The inverse association was observed for both extensive and focal gastric intestinal metaplasia.The independent dimensions of adiposity (BMI, waist circumference) are not associated with increased risk of non-cardia gastric intestinal metaplasia. The inverse association between gluteofemoral obesity and risk of gastric intestinal metaplasia warrants additional study.

Background: Diet is associated with metabolic (dysfunction)-associated fatty liver disease (MAFLD), but the dietary composition associated with MAFLD risk has not been well-examined. Aim: The purpose of this study was to assess the association of two healthy eating indices with the presence and severity of MAFLD in a sample of Veterans in a primary care setting. Methods: This was a single center cross-sectional study using a random stratified sample of Veterans enrolled in primary care. Participants underwent a Fibroscan and completed an interviewer-administered Diet History Questionnaire II from which we calculated the Healthy Eating Index-2015 and Alternate Mediterranean Diet Score. We used multivariable logistic regression models to assess associations of dietary quality with MAFLD. Results: We analyzed data from 187 participants, 53.5% of whom were female. On average, participants were 50.2 years of age (SD, 12.3 years) with an average BMI of 31.7 kg/m2. MAFLD was detected in 78 (42%) and at least moderate fibrosis in 12 (6%) participants. We found that the Alternate Mediterranean Diet Score was inversely associated with MAFLD (adjusted OR = 0.85, 95%CI 0.72–1.00), but controlling for BMI and total energy intake attenuated the association (adjusted OR = 0.92, 95%CI 0.74–1.15). We found no statistically significant associations between the Healthy Eating Index-2015 and MAFLD or advanced fibrosis. Discussion: We found that the Alternate Mediterranean Diet Score was significantly associated with lower MAFLD risk in Veterans; however, the association was mediated by BMI and total energy intake. A Mediterranean-style diet could potentially help reduce the risk of MAFLD, particularly if it helps control total energy intake and weight.

PDF file - 80K, Final multivariate logistic model for dysplastic Barrett's esophagus

Supplementary Tables S1-3. Supplementary Table S1 Description of the characteristics by study. Supplementary Table S2 Associations between confounders and body mass index and the weighted genetic risk score among controls. Supplementary Table S3 Odds ratios (OR) and 95% confidence intervals (CI) for the association between a 1-unit increase in the weighted genetic risk score (the instrumental variable [IV]) and risk of colorectal cancer.

Background: High body mass index (BMI) is consistently linked to increased risk of colorectal cancer for men, whereas the association is less clear for women. As risk estimates from observational studies may be biased and/or confounded, we conducted a Mendelian randomization study to estimate the causal association between BMI and colorectal cancer.Methods: We used data from 10,226 colorectal cancer cases and 10,286 controls of European ancestry. The Mendelian randomization analysis used a weighted genetic risk score, derived from 77 genome-wide association study–identified variants associated with higher BMI, as an instrumental variable (IV). We compared the IV odds ratio (IV-OR) with the OR obtained using a conventional covariate-adjusted analysis.Results: Individuals carrying greater numbers of BMI-increasing alleles had higher colorectal cancer risk [per weighted allele OR, 1.31; 95% confidence interval (CI), 1.10–1.57]. Our IV estimation results support the hypothesis that genetically influenced BMI is directly associated with risk for colorectal cancer (IV-OR per 5 kg/m2, 1.50; 95% CI, 1.13–2.01). In the sex-specific IV analyses higher BMI was associated with higher risk of colorectal cancer among women (IV-OR per 5 kg/m2, 1.82; 95% CI, 1.26–2.61). For men, genetically influenced BMI was not associated with colorectal cancer (IV-OR per 5 kg/m2, 1.18; 95% CI, 0.73–1.92).Conclusions: High BMI was associated with increased colorectal cancer risk for women. Whether abdominal obesity, rather than overall obesity, is a more important risk factor for men requires further investigation.Impact: Overall, conventional epidemiologic and Mendelian randomization studies suggest a strong association between obesity and the risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev; 24(7); 1024–31. ©2015 AACR.

Background: Gallbladder cancer incidence varies among racial/ethnic subgroups in the United States (US). We investigated trends in gallbladder cancer incidence rates in 50 states from 2001 to 2018. Methods: Age-adjusted incidence rates and trends in adults were calculated using data from the US Cancer Statistics registry. We used joinpoint regression to compute annual percentage of changes (APC). We analyzed incidence trends by time periods, age groups, and birth cohorts through age–period-cohort modeling. Results: Overall, age standardized incidence rates for gallbladder cancer decreased by 0.3% annually between 2001 and 2018 [95% confidence interval (CI) −0.5% to −0.1%]. However, secular trends varied by race/ethnicity. Although gallbladder cancer rates declined in other racial/ethnic groups, rates increased by 1.4% annually among non-Hispanic Blacks (NHB) between 2001 and 2018 (APC = 1.4%; 95% CI, 0.9%–2.0%). We found evidence for period and birth cohort effects with increasing rates among successive birth cohorts of NHBs. Relative to NHB cohorts born circa 1946, gallbladder cancer rates were 85% higher in NHB cohorts born circa 1971 [incidence rate ratio (IRR), 1.85; 95% CI, 1.26–2.72). The rates among NHBs in South region were higher in cohorts born circa 1971 (IRR, 2.17; 95% CI, 1.27–3.73) relative to those born circa 1946. Conclusions: The incidence of gallbladder cancer has consistently increased in the US among NHBs. A notable increase in incidence was observed among NHBs with evidence of birth cohort effects in South, Northeast, and Midwest regions. Impact: The cohort effect observed among NHBs with increasing rates in different US regions suggests that gallbladder cancer rates will continue to rise in the US in the near future.

Introduction: Non-alcoholic fatty liver disease (NAFLD) is a growing problem in the United States and Hispanics experience the highest burden of this disease. Weight loss, physical activity (PA) and a healthy diet are the mainstay for NAFLD treatment, but patients experience barriers to behavior change. The purpose of this study was to identify barriers hindering Hispanic patients with NAFLD from making changes to PA and dietary habits. Methods: Participants referred to a multidisciplinary clinic completed self-administered questionnaires that measured barriers to greater PA engagement and eating healthier, with both close-ended and open-ended responses. One bilingual coder reviewed and categorized all open-ended responses. Results: The study population included 414 patients. The top five barriers for eating healthier were cost, perceptions that healthier food does not taste good, lack of time to cook, difficulty of cooking, and difficulty in going to the grocery store. Lack of time, feeling lazy, pain, a lack of place to exercise, and the perception that exercise is difficult were the top five barriers to PA engagement. Conclusions: Since Hispanic adults with NAFLD experience similar barriers to Hispanic adults more generally, existing behavioral lifestyle interventions may work well in this clinical population with some adaption for NAFLD-specific education.

Background: Esophageal cancer (EC) incidence rates overall have declined in recent decades; however, the two main subtypes, esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC), show divergent secular trends. Methods: Age-adjusted EC incidence rates were calculated using data from the Surveillance Epidemiology and End Results (SEER) 12 Program. We examined secular trends from 1992 to 2019 overall and by age group, sex, race/ethnicity, tumor location, and SEER registry. Joinpoint regression was used to compute annual percent changes (APC) and average annual percent changes (AAPC). We used age-period-cohort models to examine the potential impact of period and birth cohort effects on trends. Results: Between 1992 and 2019, overall EC incidence rates declined by 0.54% annually (95% confidence interval [CI]: −0.75%, −0.33%). While ESCC rates declined linearly throughout the study period (AAPC = −2.85; 95%CI: −3.05%, −2.65%), EAC rates increased by over 5% annually from 1992 to 2000 (APC = 5.17; 95%CI: 3.28%, 7.10%), before stabilizing from 2000 to 2019 (APC = 0.22; 95%CI: −0.16%, 0.60%). Trends in ESCC and EAC varied by age group, sex, and race/ethnicity. Relative to ESCC rates among cohorts born circa 1950, the rates were 81% lower in cohorts born circa 1985 (rate ratio, 0.19; 95%CI: 0.04, 0.96). For EAC, rates have remained stable across successive birth cohorts since 1950. Conclusions: We observed linear declines in EC rates overall and for ESCC across age, sex, and race/ethnicity subgroups, but an inconsistent pattern for EAC. The trends in EAC cohorts born after 1955 were stable and suggest that EAC rates may have peaked in the U.S.

ObjectiveGastro-oesophageal reflux disease (GERD) has heterogeneous aetiology primarily attributable to its symptom-based definitions. GERD genome-wide association studies (GWASs) have shown strong genetic overlaps with established risk factors such as obesity and depression. We hypothesised that the shared genetic architecture between GERD and these risk factors can be leveraged to (1) identify new GERD and Barrett’s oesophagus (BE) risk loci and (2) explore potentially heterogeneous pathways leading to GERD and oesophageal complications.DesignWe applied multitrait GWAS models combining GERD (78 707 cases; 288 734 controls) and genetically correlated traits including education attainment, depression and body mass index. We also used multitrait analysis to identify BE risk loci. Top hits were replicated in 23andMe (462 753 GERD cases, 24 099 BE cases, 1 484 025 controls). We additionally dissected the GERD loci into obesity-driven and depression-driven subgroups. These subgroups were investigated to determine how they relate to tissue-specific gene expression and to risk of serious oesophageal disease (BE and/or oesophageal adenocarcinoma, EA).ResultsWe identified 88 loci associated with GERD, with 59 replicating in 23andMe after multiple testing corrections. Our BE analysis identified seven novel loci. Additionally we showed that only the obesity-driven GERD loci (but not the depression-driven loci) were associated with genes enriched in oesophageal tissues and successfully predicted BE/EA.ConclusionOur multitrait model identified many novel risk loci for GERD and BE. We present strong evidence for a genetic underpinning of disease heterogeneity in GERD and show that GERD loci associated with depressive symptoms are not strong predictors of BE/EA relative to obesity-driven GERD loci.

Identifying dysplasia of Barrett's esophagus (BE) in the electronic medical record (EMR) requires manual abstraction of unstructured data. Natural language processing (NLP) creates structure to unstructured free text. We aimed to develop and validate an NLP algorithm to identify dysplasia in BE patients on histopathology reports with varying report formats in a large integrated EMR system.We randomly selected 600 pathology reports for NLP development and 400 reports for validation from patients with suspected BE in the national Veterans Affairs databases. BE and dysplasia were verified by manual review of the pathology reports. We used NLP software (Clinical Language Annotation, Modeling, and Processing Toolkit; Melax Tech, Houston, TX) to develop an algorithm to identify dysplasia using findings. The algorithm performance characteristics were calculated as recall, precision, accuracy, and F-measure.In the development set of 600 patients, 457 patients had confirmed BE (60 with dysplasia). The NLP identified dysplasia with 98.0% accuracy, 91.7% recall, and 93.2% precision, with an F-measure of 92.4%. All 7 patients with confirmed high-grade dysplasia were classified by the algorithm as having dysplasia. Among the 400 patients in the validation cohort, 230 had confirmed BE (39 with dysplasia). Compared with manual review, the NLP algorithm identified dysplasia with 98.7% accuracy, 92.3% recall, and 100.0% precision, with an F-measure of 96.0%.NLP yielded a high degree of sensitivity and accuracy for identifying dysplasia from diverse types of pathology reports for patients with BE. The application of this algorithm would facilitate research and clinical care in an EMR system with text reports in large data repositories.

Pancreatic cancer is the seventh leading cause of cancer-related deaths worldwide with 432,242 related deaths in 2018. Unlike other cancers, the incidence of pancreatic cancer continues to increase, with little improvement in survival rates. We review the epidemiologic features of pancreatic cancer, covering surveillance and early detection in high-risk persons. We summarize data on worldwide incidence and mortality and analyze the 1975–2016 data from 9 registries of the National Cancer Institute’s Surveillance, Epidemiology, and End Results study, on the overall burden of pancreatic cancer as well as age-, sex-, and race-specific incidence, survival rates and trends. It is important to increase our knowledge of the worldwide and regional epidemiologic features of and risk factors for pancreatic cancer, to identify new approaches for prevention, surveillance, and treatment.

A recent panel of international experts proposed the disease acronym metabolic (dysfunction)-associated fatty liver disease (MAFLD) in lieu of nonalcoholic fatty liver disease (NAFLD). We aimed to estimate the burden of and risk factors for NAFLD and MAFLD, and to examine the concordance between definitions in a Veterans population.We conducted a cross-sectional study among randomly selected patients within primary care at the Houston Veterans Affairs (VA) facility. Participants completed a survey, provided blood, and underwent Fibroscan. In the absence of heavy alcohol, hepatitis C virus and hepatitis B virus, a controlled attenuation parameter median ≥290 dB/m was used to define NAFLD, whereas MAFLD was defined as controlled attenuation parameter median ≥290 dB/m and either body mass index ≥25 kg/mThe mean age of participants was 50.9 years, 55.4% were women, 42.8% were white, and 43.8% were Black. The prevalence of NAFLD was 40.6% (82/202). All 82 patients with NAFLD had a body mass index ≥25 kg/mNAFLD was present in 40% of Veterans registered in primary care; 9.4% of veterans had at least moderate hepatic fibrosis, with most having concurrent NAFLD. There was perfect concordance between NAFLD and the alternative MAFLD definition.

Background: Women with advanced cervical cancer at diagnosis have higher morbidity and mortality. Despite advancements in prevention and early detection, cervical cancer care disparities persist by race/ethnicity and geographical distribution. We aimed to identify spatial clusters of late-stage cervical cancer at diagnosis in Texas, a state with a higher than national cervical cancer rate, especially among racial/ethnic minority populations.Methods: Incident cervical cancer data were obtained from the Texas Cancer Registry for women aged 18 years or older diagnosed from 2000 to 2018. First, we conducted purely spatial scan analysis using the SaTScan Bernoulli model to identify geographic clusters (hot spots and cold spots) of late-stage cervical cancer (vs. early-stage) at diagnosis. Maximum cluster size was set at 50% of the at-risk population, and statistical significance at p Citation Format: Itunu O. Sokale, Aaron P. Thrift, Abiodun O. Oluyomi. Geospatial analyses identify hot spots of late-stage cervical cancer at diagnosis in Texas. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4211.

Cirrhosis is the main predisposing condition for hepatocellular carcinoma. Host genetic risk factors have been reported for cirrhosis; however, whether there is a genetic contribution to racial disparities in cirrhosis requires further investigation.We used an affected-only mapping by admixture linkage disequilibrium analysis to characterize the genetic risk of cirrhosis in 227 African American patients with cirrhosis genotyped at 19,804 ancestry-informative marker single nucleotide polymorphisms. We additionally performed analyses stratified by hepatitis C virus (HCV) infection status. To replicate our findings, we conducted a case-control analysis in an external study population (452 cases and 196 controls).The mean age of patients was 63.3 years and 98.2% were male. Risk factors for cirrhosis included HCV infection (83.7%) and alcohol abuse (56.4%). In the admixture mapping analysis, we found that European ancestry on chromosome 2q21.1 and African ancestry on chromosome 6p21.2 were associated with increased risk of cirrhosis in African Americans. In the fine-mapping analysis, we identified regions near POTEKP on 2q21.1 (P = .0001) and DNAH8 on 6p21.2 (P = .0017) that were associated with cirrhosis. As the admixture peaks in the HCV-positive patients were the same as those in the overall group, findings in the analysis are reflective of the HCV-positive group. In the replication analysis, the results on chromosome 2 were not significant after adjusting for multiple comparisons, and we could not replicate the results on chromosome 6.We used admixture mapping to identify novel genomic regions on 2q21.1 and 6p21.2 that may be associated with HCV-related cirrhosis risk in African Americans.

In the United States, the incidence of esophageal adenocarcinoma increased markedly since the 1970s with a recent stabilization. Despite evolving screening and surveillance strategies to diagnose, risk triage, and intervene in Barrett's esophagus patients to prevent esophageal adenocarcinoma, most cases present with advanced disease and poor resultant survival. Epidemiologic studies have identified the main risk factors for these conditions, including increasing age, male sex, white race, gastroesophageal reflux disease, abdominal obesity, cigarette smoking, and lack of infection with Helicobacter pylori. This review summarizes the current epidemiologic evidence with implications for screening and surveillance in Barrett's esophagus and esophageal adenocarcinoma.

Goal Determine whether various dimensions of smoking increase risk for gastric intestinal metaplasia. Background Cigarette smoking has been implicated in the etiology of gastric cancer, but it is not clear if smoking is a risk factor for gastric intestinal metaplasia, a precursor lesion of gastric cancer. Materials and methods We compared data from 385 gastric intestinal metaplasia cases and 1577 controls without gastric intestinal metaplasia recruited into a cross-sectional study at the Michael E. DeBakey VA Medical Center in Houston, Texas. All participants completed standardized questionnaires and underwent a study endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included participants with intestinal metaplasia on any noncardia gastric biopsy. We calculated odds ratios and associated 95% confidence intervals using multivariable logistic regression models. Results Compared with never smokers, current smokers had 2-fold increased risk for gastric intestinal metaplasia (odds ratio, 2.05; 95% confidence interval, 1.47-2.85). Among ever smokers, increasing duration and total dose were significantly associated with increased risk for gastric intestinal metaplasia (P-trend, 0.004 and 0.01, respectively). Among former smokers, risk for gastric intestinal metaplasia decreased over time and was no different to never smokers after 15 years smoking cessation. Cases with gastric intestinal metaplasia were more likely than controls to have Helicobacter pylori infection (53.2% vs. 21.7%); however, smoking effect on gastric intestinal metaplasia was not different by H. pylori infection status. Conclusions Cigarette smoking is a risk factor for gastric intestinal metaplasia. Risk of gastric intestinal metaplasia among former smokers remained significantly elevated until 15 years postcessation.

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.

These practice recommendations for the management of moderate-to-severe UC were developed using the GRADE framework and in adherence to the standards established by the Institute of Medicine for the development of trustworthy guidelines12, 13. The goal of this guideline is to promote high quality, high value evidence-based care for patients with moderate-to-severe UC. Current evidence supports use of infliximab, adalimumab, golimumab, vedolizumab, and tofacitinib for the induction and maintenance of remission in moderate-severe UC. Thiopurine monotherapy should not be used for induction of remission but may be considered for maintenance of remission; in contrast, methotrexate monotherapy, orally or subcutaneously, should not be used for induction or maintenance of remission. Network meta-analysis suggests that infliximab and vedolizumab may be preferred first-line therapy in biologic-naive patients, rather than standard-dose adalimumab or golimumab, with limited evidence to inform appropriate positioning of tofacitinib. In patients with prior exposure to infliximab, particularly those with primary non-response to induction therapy, vedolizumab or tofacitinib may be preferred over adalimumab or golimumab. Combination therapy of a biologic agent with an immunomodulator is more effective than monotherapy with either agent, though patients, particularly those with less severe disease and those averse to side effects from medications, may opt for monotherapy. In patients with moderate-severe disease activity, at high risk of colectomy, biologic agents with or without an immunomodulator, or tofacitinib, should be used early rather than gradual step up therapy after failure of 5-aminosalicylates. Patients in remission with biologic agents and/or immunomodulators or tofacitinib after prior failure of 5-ASA, may discontinue 5-aminosalicylates. Among hospitalized patients with ASUC, after excluding alternative etiologies, intravenous methylprednisolone doses of 40–60mg/day or equivalent are mainstay of therapy. Routine use of adjunctive antibiotics in patients without infections is not recommended. Patients who are refractory to 3–5 days trial of intravenous corticosteroids, who prefer ongoing medical management, may be treated with either infliximab or cyclosporine. In patients being treated with infliximab, no recommendation can be made regarding routine use of intensive vs. standard infliximab dosing.

Gastric cancer is a global health problem, with more than 1 million people newly diagnosed with gastric cancer worldwide each year. Despite its worldwide decline in incidence and mortality over the past five decades, gastric cancer remains the third leading cause of cancer-related death. Knowledge of global as well as regional epidemiology and risk factors for gastric cancer is essential for the practicing gastroenterologist to make personalized decisions about risk stratification, screening and prevention. In this article, we review the epidemiology of gastric cancer as well as screening and prevention efforts to reduce global morbidity and mortality from gastric cancer. First, we discuss the descriptive epidemiology of gastric cancer, including its incidence, mortality, survival, and secular trends. We combine a synthesis of published studies with an analysis of data from the International Agency for Research on Cancer (IARC) GLOBOCAN project to describe the global burden of gastric cancer and data from the United States Cancer Statistics (USCS) registry to discuss the change in incidence of gastric cancer in the U.S. Next, we summarize current knowledge of risk factors for gastric cancer. Finally, we discuss prevention strategies and screening efforts for gastric cancer.

Background: Obesity is a major risk factor for esophageal adenocarcinoma (EA) and its precursor Barrett's esophagus (BE). Research suggests that individuals with high genetic risk to obesity have a higher BE/EA risk. To facilitate understanding of biological factors that lead to progression from BE to EA, the present study investigated the shared genetic background of BE/EA and obesity-related traits. Methods: Cross-trait linkage disequilibrium score regression was applied to summary statistics from genome-wide association meta-analyses on BE/EA and on obesity traits. Body mass index (BMI) was used as a proxy for general obesity, and waist-to-hip ratio (WHR) for abdominal obesity. For single marker analyses, all genome-wide significant risk alleles for BMI and WHR were compared with summary statistics of the BE/EA meta-analyses. Results: Sex-combined analyses revealed a significant genetic correlation between BMI and BE/EA (rg = 0.13, P = 2 × 10−04) and a rg of 0.12 between WHR and BE/EA (P = 1 × 10−02). Sex-specific analyses revealed a pronounced genetic correlation between BMI and EA in females (rg = 0.17, P = 1.2 × 10−03), and WHR and EA in males (rg = 0.18, P = 1.51 × 10−02). On the single marker level, significant enrichment of concordant effects was observed for BMI and BE/EA risk variants (P = 8.45 × 10−03) and WHR and BE/EA risk variants (P = 2 × 10−02). Conclusions: Our study provides evidence for sex-specific genetic correlations that might reflect specific biological mecha-nisms. The data demonstrate that shared genetic factors are particularly relevant in progression from BE to EA. Impact: Our study quantifies the genetic correlation between BE/EA and obesity. Further research is now warranted to elucidate these effects and to understand the shared pathophysiology.

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 Conclusions: As a result of decreasing incidence among males aged Impact: The sex and racial disparities and strong birth cohort effect on HCC risk identified in this study have important implications for population-based HCC prevention efforts.

BACKGROUND AND AIMS: Risk of esophageal adenocarcinoma (EA) in those with Barrett’s esophagus (BE) is 11-fold greater than the general population. It remains unclear which BE patients are at highest risk of progression to EA. We aimed to validate a predictive model risk stratifying BE patients. METHODS: We conducted a retrospective cohort study at the Houston VA of consecutive patients with a new BE diagnosis from November 1990 to January 2019. Study follow-up was through 2/2020. Patients were excluded if they had no follow-up esophagogastroduodenoscopy (EGD) with esophageal biopsy after the initial BE-diagnosing EGD or evidence of high-grade dysplasia (HGD) or EA on initial EGD. We performed an external validation study of a risk model containing sex, smoking, BE length, and low-grade dysplasia (LGD) status and assessed discriminatory ability using area under the receiver operating characteristic curve (AUROC). RESULTS: Among 608 BE patients, 24 progressed to HGD/EA. The points-based model discriminated well with an AUROC of 0.72 (95% confidence interval [CI], 0.63–0.82). When categorized into low/intermediate/high-risk groups according to published cut-offs, the AUROC was poor at 0.57. Restructured into low-risk versus high-risk groups, the AUROC was 0.72 (95% CI, 0.64–0.80). Excluding baseline LGD did not reduce discriminatory ability (AUROC 0.73; 95% CI, 0.64–0.82). CONCLUSION: This external validation provides further evidence that the model including sex, LGD status, smoking status, and BE length may help to risk stratify BE patients. A simplified version excluding LGD status and/or reducing the number of risk groups has increased utility in clinical practice without loss of discriminatory ability.