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Abstract Esophageal adenocarcinoma is the most common histological subtype of esophageal cancer in Western countries and shows poor prognosis with rapid growth. EAC is characterized by a strong male predominance and racial disparity. EAC is up to fivefold more common among Whites than Blacks, yet Black patients with EAC have poorer survival rates. The racial disparity remains largely unknown, and there is limited knowledge of mutations in EAC regarding racial disparities. We used whole-exome sequencing to show somatic mutation profiles derived from tumor samples from 18 EAC male patients. We identified three molecular subgroups based on the pre-defined esophageal cancer-specific mutational signatures. Group 1 is associated with age and NTHL1 deficiency-related signatures. Group 2 occurs primarily in Black patients and is associated with signatures related to DNA damage from oxidative stress and NTHL1 deficiency-related signatures. Group 3 is associated with defective homologous recombination-based DNA often caused by BRCA mutation in White patients. We observed significantly mutated race related genes (LCE2B in Black, SDR39U1 in White) were (q-value

Introduction: Despite being almost entirely preventable, cervical cancer is the fourth most frequently diagnosed cancer among women worldwide. Cervical cancer incidence suggests missed opportunities for prevention. Geospatial analysis could strategically guide public health interventions. This study aimed to identify geographic clusters of cervical cancer incidence in Texas, a state with higher than national rates of cervical cancer incidence and mortality. Methods: In this population-based cross-sectional study, the authors analyzed incident cervical cancer data among Texas women aged 30–64 years, from 2014 to 2018. The authors conducted a purely spatial Poisson-based analysis function in SaTScan to examine geographic clusters of higher-than-expected proportions of cervical cancer incidence (i.e., hot spots) and adjusted for age. Results: A total of 5,060 women aged 30–64 years with incident cervical cancer diagnosis (mean age: 45.7 years, SD=9.6), including 1,840 (36.4%) Hispanic, 591 (11.7%) non-Hispanic Black, 2,397 (47.4%) non-Hispanic White, and 232 (4.6%) other races, were analyzed. Spatial scan analysis detected 7 significant hot spots of cervical cancer incidence. Hot spots were identified in the South Texas Plains (near Mexico border), Gulf Coast (Houston), Prairies and Lakes (North Texas), Panhandle Plains (Northwest Texas), and Piney Woods (Southeast Texas) regions of Texas. Hot spots, compared with the rest of Texas, had higher proportions of Hispanic population and individuals with socioeconomic disadvantages. Conclusions: This study found spatial variation in cervical cancer incidence in Texas. The hot spot areas can benefit from targeted, novel, scalable, and cost-effective interventions to increase human papillomavirus vaccination and screening and early detection and treatment of precancerous cervical lesions.

Summary: Background: First Nations populations have poorer colorectal cancer (CRC) survival compared to non-First Nations populations. Whilst First Nations populations across the world are distinct, shared experiences of discrimination and oppression contribute to persistent health inequities. CRC screening improves survival, however screening rates in First Nations populations are poorly described. This study seeks to define participation rates in CRC screening in First Nations populations worldwide. Methods: A systematic literature search was conducted of PubMed, Embase, Cochrane Library, CINAHL, MEDLINE, grey literature, national registries and ClinicalTrials.gov. All sources were searched from their inception date to 18 February 2024. Studies were included if they reported CRC screening rates in adult (≥18 years) First Nations populations. We aimed to undertake a meta-analysis if there were sufficient data. Quality of papers were assessed using the Joanna Briggs Institute (JBI) appraisal tool. The study was registered with PROSPERO, CRD42020210181. Findings: The literature search identified 1723 potentially eligible published studies. After review, 57 studies were included, 50 from the United States (US), with the remaining studies from Australia, Aotearoa New Zealand (NZ), Canada, Dominica and Guatemala. Additionally, eleven non-indexed reports from national programs in Australia and NZ were included. There were insufficient data to undertake meta-analysis, therefore a systematic review and narrative synthesis were conducted. CRC screening definitions varied, and included stool-based screening, sigmoidoscopy and colonoscopy. US First Nations screening rates ranged between 4.0 and 79.2%, Australia reported 10.6–35.2%, NZ 18.4–49%, Canada 22.4–53.4%, Guatemala 2.2% and Dominica 4.2%. Fifty-five studies were assessed as moderate or high quality and two as low quality. Interpretation: Our findings suggested that there is wide variation in CRC screening participation rates across First Nations populations. Screening data are lacking in direct comparator groups and longitudinal outcomes. Disaggregation of screening data are required to better understand and address First Nations CRC outcome inequities. Funding: None.

Abstract Background Cancer mortality rates overall in the U.S. have decreased significantly; however, the rate of decline has not been uniform across sociodemographic groups. We aimed to compare trends in cancer mortality rates from 1999 to 2020 between rural and urban individuals and to examine whether any rural–urban differences are uniform across racial and ethnic groups. Methods We used U.S.‐wide data from the National Center for Health Statistics, for all cancer deaths among individuals aged 25 years or older. We estimated average annual percentage change (AAPC) in age‐standardized cancer mortality rates in the U.S. by cancer type, rural–urban status, sex, and race and ethnicity. Results There was a larger reduction in cancer mortality rates among individuals from urban (males: AAPC, −1.96%; 95% CI, −2.03, −1.90; females: AAPC, −1.56%; 95% CI, −1.64, −1.48) than rural (males: AAPC, −1.43%; 95% CI, −1.47, −1.39; females: AAPC, −0.93; 95% CI, −1.03, −0.82) areas. AAPCs for cancer types were uniformly higher among urban areas compared with rural areas. Despite overall decreases, deaths rates for liver and pancreas cancers increased, including in the most recent period among males (2012–2020, APC, 1.34; 95% CI, 0.49, 2.20) and females (2013–2020, APC, 1.52; 95% CI, 0.03, 3.02) in rural areas. Conclusions Cancer death rates decreased in all racial and ethnic populations; however, the rural–urban differences varied by race/ethnicity. The rate of decline in mortality rates were lower in rural areas and death rates for liver and pancreas cancers increased, particularly for individuals living in rural America.

Summary: Background: The phenotype of combined heavy alcohol consumption and obesity has the potential to pose as a considerable health burden in the U.S. No studies using nationally representative data in the U.S. have reported their secular joint prevalence trends. We estimated the prevalence and examined the joint trends of heavy alcohol use and obesity over time among adult U.S. men and women in different age groups and according to race/ethnicity. Methods: Using data from 10 cycles of the U.S. National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020, we examined secular trends in the combined phenotype of heavy drinking and obesity overall and by age-group, sex, and race/ethnicity. The main outcome measures were prevalence of heavy alcohol consumption (>14 drinks/week in men and >7 drinks/week in women) and obesity (BMI ≥30). Findings: In 45,292 adults (22,684 men, mean age 49.26 years; and 22,608 women, mean age 49.86), the overall weighted prevalence of combined heavy alcohol drinking and obesity increased from 1.8% (95% CI: 1.2%, 3.1%) in 1999–2000 to 3.1% (95% CI: 2.7%, 3.7%) in 2017–2020 representing an increase of 72% over time. In the joinpoint regression, the combined phenotype of heavy alcohol consumption and obesity increased by 3.25% (95% CI: 1.67%, 4.85%) per year overall from 1999 to 2017. An increasing trend of 9.94% (95% CI: 2.37%, 18.06%) per year was observed among adults aged between 40 and 59 years from 2007 onwards. Prevalence of heavy alcohol consumption in obesity increased at a faster rate among women (APC, 3.96%; 95% CI: 2.14%, 5.82%) than men (APC, 2.47%; 95% CI: 0.63%, 4.35%), and increased among non-Hispanic Whites (APC, 4.12%; 95% CI: 1.50%, 6.82%) and non-Hispanic Blacks (APC, 2.78%; 95% CI: 0.47%, 5.14%), but not Hispanics. Interpretation: The prevalence of combined heavy alcohol consumption and obesity increased overall in the U.S., but the rate of increase differed by age, sex, and race/ethnic groups. Given their independent and potential synergistic effects on premature mortality, public health policies on alcohol consumption need to reflect the background obesity epidemic. Funding: Cancer Prevention & Research Institute of Texas (CPRIT) for the Systems Epidemiology of Cancer Training (SECT) Program (RP210037; PI: A. Thrift).

Introduction: Mortality rates from colorectal cancer have declined over the past decades owing to population-based life-saving screening interventions. However, screening inequalities continue among racial and ethnic minorities despite having a higher disease burden. In this study, we assessed the patterns of up-to-date colorectal cancer screening rates among racial/ethnic groups across the U.S. Census Bureau Divisions. Methods: This population-based cross-sectional study used weighted data from 4 cycles of the Behavioral Risk Factors Surveillance System (2014, 2016, 2018, and 2020) of adults aged 50‒75 years without a previous diagnosis of colorectal cancer. The primary outcome was guideline-recommended up-to-date colorectal cancer screening. We used logistic regression models to examine temporal trends in up-to-date colorectal cancer screening from 2014 to 2020. In addition, we conducted detailed descriptive statistics of up-to-date screening rates, comparing trends in 2020 with those in 2014 overall by race/ethnicity and U.S. census divisions. Results: The overall proportion of individuals with up-to-date colorectal cancer screening increased from 66.5% in 2014 to 72.5% in 2020 (p

Abstract Weight loss through behavioral modification is central to treating non-alcoholic fatty liver disease (NAFLD). To achieve this, patients need to accurately self-perceive their health behaviors. We aimed to identify predictors of concordance between self-perception and objective measures of body weight, physical activity (PA) and dietary behaviors. We used data from the Harris County NAFLD Cohort, an ongoing prospective study in a regional safety-net healthcare system. Patients completed self-administered baseline questionnaires on demographics, diet, PA, and self-perceptions. We assessed concordance between actual and self-perceived body weight and energy-balance behaviors. Multivariable logistic regression identified predictors of concordance. Patients (n = 458; average age 46.5 years) were 90% Hispanic and 76% female. PA and fruit/vegetable intake guidelines were met among 37% and 9%, respectively. Most (89%) overweight/obese patients accurately perceived themselves as such. However, 41% of insufficiently-active and 34% of patients not meeting fruit/vegetable intake guidelines inaccurately self-perceived their behaviors as “just right”. Women were 3 times more likely to accurately self-perceive weight status (adjusted odds ratio [AOR] 3.24; 95% CI 1.68–6.25) but 51% less likely to accurately self-perceive PA levels than men (AOR 0.49; 95% CI 0.29–0.81). Lower acculturation was associated with higher odds of accurate PA self-perception. Patients with prediabetes or diabetes vs normoglycemia were more likely to accurately self-perceive their fruit/vegetable intake. Most NAFLD patients accurately self-perceived their body weight. A third or more of those not meeting fruit/vegetable intake or PA guidelines had inaccurate perceptions about their behaviors. Our findings highlight key areas to target in NAFLD-specific behavioral modification programs.

Abstract We assessed differences in survival between non-Hispanic black (NHB) and non-Hispanic white (NHW) patients with multiple myeloma (MM), and the sequential effects of patient characteristics, and diagnosis and treatment-related factors on the survival disparity using data from 3319 NHB and 20,831 NHW MM patients in the SEER-Medicare (1999–2017) database. Four sets of 3319 NHWs were matched sequentially to the same set of 3319 NHBs, based on demographics (age, sex, year of diagnosis, marital status, and SEER site), socioeconomic status (SES, demographics plus SES), presentation factors (SES variables plus comorbidity), and treatment factors (presentation variables plus antimyeloma therapies). We found NHBs were less likely to receive treatment than NHWs even among patients matched for demographics, SES, and comorbidities. The absolute difference in 5-year survival between NHBs and NHWs was not significant in the demographics match (0.6%; P = 0.30) and remained non-significant after matching for SES (1.4%, P = 0.17). When matching for presentation, NHBs had significantly longer 5-year survival than NHWs (absolute difference = 3.8%, P = 0.003). Additional matching on treatment-related factors further enlarged the racial difference in 5-year survival to 4.6% (P

Background and Aims: Cholangiocarcinoma is a relatively rare malignancy with high mortality. In the U.S., incidence rates of cholangiocarcinoma have increased, particularly affecting younger age groups and Hispanic and Asian individuals. We investigated the incidence of cholangiocarcinoma in a largely under-represented, minority population. Methods: We performed a retrospective cohort study from 2005 to 2017 among adults in a county-funded healthcare system in Harris County, Texas. Incidence rate ratios were computed to compare age-standardized rates using U.S. standard population between 2 time periods: 2005–2011 and 2012–2017. Results: We identified 139 cholangiocarcinoma cases (64% intrahepatic, 36% extrahepatic). The median age at diagnosis was 57 years; 62% were Hispanic, and 56% were born outside the U.S. The incidence rate increased from 1.2 to 2.4 per 100,000 person-years (rate ratio 2.1 [95% confidence interval {CI}: 1.5, 3.0]). Hispanic individuals and those aged 40–69 years had the highest rate of incidence increase (respectively, rate ratio: 2.5 [95% CI: 1.6, 4.0] and rate ratio: 2.0 [95% CI: 1.2, 3.0]) between time periods. In 2012–2017, the risk of cholangiocarcinoma among patients with diabetes was 1.4 times relative to those without (relative risk: 1.4; 95% CI: 1.1, 1.5) and 1.2 times among those who were overweight/obese relative to those who were not (relative risk: 1.2; 95% CI: 1.1, 1.6). Conclusion: Incidence of cholangiocarcinoma doubled during the 12-year study period, with Hispanic and middle-aged individuals disproportionately affected. Individuals with diabetes mellitus and those who were overweight or obese had a high risk of being diagnosed with cholangiocarcinoma in the later time period. Further studies should focus on preventing and improving earlier diagnosis of cholangiocarcinoma among Hispanics.

Background Polygenic risk scores (PRS) hold the promise to refine prognostication in hepatocellular cancer (HCC). The few available HCC PRS include germline risk variants identified among individuals of mostly European ancestry, but data are lacking on the transportability of these PRS in multiethnic U.S patients with cirrhosis from multiple etiologies. Methods We used data from 1644 patients with cirrhosis enrolled in two prospective cohort studies in the U.S. Patients were followed until HCC diagnosis, death, liver transplantation, or last study visit through June 30, 2021. The high-risk variants in PNPLA3-MBOAT7-TM6SF2-GCKR were combined in a PRS and we evaluated its association with HCC. Discriminatory accuracy was assessed using the C-statistic. Results During 4,759 person-years of follow-up, 93 patients developed HCC. Mean age was 59.8 years, 68.6% were male, 27.2% Hispanic, 25.1% non-Hispanic Black, 25.7% had NAFLD, 42.1% had heavy alcohol use, and 19.5% had active HCV. HCC risk increased by 134% per unit increase in PRS (HR = 2.30; 95% CI, 1.35–3.92). Compared to cirrhosis patients in the lowest tertile of the PRS, those in the highest tertile had 2-fold higher risk of HCC (HR = 2.05; 95% CI, 1.22–3.44). The PRS alone had modest discriminatory ability (C-statistic = 0.58; 95% CI, 0.52–0.63); however, adding PRS to a predictive model with traditional HCC risk factors had a C-statistic of 0.70 (95% CI, 0.64–0.76), increasing from 0.68 without the PRS (p = 0.0012). Conclusions Our findings suggest that PRS may enhance risk prediction for HCC in contemporary U.S. cirrhosis patients.

Texas has the highest age-adjusted incidence rate of hepatocellular carcinoma (HCC) in the United States. To address cancer prevention and early detection through research, Cancer Prevention and Research Institute of Texas (CPRIT) has funded the Texas Collaborative Center for Hepatocellular Cancer (TeCH) to facilitate liver cancer research, education and advocacy activities. This paper describes the organizational structure, program measures, the actions completed and future plans of TeCH. This center is comprised of several cores and committees including the Administrative Core, Steering Committee, Data and Biospecimen Core, Scientific Committee, Clinical Network Committee, and the Community Outreach Committee. Each core and committee provide its own level of connectivity and necessary research support. We have developed and published a TeCH Framework, a conceptual model designed for improving primary and secondary prevention of HCC. TeCH and its committees facilitate connections and collaborations among HCC researchers and clinicians, healthcare leaders, biotechnology companies and the public to reduce liver cancer mortality in Texas by 2030.

Background/Aims The American Society for Gastrointestinal Endoscopy (ASGE) revised its guidelines for risk stratification of patients with suspected choledocholithiasis. This study aimed to assess the diagnostic performance of the revision and to compare it to the previous guidelines. Methods We conducted a retrospective cohort study of 267 patients with suspected choledocholithiasis. We identified high-risk patients according to the original and revised guidelines and examined the diagnostic accuracy of both guidelines. We measured the association between individual criteria and choledocholithiasis. Results Under the original guidelines, 165 (62%) patients met the criteria for high risk, of whom 79% had confirmed choledocholithiasis. The categorization had a sensitivity and specificity of 68% and 55%, respectively, for the detection of choledocholithiasis. Under the revised guidelines, 86 (32%) patients met the criteria for high risk, of whom 83% had choledocholithiasis. The revised categorization had a lower sensitivity and higher specificity of 37% and 80%, respectively. The positive predictive value of the high-risk categorization increased with the revision, reflecting a potential decrease in diagnostic endoscopic retrograde cholangiopancreatograpies (ERCPs). Stone visualized on imaging had the greatest specificity for choledocholithiasis. Gallstone pancreatitis was not associated with the risk for choledocholithiasis. Conclusions The 2019 revision of the ASGE guidelines decreases the utilization of ERCP as a diagnostic modality and offers an improved risk stratification tool.

Studies of the genetic association between vitamin D and cancer risk have typically been underpowered. Here the authors analyse this using Mendelian Randomisation with more than 70 vitamin D variants obtained from the UK Biobank and large-scale data from various consortia, confirming null associations between vitamin D and most cancers.

Background A number of modifiable risk factors have been designated as being causally related to cancer development. We aimed to estimate the percentage of incident cancer cases diagnosed in persons aged ≥25 years in Texas in 2015, overall and by race/ethnicity, that were attributable to these modifiable risk factors. Methods We calculated population attributable fractions (PAFs) for cancers attributable to thirteen modifiable risk factors using prevalence data from the Texas Behavioral Risk Factor Surveillance System and the National Health and Nutrition Examination Survey, as well as relative risks estimates from prior studies and cancer incidence data from the Texas Cancer Registry. Results Overall, 32.3% of all incident cancers (N = 33,416) in 2015 were attributable to modifiable risk factors. Men (35.1%) had a numerically higher overall PAF than women (29.5%). Tobacco smoking caused the highest proportion of cancers (18.4%), followed by overweight and obesity (6.6%) and excess alcohol consumption (2.9%). Non-Hispanic Blacks had a numerically higher overall PAF (36.8%) than non-Hispanic Whites (31.9%) and Hispanics (31.7%). Further, non-Hispanic Blacks had the highest combined PAFs for 85% of cancer sites analyzed, including lung/bronchus and mouth/pharynx/larynx. Conclusion Modifiable risk factors cause about one third of cancers in Texas. Non-Hispanic Blacks are especially affected by an excessive preventable cancer burden.

We estimated the percentage and number of all incident cancer cases diagnosed in Texas in 2015 that were attributable to inadequate diet and examined for racial/ethnic differences. We calculated population attributable fractions for cancers with a causal relationship with red and processed meat consumption, insufficient fiber intake, and insufficient calcium intake, using prevalence estimates from the National Health and Nutrition Examination Survey and relative risk estimates from the World Cancer Research Fund/American Institute for Cancer Research 2018 Third Expert Report. Overall, 3.3% of all new cancers (3,428 cases) diagnosed in Texas in 2015 were attributable to inadequate diet. More diet-associated cancers were diagnosed in men (3.8%) than women (2.9%). Insufficient fiber intake (1.2%) contributed more cancers than processed meat consumption (1.0%), insufficient calcium intake (0.8%), and red meat consumption (0.4%). Non-Hispanic Blacks (4.4%) had a higher proportion of cancers attributable to inadequate diet than Hispanics (3.7%) and non-Hispanic Whites (3.1%). Considering only colorectal cancers, inadequate diet caused 39.6% of cases in non-Hispanic Blacks, compared to 33.6% in non-Hispanic Whites and 33.4% in Hispanics. Inadequate diet serves as an important but preventable source of cancer. In general, and for minority populations specifically, cancer prevention programs should continue to advocate for universal compliance with recommended dietary guidelines.

OBJECTIVES Tobacco smoking is classified as carcinogenic to humans (International Agency for Research on Cancer Group 1). We aimed to estimate the percentage and number of incident cancer cases diagnosed in Texas in 2015 that were attributable to tobacco smoking, and we examined differences in the proportions of smoking-attributable cancers between the major racial/ethnic subgroups of the population. METHODS We calculated population-attributable fractions for cancers attributable to tobacco smoking using prevalence data from the Texas Behavioral Risk Factor Surveillance System and relative risks associated with smoking status from pooled analyses of cohort studies or meta-analyses. Cancer incidence data were collected from the Texas Cancer Registry. RESULTS We estimated that 19,000 excess cancer cases or 18.4% of all cancers diagnosed in 2015 in Texans aged ≥ 25 years were caused by tobacco smoking. Males had a higher overall proportion of cancers attributable to tobacco smoking than females (male, 23.3%, 11,993 excess cases; female, 13.5%, 7,006 cases). Approximately 20% of cancer cases in non-Hispanic Whites and non-Hispanic Blacks were attributable to tobacco smoking compared to 12.8% among Hispanics. CONCLUSIONS Despite ongoing public health campaigns combatting tobacco use, this preventable behavior still contributes significantly to cancer incidence in Texas. Racial/ethnic differences in smoking prevalence and smoking-attributable cancer incidence should be considered when designing cancer prevention programs.

Background Chronic alcohol use is a risk factor for non-cardia gastric adenocarcinoma. However, it is less well understood whether alcohol use is a risk factor for premalignant mucosal changes, namely gastric intestinal metaplasia. We examined the association between various parameters of alcohol use and risk of gastric intestinal metaplasia. Methods We used data from 2084 participants (including 403 with gastric intestinal metaplasia) recruited between February 2008-August 2013 into a cross-sectional study at the Michael E. DeBakey Veterans Affairs Medical Center in Houston, Texas. All participants underwent a study upper endoscopy with systematic gastric mapping biopsies. Cases had intestinal metaplasia on any non-cardia gastric biopsy. Participants self-reported lifetime history of alcohol consumption, along with other lifestyle risk factors, through a study survey. We calculated odds ratios (OR) and 95% confidence intervals (95% CI) for categories of average alcohol consumption using multivariable logistic regression, and restricted cubic spline regression to explore the potential shape of a dose-response relationship. Results Compared to lifelong non-drinkers, individuals who consumed on average ≥28 drinks per week had no elevated risk for gastric intestinal metaplasia (adjusted OR, 1.27; 95% CI, 0.74–2.19). Based on a spline regression curve and its 95% CI, there was also no demonstrable association between cumulative lifetime alcohol consumption and risk of gastric intestinal metaplasia. Similarly, we found no association between beverage type (beer, wine, liquor/spirits) and risk for gastric intestinal metaplasia. Conclusions Neither amount of alcohol consumed nor specific beverage type was associated with risk of gastric intestinal metaplasia.

BackgroundThe epidemiology of esophageal cancer has changed dramatically over the past 4 decades in many Western populations. We aimed to understand the Hungarian epidemiologic trends of esophageal squamous cell cancer (SCC) and adenocarcinoma (AC).MethodsWe performed a cross-sectional study using data from esophageal cancer patients diagnosed between 1992 and 2018 at eight tertiary referral centers in four major cities of Hungary. We retrospectively identified cases in the electronic databases of each center and collected data on gender, age at diagnosis, year of diagnosis, specialty of the origin center, histological type, and localization of the tumor. Patients were grouped based on the two main histological types: AC or SCC. For statistical analysis, we used linear regression models, chi-square tests, and independent sample t tests.ResultsWe extracted data on 3,283 patients with esophageal cancer. Of these, 2,632 were diagnosed with either of the two main histological types; 737 had AC and 1,895 SCC. There was no significant difference in the gender ratio of the patients between AC and SCC (80.1 vs 81.8% males, respectively; p = 0.261). The relative incidence of AC increased over the years (p < 0.001, b = 1.19 CI: 0.84–1.54). AC patients were older at diagnosis than SCC patients (64.37 ± 11.59 vs 60.30 ± 10.07 years, p < 0.001). The age of patients at the diagnosis of primary esophageal cancer increased over time (p < 0.001, R = 0.119).ConclusionsThe rapid increase in the relative incidence of AC and simultaneous decrease of the relative incidence of SCC suggest that this well-established Western phenomenon is also present in Hungary.

Esophageal adenocarcinoma is the most common type of esophageal cancer in most Western countries and is an important contributor to overall cancer mortality. Most cases of esophageal adenocarcinoma are believed to arise from Barrett’s esophagus. Esophageal adenocarcinoma occurs more frequently in white men over 50 years old, as well as in people with frequent symptoms of gastroesophageal reflux, in smokers and in people who are obese. Higher consumption of fruit and vegetables, use of non-steroidal anti-inflammatory drugs, and infection with Helicobacter pylori have all been shown to reduce the risk of esophageal adenocarcinoma. Here, we review the epidemiological evidence for the major risk factors of esophageal adenocarcinoma and also discuss perspectives for future research.