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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.

PURPOSE: Evidence on health disparities among patients treated with multimodality therapy protocols is still limited. We aimed to evaluate the associations between patient-level and system-level factors and the receipt of guideline-concordant therapy among patients with esophageal adenocarcinoma (EA). METHODS: This is a national cohort study of patients with stage I-III EA in the National Cancer Database (2006-2018) treated with either upfront resection or neoadjuvant therapy followed by surgery. Clinical and pathologic staging data were used for defining guideline-concordant therapy. Logistic regression models were built to identify independent associations between deviations from treatment guidelines and clinical, sociodemographic, and hospital-related factors. RESULTS: Among 18,803 patients with EA treated at 1,049 hospitals, 4,511 had an endoscopic resection, 4,866 had upfront resection, and 9,426 had neoadjuvant therapy followed by surgery. A total of 16,002 patients (85.1%) received guideline-concordant therapy. Patients who were age 70 years or older (odds ratio [OR] 1.35; 95% CI, 1.14 to 1.60), had a Charlson-Deyo modified score of ≥ 1, and were treated at hospitals with a safety-net burden of ≥ 10% (OR 1.13; 95% CI, 1.02 to 1.25) had higher risk of deviations from guidelines, whereas treatment at high-volume facilities (OR 0.84; 95% CI, 0.74 to 0.95) and diagnosis after 2011 decreased this risk. Relative to cT0-1N0 patients, those with cT2N0 disease had the highest risk of deviations from guideline-concordant therapy (OR 3.76; 95% CI, 3.30 to 4.29). Among patients treated at high-volume facilities, safety-net burden over 10% increased the risk of deviations (OR 1.26; 95% CI, 1.01 to 1.57). CONCLUSION: The delivery of guideline-concordant therapy among patients with EA varies significantly across clinical stage groups and is associated with several sociodemographic disparities. This knowledge should be a resource for future quality improvement strategies intended to address inequitable care within vulnerable populations.

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.

Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent liver disease, with the highest prevalence observed in the U.S. among Hispanic/Latino adults. While physical activity and dietary behaviors have established protective associations with NAFLD and its severity, these associations have not been well-characterized in Hispanic/Latino adults. The purpose of this study was to assess the association of lifestyle behaviors with NAFLD and advanced fibrosis in US Hispanic/Latino adults.We selected all Hispanic/Latino adults from the 2017-2018 National Health and Nutrition Examination Survey (NHANES). NAFLD was defined as CAP ≥285 dB/m, and advanced fibrosis as liver stiffness measurements ≥8.6 kPa. Multivariate-adjusted logistic regression models assessed associations of physical activity and sedentary behavior (Global Physical Activity Questionnaire), as well as diet quality (Healthy Eating Index [HEI]-2015) and total energy intake (24-hour recall) with NAFLD and advanced fibrosis.In Hispanic/Latino adults, the overall prevalence of NAFLD was 41.5%, while the prevalence of advanced fibrosis among those with NAFLD was 17.2%. We found that higher levels of physical activity and high diet quality were associated with lower risk of NAFLD. Compared to those reporting on average 0 metabolic equivalent (MET) hours/week of physical activity, participants reporting high levels of physical activity (≥32 MET hours/week) had 40% lower risk of NAFLD (Adjusted OR = 0.60, 95%CI 0.38, 0.93). High diet quality (HEI-2015) was associated with a 30% lower risk of NAFLD (Adjusted OR = 0.70, 95% CI 0.51, 0.97) and 72% lower risk of advanced fibrosis (Adjusted OR = 0.28, 95% CI 0.12, 0.66), as compared to those with low diet quality.In this population-based study, high levels of physical activity and diet quality were associated with lower risk of NAFLD in Hispanic/Latino adults. Public health and medical professionals need to concentrate efforts on lifestyle behavior change in Hispanic/Latino adults who are at high risk for serious liver disease.

Screening for gastric intestinal metaplasia (GIM) may lead to early gastric cancer detection. We developed and validated a pre-endoscopy risk prediction model for detection of GIM based on patient-level risk factors in a U.S. population. We used data from 423 GIM cases and 1796 controls from a cross-sectional study among primary care and endoscopy clinic patients at the Houston VA. We developed the model using backwards stepwise regression and assessed discrimination using area under the receiver operating characteristic (AUROC). The model was internally validated using cross-validation and bootstrapping. The final expanded model was compared to a model including H. pylori infection alone and a baseline model including remaining terms without H. pylori. Male sex, older age, non-white race/ethnicity, smoking status, and H. pylori were associated with GIM risk. The expanded model including these terms had AUROC 0.73 (95%CI 0.71–0.76) for predicting GIM and AUROC 0.82 (95%CI 0.79–0.86) for extensive GIM. This model discriminated better than a model including only H. pylori (AUROC 0.66; 95%CI 0.63–0.68) and the baseline model (AUROC 0.67; 95%CI 0.64–0.70). The expanded model performed similarly among primary care (AUROC 0.75) and endoscopy (AUROC 0.73) patients. The expanded model showed sufficient internal validity (cross-validation AUROC 0.72) with little evidence of over-fitting. We develop and validate a non-invasive risk model for GIM detection in a U.S. population that included terms for sex, age, race/ethnicity, smoking status, and H. pylori infection. Validated risk models would identify individuals with GIM who should be referred for endoscopic screening.

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.

Gastric cancer (GC) incidence rates overall in the United States have declined over recent decades and are predicted to continue declining. However, there have been mixed recent findings regarding the potential stabilization of rates and potential divergent trends by age group. We used the most recent cancer data for the United States and examined trends in GC between 1992 and 2019, overall and in important subgroups of the population.Age-adjusted GC incidence rates and trends in adults 20 years or older were calculated using data from the Surveillance, Epidemiology, and End Results (SEER) 12 program. Secular trends were examined overall and by age group, sex, race/ethnicity, SEER registry, and tumor location. We used joinpoint regression to compute annual percent changes, average annual percent changes, and associated 95% CI.GC rates decreased by 1.23% annually from 1992 to 2019. Despite overall decreases, GC incidence rates increased for age groups below 50 years, predominately driven by noncardia GC (74.3% of all GCs). Cardia GC (26.7% of GC) rates decreased in all age groups except for 80 to 84 years. Overall GC rates decreased for both sexes, all races, and for all SEER registry regions, with the largest decreases occurring in males, Asians and Pacific Islanders, and in Hawaii. Age-period-cohort analysis revealed that birth cohorts before 1940 and after 1980 both had increased rates of GC compared with the reference birth cohort of 1955.GC rates overall have continued to decline through 2019, despite increases in the rate of noncardia GC for younger age groups.

Endoscopic mucosal resection (EMR) is an effective method for removing non-pedunculated polyps ≥ 20 mm. We aimed to examine changes in EMR techniques over a 9-year period and evaluate frequency of histologic-confirmed recurrence.We identified patients who underwent EMR of non-pedunculated polyps ≥ 20 mm at a safety net and the Veteran's Affairs (VA) hospital in Houston, Texas between 2012 and 2020. Odds ratios (ORs) and 95% confidence intervals (CI) for associations with recurrence risk were estimated using multivariable logistic regression.461 unique patients were included. The histologic-confirmed recurrence was 29.0% at 15.6 months median follow up (IQR 12.3 - 17.4). Polyps removed between 2018 and 2020 had a 0.43 decreased odds of recurrenceHistologic-confirmed recurrence after EMR for non-pedunculated polyps ≥ 20 mm decreased over the seven year-period. Saline was associated with a higher risk of recurrence and the use of more viscous agents increased over time.

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.

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.

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.

Background: Although mortality from cervical cancer has declined steadily in the U.S. since the advent of population-based screening in the 1970s, the benefit has not reached all racial/ethnic groups of patients equally. This study examined the underlying role of neighborhood-level socioeconomic disadvantage as a potential mediator of the association between race/ethnicity and being diagnosed with late-stage versus early-stage cervical cancer. Methods: We analyzed Texas Cancer Registry data for cervical cancer cases diagnosed among women aged 18 or older from 2010 to 2018. Cervical cancer cases were categorized as early or late stage at diagnosis. First, we used a stepwise hierarchical logistic regression model to examine the associations between race/ethnicity and stage at diagnosis. Then, we performed causal mediation analyses using the counterfactual framework approach to estimate the direct, indirect (mediated), and total effects, and percent mediated. Results: Of the 9525 women with cervical cancer, 4869 (2200 non-Hispanic White (NHW) (45.2%), 720 non-Hispanic Black (NHB) (14.8%), 1800 Hispanic (37.0%)) had late-stage cervical cancer at diagnosis (overall, 51.1%). Women 65 years or older, NHB, Hispanic, with Medicaid/Medicare, uninsured, and those who reside in more deprived neighborhoods were more likely to present with advanced cervical cancer at diagnosis (p Citation Format: Itunu O. Sokale, Abiodun O. Oluyomi, Aaron P. Thrift. Racial/ethnic disparities in stage at diagnosis among women with cervical cancer in Texas: Mediating effects of neighborhood-level socioeconomic deprivation [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 1898.

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.

Most patients with hepatocellular carcinoma (HCC) are ≥ 65 years old at diagnosis and ~ 20% present with disease amenable to curative intent surgical therapy. The aim of this study was to examine whether treatment, the demographic variables, and clinical factors could predict 5-year survival among HCC patients. We included patients, 66 years or older, diagnosed with a first primary HCC from 1994 through 2007 in the SEER-Medicare database, and followed up until death or 31 December 2012. Curative intent treatment was defined as liver transplantation, surgery resection, or ablation. We estimated odds ratios (OR) and 95% confidence intervals (CI) for associations with 5-year survival using logistic regression. We identified 10,826 patients with HCC with mean age 75.3 (standard deviation, 6.4) years. Most were male (62.2%) and non-Hispanic white (59.7%). Overall, only 8.1% of patients were alive 5 years post-HCC diagnosis date. Among all patients that survived ≥ 5 years, 69.8% received potentially curative treatment. Conversely, patients who received potentially curative treatment represented only 15.7% of patients who survived

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.

Hepatocellular (HCC) and extrahepatic cancers have been associated with non-alcoholic fatty liver disease (NAFLD); however, the extent and nature of these relationships remain unclear. We aimed to estimate the absolute incidence rates of these cancers in adults with NAFLD with respect to key demographic and clinical factors.We searched PubMed, Embase, Cochrane Library and Web of Science databases for studies reporting the incidence rates of any cancer in adults with NAFLD from inception to 31 August 2020. The main meta-analysis outcomes were pooled incidences of cancers in NAFLD using random-effects modelling. Subgroup analyses examined the effects of NAFLD disease stage.In total, 64 studies were eligible for analysis of HCC and extrahepatic cancer incidence including 625,984 and 41,027 patients, respectively. The pooled HCC incidence rate was 1.25 per 1000 person-years (95% CI 1.01 to 1.49; Isup2/sup = 94.8%). In patients with NAFLD with advanced liver fibrosis or cirrhosis, the HCC incidence rate was 14.46 per 1000 person-years (95% CI 10.89 to 18.04; Isup2/sup = 91.3%). The pooled extrahepatic cancer incidence rate was 10.58 per 1000 person-years (95% CI 8.14 to 13.02; Isup2/sup = 97.1%). The most frequently occurring extrahepatic cancers were uterine, breast, prostate, colorectal, and lung. Extrahepatic cancer incidence rates were not higher in patients with NAFLD with advanced liver fibrosis or cirrhosis.The rate of HCC development in patients with NAFLD who have progressed to advanced liver fibrosis or cirrhosis supports current HCC surveillance recommendations targeted for this group. Extrahepatic cancers are over eight-fold more frequent than HCC in NAFLD and not associated with liver fibrosis stage. As the global prevalence of NAFLD is approximately 25% and increasing, these findings support a focus on its prevention and the early detection of cancer in adults with NAFLD.

Screening for gastric cancer is not recommended despite rising rates in certain U.S.We determined possible missed opportunities for the detection and surveillance of preneoplastic lesions among gastric cancer patients in a VA hospital.This retrospective cohort study included consecutive, newly diagnosed non-cardia gastric adenocarcinoma patients from 11/2007 to 10/2018 at the Houston VA Hospital. We identified missed opportunities for screening based on risk factors (non-White race, smoking, alcohol, Helicobacter pylori infection, gastric ulcers, family history of gastric cancer). We additionally determined missed opportunities for surveillance of known high-risk lesions. Associations between receipt of prior endoscopy for screening or surveillance and cancer-related outcomes (stage, treatment, survival) were determined using logistic regression models.Among 91 gastric cancer patients, 95.6% were men, 51.6% were black, 12.1% were Hispanic, with mean age of 68.0 years (standard deviation 10.8 years). The most common risk factors included non-white race (68.1%), smoking (76.9%), alcohol use (59.3%) and prior H. pylori (12.1%). Most patients had ≥ 1 risk factor for gastric cancer (92.6%), and 76.9% had ≥ 2 risk factors. Only 25 patients (27.5%) had undergone endoscopy prior to cancer diagnosis. Of 14 with known high-risk lesions (i.e., gastric intestinal metaplasia, dysplasia, ulcer), only 2 (14.3%) underwent surveillance endoscopy. Receipt of prior endoscopy was not associated with differences in cancer outcomes.Most patients with newly diagnosed gastric cancer had ≥ 2 known risk factors for gastric cancer but never received prior screening endoscopy. Among the few with known prior preneoplastic lesions, endoscopic surveillance was not consistently performed.

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.

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.

The development of point-of-care biomarkers of disease has become a major focus of interest in nonalcoholic fatty liver disease (NAFLD). The NAFLD fibrosis score (NFS), BARD, FIB-4, and aspartate aminotransferase-to-platelet ratio index (APRI) are commonly used for advanced NAFLD fibrosis prediction. However, the performance of these scores among in a predominantly Hispanic patient population, a population with the highest prevalence of NAFLD, has not been examined. We performed a retrospective study among patients with histologically confirmed and staged NAFLD at the Ben Taub General Hospital, Houston, Texas, to externally validate four noninvasive advanced fibrosis prediction scores. Their discriminatory ability was assessed using the area under the receiver operating characteristic curve (AUROC). Sensitivity, specificity, positive, and negative predictive values were calculated. We included 99 NAFLD patients, of whom 37 (37.4%) had advanced fibrosis. The cohort was predominantly Hispanic (73.7%). The AUROC for detecting advanced fibrosis were: NFS 0.79 (95% confidence interval, 0.69–0.88), BARD 0.76 (0.67–0.86), FIB-4 0.77 (0.68–0.87), and APRI 0.70 (0.59–0.81). Using the low cutoff for the NFS (− 1.455) had the highest sensitivity (81.1%) and the highest negative predictive value (85.4%) among the overall study population. Noninvasive scores for advanced NAFLD fibrosis have moderate discriminatory ability in Hispanic patients with NFS having a small advantage. The AUROCs of these scores were similar to those reported in Caucasian populations. However, they had uniformly lower negative predictive values among our predominantly Hispanic study population, suggesting that they are not reliable for ruling out advanced fibrosis among this high-risk population.

The risk and determinants of HCC in patients with primary biliary cholangitis (PBC) are unclear. We conducted a systematic review and meta-analysis of the incidence of HCC and risk factors associated with HCC risk among patients with PBC. We searched PubMed, EMBASE, MEDLINE, Cochrane databases and reference lists from relevant articles to identify cohort studies that examined incidence of HCC in patients with PBC from inception through November 2019. A total of 29 studies including 22,615 patients met the eligibility criteria. The median cohort size was 292 patients followed for an average of 76 months. The pooled incidence rate for patients with PBC was 4.17 per 1000 patient-years (95% CI 3.17–5.47). On subgroup analysis, the incidence of HCC in patients with PBC cirrhosis was 15.7 per 1000 patient-years (95% CI 8.73–28.24). The HCC incidence rate was 9.82 per 1000 person-years (95% CI 5.92–16.28) in men and 3.82 per 1000 person-years (95% CI 2.85–5.11) in women. Cirrhosis is the strongest risk factor for HCC in patients with PBC. Male gender was also a risk factor. Our meta-analysis supports current recommendations of HCC surveillance in patients with PBC cirrhosis. Further studies are needed to evaluate risk factors in this population.

Recent findings indicate a shift in the epidemiology of non-cardia gastric cancer in the USA. In particular, an uprising trend in incidence rates among non-Hispanic whites aged

Alcohol consumption, especially at levels above 3 drinks/day, causes eight different types of cancer. We aimed to estimate the percentage and number of incident cancer cases diagnosed in Texas in 2015 that were attributable to alcohol consumption. We further examined for differences in these estimates across major population racial/ethnic subgroups. We calculated population-attributable fractions for cancers attributable to alcohol consumption using prevalence estimates of alcohol consumption from the Texas Behavioral Risk Factor Surveillance System and relative risks associated with alcohol consumption from the third World Cancer Research Fund/American Institute for Cancer Research expert report. Cancer incidence data were retrieved from the Texas Cancer Registry. We estimated 2.9% of all cancers or 2974 excess cancer cases diagnosed in 2015 in Texans aged ≥25 years were attributable to alcohol consumption. Non-Hispanic Blacks (2.2%) had the lowest proportion of alcohol-attributable cancers. Despite Hispanics having the highest percent of non-consumption of alcohol (65.3%, compared with 45.5% of non-Hispanic Whites), Hispanics had a slightly higher proportion of alcohol-attributable cancers than non-Hispanic Whites (3.0% and 2.7%, respectively). Alcohol consumption is an important target for intervention by public health programs aimed toward addressing cancer prevention. Differences in alcohol-attributable cancer burden among racial/ethnic subgroups should be acknowledged to provide appropriately tailored prevention recommendations.

Texas is the second largest state by area and population in the USA and is reported to have high incidence and mortality rates for hepatocellular carcinoma (HCC). The reasons for the increasingly high burden of HCC in Texas are not clear. We explored trends and demographic and regional variations in HCC incidence to better understand reasons for the high burden in Texas. We analyzed Texas Cancer Registry incidence data from 2001 to 2015 and compared results to the U.S. National Program of Cancer Registries and SEER for the same period. Rates were stratified by sex, race/ethnicity, and age at diagnosis. Rates were also compared between the US/Mexico border region of Texas and the rest of Texas. Texas had the highest HCC age-adjusted incidence rate of all states, 13.2/100,000, which was 45% higher than the national average. In Texas and nationally, rates increased by 4% per year between 2001 and 2015. Rates in Texas were 26–37% greater than national rates for Hispanics, African-Americans, and non-Hispanic whites. Among Hispanics in states with the largest percentage of Hispanics, Texas-based Hispanics had the highest HCC incidence rate in 2015 (21.2/100,000) compared with Hispanics in New Mexico, California, Arizona, Nevada, and Florida. Incidence rates were highest in South Texas and US/Mexico border regions. Increasing rates in the large Hispanic population may explain why Texas now has the highest HCC incidence rate in the USA.

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.

Etiological risk factors for cirrhosis have changed in the last decade. It remains unclear to what extent these trends in cirrhosis risk factors have changed HCC risk.We used data from two contemporary, prospective multiethnic cohorts of patients with cirrhosis: the Texas Hepatocellular Carcinoma Consortium Cohort and the Houston Veterans Administration Cirrhosis Surveillance Cohort. Patients with cirrhosis were enrolled from seven US centers and followed until HCC diagnosis, transplant, death, or June 30, 2021. We calculated the annual incidence rates for HCC and examined the effects of etiology, demographic, clinical, and lifestyle factors on the risk of HCC. We included 2733 patients with cirrhosis (mean age 60.1 years, 31.3% women). At enrollment, 19.0% had active HCV, 23.3% had cured HCV, 16.1% had alcoholic liver disease, and 30.1% had NAFLD. During 7406 person-years of follow-up, 135 patients developed HCC at an annual incidence rate of 1.82% (95% CI, 1.51-2.13). The annual HCC incidence rate was 1.71% in patients with cured HCV, 1.32% in patients with alcoholic liver disease, and 1.24% in patients with NAFLD cirrhosis. Compared to patients with NAFLD, the risk of progression to HCC was 2-fold higher in patients with cured HCV (HR, 2.04; 95% CI, 1.24-3.35). Current smoking (HR, 1.63; 95% CI, 1.01-2.63) and overweight/obesity (HR, 1.79; 95% CI, 1.08-2.95) were also associated with HCC risk.HCC incidence among patients with cirrhosis was lower than previously reported. HCC risk was variable across etiologies, with higher risk in patients with HCV cirrhosis and lower risk in those with NAFLD cirrhosis. Current smoking and overweight/obesity increased HCC risk across etiologies.