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Background: There is a large Barrett’s esophagus patient population undergoing endoscopic surveillance. Methods to stratify patients into higher and lower risk groups may enable more varied surveillance intervals for patients with non-dysplastic Barrett’s esophagus that could optimise use of endoscopy resources. Objective: We aimed to assess whether risk of progression to esophageal adenocarcinoma differed in patients with multiple endoscopic biopsies negative for dysplasia.Methods: We conducted a retrospective cohort study among individuals from the population-based Northern Ireland Barrett’s register with a histologically confirmed diagnosis of non-dysplastic Barrett’s esophagus (with intestinal metaplasia) between 1993 and 2010, who had at least one endoscopic biopsy conducted at least 12 months after diagnosis. We used Poisson regression to estimate incidence rate ratios (IRR) and 95% confidence intervals (CI) for the association between number of successive endoscopies showing non-dysplastic Barrett’s esophagus and risk of esophageal adenocarcinoma alone, and combined with high-grade dysplasia, at the next endoscopy.Results: We identified 1,761 individuals who met our eligibility criteria. Subsequent risk of progression to esophageal adenocarcinoma was lower at the next endoscopy following two endoscopies showing non-dysplastic Barrett’s esophagus (IRR 0.26, 95% CI 0.10-0.66) than following one endoscopy showing non-dysplastic Barrett’s esophagus. Similar findings were apparent for risk of progression to esophageal adenocarcinoma or high-grade dysplasia (IRR 0.41, 95% CI 0.22-0.79).Conclusion: The lower risk of malignant progression in individuals with persistent non-dysplastic Barrett’s esophagus over two consecutive endoscopic biopsies but not for longer term persistence does not support hypotheses of persistence being an indicator of less biologically aggressive lesions. Instead, the initial difference may be attributable to post-endoscopy cancers and support the necessity of adhering to robust quality standards for endoscopic procedures.

Previous Mendelian randomization (MR) studies on 25-hydroxyvitamin D (25(OH)D) and cancer have typically adopted a handful of variants and found no relationship between 25(OH)D and cancer; however, issues of horizontal pleiotropy cannot be reliably addressed. Using a larger set of variants associated with 25(OH)D (74 SNPs, up from 6 previously), we perform a unified MR analysis to re-evaluate the relationship between 25(OH)D and ten cancers. Our findings are broadly consistent with previous MR studies indicating no relationship, apart from ovarian cancers (OR 0.89; 95% C.I: 0.82 to 0.96 per 1 SD change in 25(OH)D concentration) and basal cell carcinoma (OR 1.16; 95% C.I.: 1.04 to 1.28). However, after adjustment for pigmentation related variables in a multivariable MR framework, the BCC findings were attenuated. Here we report that lower 25(OH)D is unlikely to be a causal risk factor for most cancers, with our study providing more precise confidence intervals than previously possible., 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.

A community outreach hepatitis C virus (HCV) infection screening program provided low yield of detecting HCV-infected patients, linking them to our hepatology clinic for treatment. Our data underscore that most of the yield was related to addiction centers and birth cohort; these groups should be targeted by future interventions.

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 5 years. Curative intent treatment was the strongest predictor for surviving ≥ 5 years (vs. none/palliative treatment; adjusted OR 8.12, 95% CI 6.90-9.64). While stage at diagnosis and comorbidities were also independently associated with ≥ 5-year survival in HCC patients, these factors did not improve discrimination between short- and long-term survivors.Curative intent treatment was the strongest predictor for survival ≥ 5 years among HCC patients. Given the limited availability of liver transplant and limited eligibility for surgical resection, finding curative intent HCC therapies remain critically important.

Background & Aims There is a need to identify individuals with gastric intestinal metaplasia, a precursor to gastric cancer, so they can be offered screening and surveillance. We examined the prevalence of gastric intestinal metaplasia, detected by upper endoscopy biopsy analysis, in different race and ethnic subgroups. We also investigated the extent to which Helicobacter pylori infection, with or without acute and chronic gastritis, accounts for observed associations between race or ethnicity and risk of gastric intestinal metaplasia. Methods We used data from a cross-sectional study of consecutively recruited patients at the Michael E. DeBakey Veterans Affairs Medical Center in Houston, Texas, from February 2008 to August 2013. All participants completed a study questionnaire on sociodemographic and clinical characteristics and underwent upper endoscopy with gastric mapping (7 biopsy sites). Cases were classified as having gastric intestinal metaplasia if intestinal metaplasia was detected in 1 or more noncardia gastric biopsies; noncases were participants without evidence of gastric intestinal metaplasia. We used logistic regression models to estimate odds ratios (ORs) and 95% CI values to examine the association between race or ethnicity and gastric intestinal metaplasia and performed a mediation analysis to determine whether H pylori and gastritis affected observed associations. Results We included 415 cases with gastric intestinal metaplasia and 1764 noncases. The prevalence of gastric intestinal metaplasia was highest among Hispanic patients (29.5%; 95% CI, 23.7%–36.1%), followed by African American (25.5%; 95% CI, 22.4%–28.9%) and non-Hispanic white patients (13.7%; 95% CI, 11.9%–15.7%). After we adjusted for age, sex, and smoking, African American (OR, 1.87; 95% CI, 1.44–2.44) and Hispanic race or ethnicity (OR, 2.32; 95% CI, 1.61–3.34) and H pylori infection (OR, 3.65; 95% CI, 2.79–4.55) were associated with an increased risk of gastric intestinal metaplasia. H pylori infection alone accounted for 33.6% of the association of race or ethnicity with gastric intestinal metaplasia, and 55.5% of the association when combined with acute and chronic gastritis. Conclusions Hispanic and African American patients have an increased risk for gastric intestinal metaplasia, determined by upper endoscopy biopsy analysis, compared with non-Hispanic white patients. This increase in risk was partially independent of H pylori infection.

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.

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

Background & Aims The risk of nonalcoholic fatty liver disease (NAFLD) and its progression may differ between men and women. We conducted a systematic review and meta-analysis to determine the relationship between sex and NAFLD, nonalcoholic steatohepatitis (NASH), and advanced NAFLD fibrosis. Methods Studies reporting sex-stratified NAFLD prevalence among population-based samples and either NASH or advanced fibrosis among patients with biopsy-proven NAFLD were identified from MEDLINE, EMBASE, and Cochrane databases through December 2017. We calculated pooled relative risk ratios comparing women vs men for each outcome. Results Our final analysis comprised 54 studies. Samples sizes were 62,239 for the NAFLD analysis, 5428 for the NASH analysis, and 6444 for the advanced fibrosis analysis. Women had a 19% lower risk of NAFLD than men in the general population (pooled risk ratio [RR], 0.81; 95% CI, 0.68–0.97; I2 = 97.5%). Women had a similar risk of NASH (RR, 1.00; 95% CI, 0.88–1.14; I2 = 85.1%), and a 37% higher risk of advanced fibrosis (RR, 1.37; 95% CI, 1.12–1.68; I2 = 74.0%) than men. Age modified the effect of sex on NAFLD severity. Risks of NASH (RR, 1.17; 95% CI, 1.01–1.36) and advanced fibrosis (RR, 1.56; 95% CI, 1.36–1.80; I2 = 0) were substantially higher in women in study populations with average ages of 50 years and older; sex differences in NASH and advanced fibrosis were attenuated in younger populations. Conclusions In a systematic review and meta-analysis, we found women to have a lower risk of NAFLD than men. However, once NAFLD is established, women have a higher risk of advanced fibrosis than men, especially after age 50 years.

OBJECTIVES The risk of noncardia gastric cancer is increased in the presence of gastric intestinal metaplasia. We aimed to identify demographic and lifestyle factors independently associated with the risk of gastric intestinal metaplasia. METHODS We used data from a cross-sectional study of patients attending primary care and endoscopy clinics at the Michael E. DeBakey VA Medical Center in Houston, Texas, between February 2008 and August 2013. All patients completed standardized questionnaires and underwent endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included patients with intestinal metaplasia on any noncardia gastric biopsy; we defined extensive gastric intestinal metaplasia as antrum and corpus involvement. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic regression models. RESULTS We identified 423 cases with gastric intestinal metaplasia and 1,796 controls without gastric intestinal metaplasia. Older age (vs

Contains fulltext : 229320.pdf (Publisher’s version ) (Closed access) BACKGROUND & AIMS: Esophageal adenocarcinoma (EA) and its premalignant lesion, Barrett's esophagus (BE), are characterized by a strong and yet unexplained male predominance (with a male-to-female ratio in EA incidence of up to 6:1). Genome-wide association studies (GWAS) have identified more than 20 susceptibility loci for these conditions. However, potential sex differences in genetic associations with BE/EA remain largely unexplored. METHODS: Given strong genetic overlap, BE and EA cases were combined into a single case group for analysis. These were compared with population-based controls. We performed sex-specific GWAS of BE/EA in 3 separate studies and then used fixed-effects meta-analysis to provide summary estimates for >9 million variants for male and female individuals. A series of downstream analyses were conducted separately in male and female individuals to identify genes associated with BE/EA and the genetic correlations between BE/EA and other traits. RESULTS: We included 6758 male BE/EA cases, 7489 male controls, 1670 female BE/EA cases, and 6174 female controls. After Bonferroni correction, our meta-analysis of sex-specific GWAS identified 1 variant at chromosome 6q11.1 (rs112894788, KHDRBS2-MTRNR2L9, P(BONF) = .039) that was statistically significantly associated with BE/EA risk in male individuals only, and 1 variant at chromosome 8p23.1 (rs13259457, PRSS55-RP1L1, P(BONF) = 0.057) associated, at borderline significance, with BE/EA risk in female individuals only. We also observed strong genetic correlations of BE/EA with gastroesophageal reflux disease in male individuals and obesity in female individuals. CONCLUSIONS: The identified novel sex-specific variants associated with BE/EA could improve the understanding of the genetic architecture of the disease and the reasons for the male predominance.

Although substantial progress is currently being made in the development of novel and more effective therapeutics, cancer remains a largely unsolved clinical problem with high mortality. Cancer incidence is on the rise in the United States and worldwide. Between 2005 and 2015, the number of cancer cases increased by 33%, owing in part to population aging, which contributed 16%, and population growth and changes in age-specific rates, which contributed the remainder. Cancer incidence and the societal cancer burden are expected to increase further. Beyond therapeutics, substantial reduction in cancer mortality necessitates improved understanding of cancer risk, implementation of effective preventive intervention strategies, and early detection of cancers that are likely to progress to avoid the problem of overdiagnosis, all of which represent substantial challenges that can be overcome. Identifying individuals at increased risk of developing a particular cancer type would allow for a range of preventive interventions to be implemented, from altered lifestyle and health behaviors to the use of vaccines, and early detection of particular cancer(s) for which these persons are at risk. A case in point is obesity, which is a risk factor for at least 13 different cancers. Elucidation of metabolic, immune, and other molecular profiles that contribute to the increased risk would allow for more focused screening strategies for persons with these risk profiles and would allow implementation of targeted preven­tion strategies aimed at the cancer(s) for which they are at risk.

BACKGROUND: Efforts to reduce mortality from esophageal adenocarcinoma (EA) have focused on screening and surveillance of Barrett’s esophagus (BE). AIMS: We sought to determine the frequency of prior diagnosis of BE in patients with EA, and to evaluate the impact of a prior BE diagnosis on mortality in EA patients. METHODS: This was a retrospective cohort study of patients diagnosed with EA in the VA during 2002–2016. We compared the distributions of EA stage and receipt of treatment between EA patients with and without a prior BE diagnosis and used Cox proportional hazards models to compare mortality risk (all-cause and cancer specific) unadjusted and adjusted for stage and treatment to assess their impact on any survival differences. RESULTS: Among 8564 EA patients, only 4.9% had a prior BE diagnosis. The proportion with prior BE diagnosis increased from 3.2% in EA patients diagnosed during 2005–2007 to 7.0% in those diagnosed during 2014–2016. EA patients with a prior BE diagnosis were more likely to have stage 1 disease and receive any treatment. A prior BE diagnosis was associated with lower all-cause mortality risk (hazard ratio [HR] unadjusted for stage, 0.69; 95% CI, 0.61–0.80), which was largely explained by the earlier stage of EA at the time of diagnosis (HR adjusted for stage, 0.87; 95% CI, 0.75–0.99). There was no evidence of lead time bias or length time bias. CONCLUSIONS: Prior diagnosis of BE was associated with better survival, largely due to earlier EA stage at diagnosis.

Since the early 1970s, the incidence of esophageal adenocarcinoma (EA) has increased dramatically in most Western populations while the incidence of esophageal squamous cell carcinoma has decreased. As a result, EA has become the predominant subtype of esophageal cancer in North America and Europe and is an important contributor to overall cancer mortality. Barrett's esophagus (BE), a metaplastic columnar epithelium of the distal esophagus, is the known precursor lesion for EA. EA and BE occur 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. Conversely, EA and BE are less common in persons using nonsteroidal anti-inflammatory drugs and in person with Helicobacter pylori infection. The 5-year survival rate for patients with EA, although generally poor, has improved during the past decade, and long-term survival is increasingly possible for patients with early or locally advanced disease. This review combines a synthesis of published studies with an analysis of data from the United States National Cancer Institute's Surveillance, Epidemiology, and End Results program to discuss the change in incidence of EA and summarize current knowledge of risk factors.

BACKGROUND: The incidence of gastric cancer, while declining in many places worldwide, is characterized by considerable geographical variability. The USA has large racial, ethnic and regional variation; we collected data from all 50 states to better characterize recent changes in gastric cancer incidence nationwide. METHODS: Annual gastric cancer incidence rates from 1999 to 2013 were extracted from the United States Cancer Statistics (USCS) registry. Secular trends of gastric cancer incidence were examined overall and by sociodemographic factors and states. We used Joinpoint regression to compute annual percent change (APC) and average annual percent change (AAPC) and corresponding 95% confidence intervals (CIs). SEER 13 registries data were extracted to examine the secular trends by cardia and non-cardia gastric cancers. RESULTS: Overall gastric cancer incidence decreased until 2007 (APC = −1.55, 95% CI: −1.88, −1.21), and remained stable thereafter (APC = −0.32, 95% CI: −0.84, 0.20). However, rates increased among persons

Endoscopic surveillance is recommended for patients with Barrett's esophagus (BE). However, it remains unclear if all BE patients benefit from long-term surveillance. We investigated the risk of esophageal adenocarcinoma (EAC) in BE patients in relation to number of successive endoscopies, years of follow-up, and calendar year.We conducted a retrospective cohort study of male veterans with newly diagnosed BE during 2004-2009 with follow-up until 30 September 2011. EAC was verified using detailed structured electronic medical records reviews. We used Poisson regression to determine incidence rates, rate ratios (RR), and corresponding 95% confidence intervals (CI) for EAC according to number of successive endoscopies, years of follow-up independent of number of follow-up endoscopies, and calendar year of BE diagnosis.Among 28,561 male patients with BE, 406 developed EAC during 140,499 person-years of follow-up (median 4.9 years). EAC incidence rates increased with each additional endoscopy following a previous negative endoscopy (RR per additional endoscopy, 1.43; 95% CI, 1.25-1.64). Compared to the EAC incidence rate at the 1st follow-up EGD, the EAC incidence rate at the 5th follow-up EGD was ninefold higher (adjusted RR, 8.82; 95% CI, 4.90-15.9). EAC incidence was highest at the first year of follow-up (5.34 per 1,000 person-years); however, EAC rates starting from the second follow-up year increased during successive years of follow up. Compared to the EAC incidence rate in the 2nd year of follow-up, the EAC incidence rate was 1.5-fold higher in EGDs conducted ≥5 years after the index BE date (adjusted RR, 1.49; 95% CI, 1.07-2.10). In contrast, we found no significant change in EAC incidence rates by calendar year.Persistence of non-neoplastic BE on multiple consecutive endoscopies was not associated with lower EAC risk. These findings argue against discontinuation of endoscopic surveillance in patients with persistent nondysplastic BE after multiple negative endoscopies.

The purpose of this study is to review the recent literature on the epidemiology of NAFLD-related HCC and discuss published data on primary and secondary prevention of NAFLD-related HCC, including surveillance for HCC. Hepatocellular cancer (HCC) is the fastest rising cause of cancer-related deaths in the USA. Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the USA, afflicting nearly one in three Americans and is increasingly linked to the development of HCC. NAFLD will likely become the major contributor to the burden of HCC in the USA. While cirrhosis remains the most important risk factor for HCC in NAFLD, mounting evidence indicates that NAFLD patients can rarely develop HCC in the absence of cirrhosis. While effective medical therapies for NAFLD exist, their role as chemopreventive agents against HCC is unclear. Major knowledge gaps remain in our understanding of the risk of HCC and the interplay between HCC-promoting factors in patients with NAFLD. Currently, efforts should focus on prompt diagnosis of NAFLD and cirrhosis with non-invasive methods, or liver biopsy as needed. This will identify the great majority of NAFLD patients at risk for HCC. Valid and reliable methods for identifying non-cirrhotic NAFLD patients at risk for HCC are lacking, so surveillance cannot be currently recommended in the absence of cirrhosis. Meanwhile, further studies are needed to determine the magnitude of risk and specific risk factors or biomarkers for HCC in patients with NAFLD with or without cirrhosis.

To investigate trends in colorectal cancer (CRC) incidence and survival among Hispanics in Texas.The incidence of CRC is rising among young adults in the United States. Given Texas' large Hispanic population, investigating CRC trends in Texas may provide valuable insight into the future of CRC epidemiology in an ever-diversifying US population.Data from the Texas Cancer Registry (1995 to 2010) were used to calculate age-adjusted CRC rates based on the 2000 US standard population. Annual percentage change (APC) and 5-year cancer-specific survival (CSS) rates were reported by age, race/ethnicity, stage, and anatomic location.Of 123,083 CRC cases, 11% occurred in individuals below 50 years old, 26% of whom were Hispanic. Incidence was highest among African Americans (AAs; 76.3/100,000), followed by non-Hispanic whites (NHWs; 60.2/100,000) and Hispanics (50.8/100,000). Although overall CRC incidence declined between 1995 and 2010 (APC, -1.8%; P0.01), trends differed by age and race/ethnicity. Among individuals 50 years and above, the rate of decline was statistically significant among NHWs (APC, -2.4%; P0.01) and AAs (APC, -1.3%; P0.01) but not among Hispanics (APC, -0.6%; P=0.13). In persons aged 20 to 39 years, CRC incidence rose significantly among Hispanics (APC, 2.6%; P0.01) and NHWs (APC, 2.4%; P0.01), but not AAs (APC, 0.3%; P=0.75). CSS rates among Hispanics and NHWs were comparable across most age groups and cancer stages, whereas CSS rates among AAs were generally inferior to those observed among NHWs and Hispanics.Although CRC incidence has declined in Texas, it is rising among young Hispanics and NHWs while declining more slowly among older Hispanics than among older NHWs and AAs.

Chronic HCV infection is a global health problem that affects >184 million people worldwide. HCV is associated with several hepatic and extrahepatic disorders, including several malignancies. The burden of HCV-related disorders is influenced by the number of new and existing cases, number of existing cases and the natural history of the infection. The natural history of HCV is affected by several demographic, virological, clinical and lifestyle factors. Major variations exist in the burden of HCV among different populations and geographical regions, as well as over time. With the advent of new and efficacious antiviral treatments, it is important to learn the determinants of HCV burden to design appropriate strategies for detection, prognostication and treatment. Furthermore, with the expected growth of patients cured of HCV, it is essential to learn about the possible change in natural history and burden of disease in these patients. In this Review, we will discuss the global epidemiology and burden of HCV and its complications, as well as the natural history and clinical course of chronic and cured HCV infection.

Background & Aims Esophageal adenocarcinoma (EAC) occurs most frequently in men. We performed a Mendelian randomization analysis to investigate whether genetic factors that regulate levels of sex hormones associated with risk of EAC or Barrett’s esophagus (BE). Methods We conducted a Mendelian randomization analysis using data from patients with EAC (n=2488) or BE (n=3247) and control participants (n=2127), included in international consortia of genome-wide association studies in Australia, Europe, and North America. Genetic risk scores or single nucleotide variants were used as instrumental variables for 9 specific sex hormones. Logistic regression provided odds ratios (ORs) with 95% CIs. Results Higher genetically predicted levels of follicle stimulating hormones were associated with increased risks of EAC and/or BE in men (OR, 1.14 per allele increase; 95% CI, 1.01-1.27) and in women (OR, 1.28; 95% CI, 1.03-1.59). Higher predicted levels of luteinizing hormone were associated with a decreased risk of EAC in men (OR, 0.92 per standard deviation increase; 95% CI, 0.87-0.99) and in women (OR, 0.93; 95% CI, 0.79-1.09), and decreased risks of BE (OR, 0.88; 95% CI, 0.77-0.99) and EAC and/or BE (OR, 0.89; 95% CI, 0.79-1.00) in women. We found no clear associations for other hormones studied, including sex hormone-binding globulin, dehydroepiandrosterone sulphate, testosterone, dihydrotestosterone, estradiol, progesterone, or free androgen index. Conclusions In a Mendelian randomization analysis of data from patients with EAC or BE, we found an association between genetically predicted levels of follicle stimulating and luteinizing hormones and risk of BE and EAC.

BACKGROUND: The proportions of patients with oesophageal adenocarcinoma (OAC) diagnosed by Barrett’s oesophagus surveillance or with preexisting Barrett’s oesophagus are unclear. AIM: A systematic review and meta-analysis to estimate the prevalence of prior and concurrent Barrett’s oesophagus diagnosis among patients with OAC or oesophagogastric junction adenocarcinomas (OGJAC). METHODS: We searched PubMed and Embase to identify studies published 1966–1/8/2020 that examined the prevalence of prior (≥6 months) or concurrent Barrett’s diagnosis (at cancer diagnosis) among OAC and OGJAC patients. Random effects models estimated overall and stratified pooled prevalence rates. RESULTS: A total of 69 studies, including 33,002 OAC patients (53 studies) and 2,712 with OGJAC (28 studies) were included. The pooled prevalence of prior Barrett’s oesophagus diagnosis in OAC was 11.8% (95% confidence interval [CI] 8.4–15.6%). The prevalence of prior Barrett’s oesophagus diagnosis was higher in single-center resection studies (16.0%, 95%CI 8.7–24.9%) than population-based cancer registry studies (8.4%, 95%CI 5.5–11.9%). The prevalence of concurrent Barrett’s oesophagus in OAC was 56.6% (95%CI 48.5–64.6%). Studies with 100% early stage OAC had higher prevalence of concurrent Barrett’s oesophagus (91.3%, 95%CI 82.4–97.6%) than studies with

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.

Background: Barrett's esophagus is the precursor to the highly lethal esophageal adenocarcinoma. Risk prediction models have been developed to assist in its detection, potentially improving early identification and treatment of esophageal adenocarcinoma. Six models have been developed. Aims: To externally validate three models (Rubenstein, Thrift, and Baldwin-Hunter models) and compare them to a fourth risk prediction model (Ireland model) for Barrett's esophagus. Methods: Data from 120 Barrett's cases and 235 population controls were available to externally validate the three models. Discriminatory ability of these models was assessed by the area under the receiver operating characteristic curve. Calibration was assessed with the calibration slope, Hosmer-Lemeshow test, and Lowess smoother calibration plot. Following external validation, diagnostic accuracy of the three models was compared to that of the Ireland model. Results: On external validation, the Rubenstein model had an area under the receiver operating characteristic curve of 0.71 and was well calibrated (Hosmer-Lemeshow test, p = 0.67). Likewise, the Thrift and Baldwin-Hunter models had similar discrimination (0.71 and 0.70, respectively) and were also well calibrated (p = 0.69 and p = 0.28). Our previous external validation of the Ireland model provided an area under the receiver operating characteristic curve of 0.83 and was well calibrated (p = 0.14). The Ireland model demonstrated a statistically significantly greater area under the receiver operating characteristic curve than the Rubenstein (p = 0.02), Thrift (p = 0.001), and Baldwin-Hunter (p = 0.002) models. Conclusion: We externally validated the Rubenstein, Thrift, and Baldwin-Hunter risk prediction models and compared them to the Ireland model. The Ireland model demonstrated improved accuracy, albeit with slightly poorer calibration. Refereed/Peer-reviewed

Background Although declining rates of incident AIDS-related Kaposi sarcoma (KS) have been reported, KS incidence rates have noted race/ethnic, age, and geographic diversity. We performed a comprehensive assessment of recent secular trends in AIDS-related KS incidence in the United States. Methods We identified incident KS diagnosed in men aged 20-54 years (who comprise most AIDS-related KS in the United States) using the US Cancer Statistics registry data. Joinpoint analysis assessed for trends in age-adjusted incidence rates between 2000 and 2014 calculating average annual percentage changes (AAPCs) with 95% confidence intervals. Heat maps were generated to compare age-adjusted HIV incidence rates with KS incidence rates. Results Age-adjusted KS incidence rates nationwide decreased from 1.44/100,000 to 0.95/100,000 between 2000 and 2014. Observed rate changes varied across subgroups; eg, there were significant decreases in 30-44 years (AAPC = -5.4%), particularly in Whites and Blacks, significant increases among 20-29 years (AAPC = 2.7), primarily in Blacks, and stable rates among 45-54 years (AAPC = -0.03). In Southern United States, the incidence rates among Blacks did not significantly change. The states with highest average age-adjusted rates over the study period were Georgia (2.71/100,000), New York (2.16/100,000), California (2.02/100,000), Florida (1.90/100,000), and Texas (1.39/100,000), with significantly decreasing trends over time, except Georgia where rates increased (AAPC = 1.8). Conclusions Although KS incidence rates have decreased nationally, age, racial, and geographic disparities persist, including increasing risk among younger Black men and particularly elevated rates in some southern states and urban areas. Further research is needed to address racial and geographic AIDS-related KS disparities.

Epidemiological studies of statin use and liver cancer risk have produced conflicting results. We examined the association between statin use and risk of primary liver cancer in two large independent study populations taking account of important covariates and main indications of statins such as high cholesterol and chronic liver disease. We performed a nested case-control study within the Scottish Primary Care Clinical Informatics Unit (PCCIU) database. Five controls were matched to cases with primary liver cancer and we used conditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with statin use. We also conducted a prospective cohort study within the UK Biobank using self-reported statin use and cancer-registry recorded primary liver cancer outcomes. Cox regression was used to calculate hazard ratios (HRs) and 95% CIs. In the PCCIU case-control analysis, 434 liver cancer cases were matched to 2,103 controls. In the UK Biobank cohort, 182 out of 475,768 participants developed incident liver cancer. Statin use was associated with 39% lower risk of liver cancer in the PCCIU (adjusted OR 0.61, 95% CI 0.43-0.87). When we examined specific subtypes of liver cancer in the UK Biobank, statin use was associated with lower risk of hepatocellular carcinoma (HCC) (adjusted HR, 0.48; 95% CI, 0.24-0.94) but not intrahepatic bile duct carcinoma (IBDC) (adjusted HR, 1.09; 95% CI, 0.45-2.64). In conclusion, we found a consistent inverse relationship between statin use and risk of primary liver cancer which was only seen for HCC but not IBDC. This article is protected by copyright. All rights reserved.

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.

Background Metastatic colorectal cancer (CRC) outcomes continue to improve, but they vary significantly by race and ethnicity. We hypothesize that these disparities arise from unequal access to care. Materials and Methods The Harris Health System (HHS) is an integrated health delivery network that provides medical care to the underserved, predominantly minority population of Harris County, Texas. As the largest HHS facility and an affiliate of Baylor College of Medicine’s Dan L. Duncan Comprehensive Cancer Center, Ben Taub Hospital (BTH) delivers cancer care through multidisciplinary subspecialty that prioritize access to care, adherence to evidence-based clinical pathways, integration of supportive services, and mitigation of financial toxicity. We performed a retrospective analysis of minority patients diagnosed with and treated for metastatic CRC at BTH between January 2010 and December 2012. Kaplan-Meier survival curves were compared with survival curves from randomized control trials reported during that time period. Results We identified 103 patients; 40% were black, 49% were Hispanic, and 12% were Asian or Middle Eastern. Thirty-five percent reported a language other than English as their preferred language. Seventy-four percent of patients with documented coverage status were uninsured. Eighty-four percent of patients received standard chemotherapy with a clinician-reported response rate of 63%. Overall survival for BTH patients undergoing chemotherapy was superior to that of subjects enrolled in the CRYSTAL (Cetuximab Combined with Irinotecan in First-Line Therapy for Metastatic Colorectal Cancer) trial (median, 24.0 vs. 19.9 months; P = .014). Conclusion HHS provides a health delivery infrastructure through which minority patients with socioeconomic challenges experience clinical outcomes comparable with highly selected patients enrolled in randomized control trials. Efforts to resolve CRC disparities should focus on improving access of at-risk populations to high-quality comprehensive cancer care.

Objectives The US Department of Veterans Affairs (VA) is the largest integrated health care provider for HIV-infected patients in the USA. VA data for HIV-specific clinical and quality improvement research are an important resource. We sought to determine the accuracy of using the VA Corporate Data Warehouse (CDW), a fully automated medical records database for all VA users nationally, to identify HIV-infected patients compared with a gold-standard VA HIV Clinical Case Registry (CCR). Methods We assessed the test performance characteristics of each of our CDW criteria-based algorithms (presence of one, two or all of the following: diagnostic codes for HIV, positive HIV laboratory tests, and prescription for HIV medication) by calculating their sensitivity (proportion of HIV-positive patients in the CCR accurately detected as HIV-positive by the CDW algorithm) and positive predictive value (PPV; the proportion of patients identified by the CDW algorithm who were classified as HIV-positive from the CCR). Results We found that using a CDW algorithm requiring two of three HIV diagnostic criteria yielded the highest sensitivity (95.2%) with very little trade-off in PPV (93.5%). Conclusions A two diagnostic criteria-based algorithm can be utilized to accurately identify HIV-infected cohorts seen in the nationwide VA health care system.

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

We previously developed a tool that identified individuals who later developed esophageal adenocarcinoma (based on age, sex, body mass index, smoking status, and prior esophageal conditions) with an area under the curve of 0.80. In this study, we collected data from 329,463 individuals in the UK Biobank cohort who were tested for genetic susceptibility to esophageal adenocarcinoma (a polygenic risk score based on 18 recognized genetic variants). We found that after inclusion of this genetic information, the area under the curve for identification of individuals who developed esophageal adenocarcinoma remained at 0.80. Testing for genetic variants associated with esophageal adenocarcinoma therefore seems unlikely to improve identification of individuals at risk of esophageal adenocarcinoma.

Increased body fat, particularly abdominal visceral fat, is central in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) (1, 2). Identifying a clinically feasible fat assessment method is thus important. Body mass index (BMI) and waist circumference (WC) convey insufficient information on body composition, fat distribution, and visceral fat (3, 4). BMI’s limitations are most evident in cases of “lean” but “metabolically unhealthy” individuals who despite a normal BMI have increased central adiposity and predisposition to cardiometabolic complications including NAFLD (5). While computerized tomography (CT), magnetic resonance imaging (MRI), and DEXA are precise fat assessment methods, they are impractical for routine use. Bioelectrical impedance analysis (BIA) is a simple non-invasive assessment tool for body composition. BIA-estimated abdominal fat was found to have greater discriminatory ability than WC for identifying NAFLD in the only previous study to specifically address the issue (6). However it remains unclear whether BIA-estimated abdominal fat is truly superior to conventional measures for prediction of NAFLD risk as this previous study did not assess the association independent of BMI. Therefore, we sought to determine whether BIA-derived total body and trunk fat measures are more strongly associated with NAFLD risk than BMI and WC.

Background: Studies have shown high but variable mortality following gastrostomy tube (GT) placement. There are no standard practice guidelines for GT placement. Aim: To evaluate if implementation of patient selection and prognosis algorithms for GT insertion has favorable effects on patient outcomes. Methods: This was a pre-, post-cohort analysis in a Veterans Affairs hospital. We implemented a patient selection algorithm aided by the Sheffield Gastrostomy Scoring System (SGSS) in July 2015. We reviewed all referrals to the inpatient service for a GT between July 2014 and June 2016 (pre-, post- implementation), and collected albumin and SGSS at time of consultation, date of GT insertion, and outcomes including vital status and albumin 30 days post-consultation. Patients were followed until 30 October 2016. We compared outcomes pre- and post-implementation. Results: A total of 126 referrals were reviewed, 68 pre- and 58 post-algorithm implementation. Seventy-seven GTs were placed; 58 (75.3%) fulfilled the algorithm-appropriate indications. The mean SGSS was significantly lower among patients in whom GT was placed for algorithm-appropriate indications 2.03 (SD =0.86) vs inappropriate indications (2.59, SD =0.63; p

Background and Aims Less than 10% of patients diagnosed with esophageal adenocarcinoma have a pre-existing Barrett’s esophagus (BE) diagnosis, possibly due to suboptimal performance of guidelines. We examined the prevalence of BE in a previously unscreened primary care population and the potential yield of practice BE screening guidelines. Methods This was a retrospective analysis of a prospective cross-sectional study of consecutively recruited unreferred patients from primary care clinics who underwent study upper endoscopy. We examined the performance of BE screening guidelines of the European Society of Gastrointestinal Endoscopy (ESGE), British Society of Gastroenterology (BSG), American Society for Gastrointestinal Endoscopy (ASGE), American College of Gastroenterology (ACG), American Gastroenterological Association (AGA), and our own modification of guidelines. Results We identified 44 BE cases and 469 controls (prevalence, 8.6%). Among 371 patients without GERD symptoms, 25 (6.7%) had BE. The AGA guidelines requiring ≥2 BE risk factors had sensitivity of 100% and specificity of only 0.2%, whereas ACG, ASGE, ESGE, and BSG guidelines (all requiring GERD first) had low sensitivities (38.6%-43.2%), specificities ranging 67.4% to 76.5%, and area under the receiver operating curve (AUROC) of 0.50 to 0.60. Our 2-pronged approach depending on presence of GERD symptoms or absence of GERD symptoms but with other risk factors achieved sensitivity of 81.8%, specificity of 51.2%, and AUROC of 0.66. Conclusions Over half of BE cases were without frequent GERD symptoms, but virtually all had at least one known BE risk factor. Practice guidelines requiring GERD symptoms have low sensitivity, whereas those not requiring GERD have low specificity. We have proposed a screening guideline with better use of known risk factors.

OBJECTIVES: Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced risk of esophageal adenocarcinoma. Epidemiological studies examining the association between NSAID use and the risk of the precursor lesion, Barrett’s esophagus, have been inconclusive.METHODS: We analyzed pooled individual-level participant data from six case-control studies of Barrett’s esophagus in the Barrett’s and Esophageal Adenocarcinoma Consortium (BEACON). We compared medication use from 1474 patients with Barrett’s esophagus separately with two control groups: 2256 population-based controls and 2018 gastroesophageal reflux disease (GERD) controls. Study-specific odds ratios (OR) and 95% confidence intervals (CI) were estimated using multivariable logistic regression models and were combined using a random effects meta-analytic model.RESULTS: Regular (at least once weekly) use of any NSAIDs was not associated with the risk of Barrett’s esophagus (vs. population-based controls, adjusted OR = 1.00, 95% CI = 0.76–1.32; I2=61%; vs. GERD controls, adjusted OR = 0.99, 95% CI = 0.82–1.19; I2=19%). Similar null findings were observed among individuals who took aspirin or non-aspirin NSAIDs. We also found no association with highest levels of frequency (at least daily use) and duration (≥5 years) of NSAID use. There was evidence of moderate between-study heterogeneity; however, associations with NSAID use remained non-significant in “leave-one-out” sensitivity analyses.CONCLUSIONS: Use of NSAIDs was not associated with the risk of Barrett’s esophagus. The previously reported inverse association between NSAID use and esophageal adenocarcinoma may be through reducing the risk of neoplastic progression in patients with Barrett’s esophagus.

Basal cell and squamous cell carcinomas of the skin are the commonest cancers in humans, yet no validated tools exist to estimate future risks of developing keratinocyte carcinomas. To develop a prediction tool, we used baseline data from a prospective cohort study (n = 38,726) in Queensland, Australia, and used data linkage to capture all surgically excised keratinocyte carcinomas arising within the cohort. Predictive factors were identified through stepwise logistic regression models. In secondary analyses, we derived separate models within strata of prior skin cancer history, age, and sex. The primary model included terms for 10 items. Factors with the strongest effects were >20 prior skin cancers excised (odds ratio 8.57, 95% confidence interval [95% CI] 6.73–10.91), >50 skin lesions destroyed (odds ratio 3.37, 95% CI 2.85–3.99), age ≥ 70 years (odds ratio 3.47, 95% CI 2.53–4.77), and fair skin color (odds ratio 1.75, 95% CI 1.42–2.15). Discrimination in the validation dataset was high (area under the receiver operator characteristic curve 0.80, 95% CI 0.79–0.81) and the model appeared well calibrated. Among those reporting no prior history of skin cancer, a similar model with 10 factors predicted keratinocyte carcinoma events with reasonable discrimination (area under the receiver operator characteristic curve 0.72, 95% CI 0.70–0.75). Algorithms using self-reported patient data have high accuracy for predicting risks of keratinocyte carcinomas.

Epidemiological data regarding coffee and tea consumption and risk of esophageal inflammation, Barrett’s esophagus (BE), and adenocarcinoma are sparse and inconclusive. This study examined the association between consumption of tea or coffee with risk of BE. We conducted a cross-sectional study among United States veterans, comparing 310 patients with histologically confirmed BE with 1728 individuals with no endoscopic or histopathologic features of BE (controls). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression models. In univariate models, we found a statistically significant association between risk of BE and consumption of coffee (OR, 1.41; 95% CI, 1.06–1.87) or tea (OR, 1.34; 95% CI, 1.05–1.71). However, in multivariate analysis, in which models were adjusted for confounders including sex and race, we found no association between risk of BE and consumption of coffee (adjusted OR, 1.04; 95% CI, 0.76–1.42) or tea (adjusted OR, 1.11; 95% CI, 0.85–1.44). These data do not support an association between consumption of coffee or tea and risk of BE. It is unlikely that avoidance of coffee or tea will protect against BE.

Since the early 1970s, the incidence of oesophageal adenocarcinoma has increased dramatically in most Western populations. In contrast, the incidence of oesophageal squamous-cell carcinoma has decreased in these same populations. Epidemiological studies conducted over the past decade have provided great insights into the etiology of oesophageal cancer. These studies have identified gastro-oesophageal reflux disease, obesity and cigarette smoking as risk factors for oesophageal adenocarcinoma, while use of nonsteroidal anti-inflammatory drugs and infection with Helicobacter pylori are associated with reduced risk of oesophageal adenocarcinoma. For oesophageal squamous-cell carcinoma, alcohol and cigarette smoking are the two major risk factors underlying most cases. This review combines a synthesis of these studies with an analysis of data from the United States National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program to discuss the change in incidence of oesophageal cancer and summarize current knowledge of risk factors.

The incidence of esophageal adenocarcinoma has increased rapidly in the USA and other western populations. Barrett’s esophagus, a metaplastic change in the distal esophagus, is the only known precursor for esophageal adenocarcinoma. Epidemiological studies strongly implicate gastroesophageal reflux disease symptoms and obesity as the primary causal factors for esophageal adenocarcinoma and Barrett’s esophagus. Recent studies suggest that abdominal obesity, rather than overall obesity, is associated with esophageal adenocarcinoma and Barrett’s esophagus and that these associations are not entirely explained by gastroesophageal reflux disease symptoms. Evidence from these studies indicates that abdominal obesity has both mechanical (for example, via disruption of the gastroesophageal junction and resulting gastroesophageal reflux symptoms) and nonmechanical metabolic and inflammatory effects on esophageal adenocarcinoma and Barrett’s esophagus. Overall, the current body of literature provides some insights into the potential biological mechanisms linking abdominal obesity with esophageal adenocarcinoma and Barrett’s esophagus.

Contains fulltext : 170949.pdf (Publisher’s version ) (Closed access) BACKGROUND: Observational studies have reported a positive association between body mass index (BMI) and ovarian cancer risk. However, questions remain as to whether this represents a causal effect, or holds for all histological subtypes. The lack of association observed for serous cancers may, for instance, be due to disease-associated weight loss. Mendelian randomization (MR) uses genetic markers as proxies for risk factors to overcome limitations of observational studies. We used MR to elucidate the relationship between BMI and ovarian cancer, hypothesizing that genetically predicted BMI would be associated with increased risk of non-high grade serous ovarian cancers (non-HGSC) but not HGSC. METHODS: We pooled data from 39 studies (14 047 cases, 23 003 controls) in the Ovarian Cancer Association Consortium. We constructed a weighted genetic risk score (GRS, partial F-statistic = 172), summing alleles at 87 single nucleotide polymorphisms previously associated with BMI, weighting by their published strength of association with BMI. Applying two-stage predictor-substitution MR, we used logistic regression to estimate study-specific odds ratios (OR) and 95% confidence intervals (CI) for the association between genetically predicted BMI and risk, and pooled these using random-effects meta-analysis. RESULTS: Higher genetically predicted BMI was associated with increased risk of non-HGSC (pooled OR = 1.29, 95% CI 1.03-1.61 per 5 units BMI) but not HGSC (pooled OR = 1.06, 95% CI 0.88-1.27). Secondary analyses stratified by behaviour/subtype suggested that, consistent with observational data, the association was strongest for low-grade/borderline serous cancers (OR = 1.93, 95% CI 1.33-2.81). CONCLUSIONS: Our data suggest that higher BMI increases risk of non-HGSC, but not the more common and aggressive HGSC subtype, confirming the observational evidence.

Esophageal adenocarcinoma has undergone a continuous rise in incidence since the early 1970s and is the fastest rising cancer among white men in the United States. Epidemiologic studies have demonstrated that medications commonly used to treat multiple chronic conditions (for example, aspirin, non-aspirin nonsteroidal anti-inflammatory drugs, and statins) as well as powerful acid suppressants such as proton pump inhibitors are associated with a reduced risk of esophageal adenocarcinoma. The chemopreventive potential of these classes of medications appears to be especially applicable to persons with Barrett's esophagus, the only known premalignant condition for esophageal adenocarcinoma. However, it is not known whether these medications also influence cancer recurrence and cancer-specific mortality in persons diagnosed with esophageal adenocarcinoma. This is an important question because most patients with esophageal adenocarcinoma have 1 or more comorbid conditions at the time of their cancer diagnosis and are receiving medication to treat these conditions. This article summarizes the evidence on the associations between 4 commonly used classes of medications and (1) risk of developing esophageal adenocarcinoma and Barrett's esophagus and (2) risk of cancer recurrence and cancer-specific mortality in patients with esophageal adenocarcinoma.

Background. Non-alcoholic fatty liver disease (NAFLD) is a growing problem in the U.S. and has become an important risk factor for hepatocellular carcinoma (HCC). Hispanics experience the highest burden of both NAFLD and HCC. Increasing physical activity and making dietary changes to achieve weight loss are the mainstay for NAFLD treatment and potentially for HCC prevention. While newly diagnosed NAFLD patients usually get brief information on the etiology and management of their disease, it is unclear exactly what patients actually think about their current health behaviors and their need to be more active or eat healthier. The purpose of this study was to describe Hispanic NAFLD patients’ current physical activity and dietary behaviors, perceptions of those behaviors, and any barriers they perceive to be hindering them from making a change. Methods. We conducted a cross-sectional study among 414 Hispanic patients participating in the Harris County NAFLD Cohort, a prospective cohort study that recruits consecutive adult patients with NAFLD referred to a multidisciplinary specialty clinic within a safety-net healthcare system in Texas. NAFLD was diagnosed based on liver imaging, excluding other known causes. Height and weight were measured at baseline to obtain Body Mass Index (BMI); diabetes was classified based on pre-existing diagnosis reported by the patients and verified in the medical records. Self-administered questionnaire measured demographic factors, physical activity (Rapid Assessment of Physical Activity Scale), diet (NCI FLASHE questionnaire), and perceptions of and barriers to doing physical activity or eating healthy. We used descriptive statistics to explore demographics, behaviors, perceptions, and barriers. Results. Average age was 46 years, 84% spoke primarily Spanish, and 59% were born in Mexico. More than half of the sample were insufficiently active (55%), but encouragingly 90.1% reported wanting to be more active. Most of the sample (79%) did not meet fruit and vegetable intake guidelines. While 92% of the sample reported that they could eat healthier, only 61% of the total sample thought that they should eat more fruits and vegetables, 70% thought that they should eat less fat and 65% thought that they should eat less sugar. The top 5 barriers to eating healthier were cost, perceptions that healthier food doesn’t taste good, lack of time to cook, difficulty of cooking and difficulty of going to the grocery store. Top barriers to doing more physical activity were Lack of time, feelings of laziness, pain, nowhere to exercise, and feeling that is it too difficult to exercise. Discussion. Interventions will be necessary to encourage physical activity and health dietary behaviors, as well as correct certain perceptions among Hispanic patients diagnosed with NAFLD. Multi-level interventions may be needed to help patients address barriers to these two behaviors. Citation Format: Aaron Thrift, Maya Balakrishnan, Natalia I. Heredia, Yan Liu. Physical activity and nutrition behaviors in Hispanic patients with non- alcoholic fatty liver disease [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-185.