bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4803: Metabolic syndrome is associated with an increased risk of Barrett's esophagus in those without symptomatic reflux.
Authors: Drahos Jennifer , Ricker Winnie , Pfiffer Ruth M. , Warren Joan L. , Cook Michael B. 
Published: August 2014

Abstract
Background: Obesity is known to increase the propensity for gastroesophageal reflux, a discrete inflammatory effect which may lead to the development of an esophageal metaplasia termed Barrett's esophagus (BE). BE is a precancerous lesion that drastically increases the risk of esophageal adenocarcinoma. Obesity is also associated with BE independent of reflux, through unknown pathways. Metabolic syndrome (MetS) is an exposure closely aligned with obesity and represents one possible pathway. MetS produces a global inflammatory state which could increase the risk of BE.
Methods: We used the SEER-Medicare linked database to evaluate the association between MetS and BE with comparison to two control groups- a general Medicare group and an endoscopy BE-negative group. MetS was defined as diagnosis of at least three of the following conditions: obesity, dyslipidemia, hypertension, and impaired fasting glucose. Multivariable logistic regression was used to estimate adjusted odds ratios (OR) and 95% confidence intervals (95%CI). All analyses were adjusted for age, sex, SEER registry, smoking-related conditions, Medicaid dual enrollment, reflux, and a modified Charlson comorbidity score.
Results: We identified 2,212 incident Barrett's esophagus cases among 251,196 eligible beneficiaries. MetS increased the risk of BE [OR 1.20; 95%CI 1.07, 1.36] compared with Medicare controls. However, reflux status modified the association; among those without a prior reflux diagnosis, MetS was associated with a 35% increased risk of BE [OR 1.35; 95%CI 1.18, 1.55], but no association was observed among those with a history of reflux [OR 0.97; 95%CI 0.65, 1.43]. Assessment of individual components of MetS reiterated these findings. MetS was not associated with an increased risk of BE compared with endoscopy controls [OR 0.99; 95%CI 0.88, 1.10].
Conclusions: MetS was positively associated with BE; however not in a reflux population or compared to endoscopy BE-negative controls. Our findings may be explained by a saturated inflammatory state in which MetS global inflammation contributes little to the risk of BE in the presence of discrete inflammatory effects conferred by gastroesophageal reflux. Conversely, in individuals without reflux, the effects of MetS global inflammation in relation to BE are detectable.
Citation Format: Jennifer Drahos, Winnie Ricker, Ruth M. Pfiffer, Joan L. Warren, Michael B. Cook. Metabolic syndrome is associated with an increased risk of Barrett's esophagus in those without symptomatic reflux. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4803. doi:10.1158/1538-7445.AM2013-4803
Abstract 4805: Index-based dietary patterns and risk of esophageal cancer and gastric cancer in the NIH-AARP diet and health study.
Authors: Li Wen-qing , Park Yikyung , Wu Jennifer W. , Ren Jian-song , Goldstein Alisa M. , Taylor Philip R. , Hollenbeck Albert R. , Freedman Neal D. , Abnet Christian C. 
Published: August 2014

Abstract
Background Diet may affect esophageal and gastric cancer risk, but associations have been inconsistent. Due to the complexity of the diet, studies of dietary patterns may elucidate the associations between diet and cancer better than studies of individual foods. Yet, studies evaluating the association between index-based dietary patterns and incident esophageal and gastric cancers have been sparse. Objectives We aimed to prospectively evaluate the association between two diet quality indices, the Healthy Eating Index-2005 (HEI-2005) and the alternate Mediterranean Diet Score (aMED), and risk of esophageal and gastric cancers in the United States.
Methods In sum, 494,968 participants from the National Institutes of Health-AARP Diet and Health study completed a self-administered baseline food frequency questionnaire which was used to estimate scores for each index.
Results During the follow-up (1995-2006), we documented 215 esophageal squamous cell carcinomas (ESCC), 633 esophageal adenocarcinomas (EAC), 453 gastric cardia adenocarcinomas, and 501 gastric noncardia adenocarcinomas. Higher scores in the HEI-2005, reflecting healthy eating patterns, were associated with a reduced risk of ESCC (the highest quintile compared to lowest: hazard ratio (HR) =0.51, 95% confidence interval (CI): 0.31-0.86, Ptrend =0.001), and EAC (HR=0.75, 95% CI: 0.57-0.98, Ptrend=0.01). We observed an inverse association of ESCC with higher diet quality as assessed by aMED, but not for EAC. No significant associations for gastric cardia or noncardia adenocarcinomas were found with either HEI-2005 or aMED. Conclusions In this prospective study, the HEI-2005 was inversely associated with risk of both ESCC and EAC, while the aMED was associated with reduced risk of ESCC, suggesting that adherence to dietary recommendations may help prevent esophageal cancer.
Citation Format: Wen-qing Li, Yikyung Park, Jennifer W. Wu, Jian-song Ren, Alisa M. Goldstein, Philip R. Taylor, Albert R. Hollenbeck, Neal D. Freedman, Christian C. Abnet. Index-based dietary patterns and risk of esophageal cancer and gastric cancer in the NIH-AARP diet and health study. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4805. doi:10.1158/1538-7445.AM2013-4805
Abstract 4809: Dietary fat intake and risk of pancreatic cancer in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial.
Authors: Arem Hannah E. , Mayne Susan T. , Sampson Joshua , Risch Harvey , Stolzenberg-Solomon Rachael Z. 
Published: August 2014

Abstract
Background: Some published studies on dietary fat and risk of pancreatic cancer suggest that dietary fat and specific fat sources may increase risk of pancreatic cancer.
Methods: We examined the association between fat intake (measured by food frequency questionnaire) and pancreatic cancer risk among 111,416 participants in the PLCO Cancer Screening Trial using Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs).
Results: There were 411 incident pancreatic cancer cases over the median 8.9 years of follow up. We observed an inverse association between saturated fat intake and pancreatic cancer risk comparing extreme quintiles (HR=0.64, 95% CI 0.46-0.88), but the association became weaker and non-significant when excluding individuals with &lt;4 years of follow up to assess reverse causation HR=0.88 (95% CI 0.58-1.33). Total fat intake showed a similar pattern of association, while monounsaturated and polyunsaturated fat intakes and analysis by animal or plant source showed no association with risk.
Conclusions: Despite more cases and longer follow up than most previous studies, our results do not suggest that higher fat consumption increases risk of pancreatic cancer. Lower fat intake in cases prior to diagnosis may reflect early manifestations of the disease (e.g. dyspepsia), and avoidance of fat which can exacerbate symptoms.
Citation Format: Hannah E. Arem, Susan T. Mayne, Joshua Sampson, Harvey Risch, Rachael Z. Stolzenberg-Solomon. Dietary fat intake and risk of pancreatic cancer in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4809. doi:10.1158/1538-7445.AM2013-4809
Abstract 481: Oligodeoxynucleotides expressing Poly-G motifs promote anti-tumor activity through the up-regulation of IL-2.
Authors: Kobayashi Nobuaki , Klinman Dennis M. , Sasaki Masahiro , Kaneko Takeshi , Ishigatsubo Yoshiaki , Shirota Hidekazu 
Published: August 2014

Abstract
The primary goal of cancer immunotherapy is to elicit an immune response capable of eliminating the tumor. One approach towards accomplishing that goal utilizes general (rather than tumor-specific) immunomodulatory agents to boost the number and activity of pre-existing cytotoxic T lymphocytes. We find that the intra-tumoral injection of poly-G ODN has such an effect, boosting anti-tumor immunity and promoting tumor regression. The anti-tumor activity of poly-G ODN was mediated through CD8 T cells in a TLR9 independent manner. Mechanistically, poly-G ODN directly induced the phosphorylation of Lck (an essential element of the T cell signaling pathway), thereby enhancing the production of IL-2 and CD8 T cell proliferation. These findings establish poly-G ODN as a novel type of cancer immunotherapy.
Citation Format: Nobuaki Kobayashi, Dennis M. Klinman, Masahiro Sasaki, Takeshi Kaneko, Yoshiaki Ishigatsubo, Hidekazu Shirota. Oligodeoxynucleotides expressing Poly-G motifs promote anti-tumor activity through the up-regulation of IL-2. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 481. doi:10.1158/1538-7445.AM2013-481
Abstract 4812: HCV infected elderly are at excess risk of pancreatic cancer: a population based SEER-Medicare study.
Authors: Shebl Fatma M. 
Published: August 2014

Abstract
Background: Pancreatic cancer is uncommon, however, it is a fatal cancer that ranks the fourth in mortality in United States. Risk factors of pancreatic cancer include infections, smoking, hormonal, alcoholism, genetic, and environmental factors. Pancreatitis is one of the risk factors of pancreatic cancer which is also, one of the observed extrahepatic manifestations of hepatitis C virus (HCV) infection. HCV infection mortality and morbidity are increasing; therefore it is important to understand the relationship between HCV infection and pancreatic cancer and the role of HCV-related pancreatitis.
Methods: We used the Surveillance, Epidemiology, and End Results (SEER) Medicare linked (SEER-Medicare) database to employ a population-based nested case control study among United States elder. The study included 29,892 pancreatic cancer cases and 100,000 controls. In this study, we calculated adjusted odds ratios (ORs) and 95% confidence intervals (CI) using unconditional logistic regression. Models were adjusted for the matching variables including age, sex, and calendar year. To examine the hypothesis that pancreatitis is in the causal pathway between HCV and pancreatic cancer; and therefore, is a mediator (intermediate endpoint), we used mediation modeling to calculate the percentage of the total effect of HCV that is mediated by pancreatitis.
Results: HCV infection was reported in 0.42% pancreatic cancer cases and 0.32% controls. Pancreatitis was observed in 6.2% of HCV infected, and 1.4% non-HCV infected. Pancreatitis was reported in 2.6%, and 1.4% of cancer and controls respectively. Adjusting for matching variables, HCV infection was associated with higher odds of pancreatic cancer [OR (95% CI); 1.36(1.10-1.68)]. In the mediation modeling, pancreatitis significantly mediated the HCV effect, such that 11.4% of HCV effect was mediated by pancreatitis.
Conclusion: HCV is a risk factor of pancreatic cancer. HCV effect is mediated in part by pancreatitis. Further studies are warranted to understand the various mechanisms that might explain the excess risk of pancreatic cancer among HCV infected individuals, and to determine the effect of HCV treatment on pancreatic cancer risk.
Citation Format: Fatma M. Shebl. HCV infected elderly are at excess risk of pancreatic cancer: a population based SEER-Medicare study. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4812. doi:10.1158/1538-7445.AM2013-4812
Abstract 4813: The increased risk of colon cancer due to cigarette smoking may be greater in women than men.
Authors: Parajuli Ranjan , Bjerkaas Eivind , Tverdal Aage , Selmer Randi , Le Marchand Loic , Weiderpass Elisabete , Gram Inger Torhild 
Published: August 2014

Abstract
Background: The International Agency for Research on Cancer (IARC) has recently established cigarette smoking as a risk factor for colon cancer. Norway has one of the highest incidence rates of colon cancer in the world especially among women. We examined the association between different measures of smoking exposure and colon cancer by gender in a large Norwegian cohort.
Methods: We followed 602,242 participants aged 19-67 years at enrollment who completed a questionnaire in 1972-2003, by linkage to national registries through December 2007. We used Cox proportional hazard regression models to estimate hazard ratios (HR) and 95% confidence intervals (CIs) adjusting for age, body mass index, physical activity and education.
Results: During a mean follow-up time of 14 years, 2,152 men and 1,846 women developed colon cancer. Women ever smokers had a 19% increased risk (HR=1.19, 95% CI=1.09-1.32) and men ever smokers had an 8% increased risk (HR=1.08, 95% CI=0.97-1.19) compared with never smokers. The association was more consistent for proximal than distal colon cancer among women ever smokers. The dose-response association between latency, number of years smoked, number of cigarettes per/day, number of pack-years and colon cancer risk among women was stronger than in men. Test for heterogeneity of the smoking effect between men and women was significant among ever smokers only for proximal colon cancer (Wald p=0.02).
Conclusions: The results provide further evidence that smoking plays a role in the etiology of colon cancer. Female smokers may be more susceptible to proximal colon cancer than male smokers.
Citation Format: Ranjan Parajuli, Eivind Bjerkaas, Aage Tverdal, Randi Selmer, Loic Le Marchand, Elisabete Weiderpass, Inger Torhild Gram. The increased risk of colon cancer due to cigarette smoking may be greater in women than men. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4813. doi:10.1158/1538-7445.AM2013-4813
Abstract 4815: Colorectal Cancer Mortality in Hong Kong, Japan, Korea, and Singapore.
Authors: Shin Aesun , Jung Kyu Won , Won Young-Joo 
Published: August 2014

Abstract
Although colorectal cancer mortality has started to decrease in many Western countries, its high incidence and mortality in most Asian countries are challenging health problems. We analyzed the colorectal cancer mortality in four Asian countries using the World Health Organization mortality database and the Korea National Statistics Office database. The annual age-standardized rates and truncated rated for the three age groups (30-49/50-69/70+ years) for Hong Kong (1969-2009), Japan (1955-2009), Korea (1985-2006), and Singapore (1966-2009) were estimated. A joinpoint regression model was used to detect significant trends in mortality rates. Colorectal cancer mortality in men started to decrease in 1992 in Japan followed by Singapore and Hong Kong in 1995. The mortality rates in women stared to decrease in 1980 in Singapore, followed by Hong Kong and Japan in 1996. In all countries and both genders, except for women in Singapore, the decrease in mortality began in the younger age groups. In conclusion, the colorectal cancer mortality in the four studied Asian countries has started to decrease, and the decrease occurred first in the younger age groups.
Citation Format: Aesun Shin, Kyu Won Jung, Young-Joo Won. Colorectal Cancer Mortality in Hong Kong, Japan, Korea, and Singapore. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4815. doi:10.1158/1538-7445.AM2013-4815
Abstract 4816: Paleolithic and Mediterranean diet scores and risk of colorectal adenoma.
Authors: Whalen Kristine A. , Yang Baiyu , Bostick Roberd M. 
Published: August 2014

Abstract
Background: A Westernized diet and lifestyle is associated with risk for colorectal cancer and adenomas. Evolutionary discordance could explain this association.
Objective: We investigated associations of scores for two proposed healthy diet patterns, the “Paleolithic” and Mediterranean diets, with risk for incident, sporadic colorectal adenomas.
Methods: In the Minnesota Cancer Prevention Research Unit case-control study of colorectal polyps, 1,248 participants with no history of colorectal neoplasms completed extensive questionnaires, including a Willett food frequency questionnaire, prior to an elective, outpatient colonoscopy. Of these participants 564 were identified as cases and 684 as colonoscopy-negative controls. An additional group of 535 age and sex frequency-matched population controls were also recruited. Paleolithic and the Mediterranean diet scores were calculated and categorized into quintiles, and associations estimated using unconditional logistic regression.
Results: The Paleolithic and the Mediterranean diet patterns were similarly inversely associated with colorectal adenomas. The multivariable-adjusted odds ratios [OR] comparing those in the highest relative to the lowest quintiles of the Paleolithic and Mediterranean diet scores, respectively, were 0.51 (95% confidence interval [CI] 0.35-0.76) and 0.50 (95% CI 0.33-0.75) when comparing the cases to the colonoscopy negative controls, and 0.66 (95% CI 0.45 - 0.96, ptrend = 0.03) and 0.65 (95% CI 0.44 - 0.96, ptrend = 0.03) when comparing the cases to the population controls. These findings tended to be somewhat stronger among men and those who were overweight or obese.
Conclusion: These findings suggest that higher adherence to the Paleolithic or Mediterranean diet patterns may be similarly associated with lower risk for incident, sporadic colorectal adenomas.
Citation Format: Kristine A. Whalen, Baiyu Yang, Roberd M. Bostick. Paleolithic and Mediterranean diet scores and risk of colorectal adenoma. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4816. doi:10.1158/1538-7445.AM2013-4816
Abstract 4825: Metabolic factors and hepatocarcinogenesis in steatohepatitis.
Authors: Zarrinpar Ali , Agopian Vatche , Hiatt Jonathan , Busuttil Ronald 
Published: August 2014

Abstract
Background: With the rising prevalence in the US of alcoholism, obesity, and metabolic syndrome and better treatments for hepatitis B and C, steatohepatitis is projected to become the leading cause of end-stage liver disease and hepatocellular carcinoma (HCC) by 2025.
Objective, Setting, and Design: Using a prospectively collected database, we analyzed clinical and pathologic features of HCC in patients who underwent liver transplantation (LT) for steatohepatitis due to non-alcoholic (NASH) and alcoholic causes (ALD) between 1/1/02 and 12/31/11 in a large urban transplant center. We further compared patients with HCC due to NASH (N-HCC) and ALD (A-HCC).
Results: HCC was present in 80 of 317 patients who underwent LT for steatohepatitis with equivalent distribution in NASH and ALD patients (24% vs 26%;P=0.8). On multivariate analysis, age and diabetes were associated with HCC in the explant but not BMI, hypertension, or smoking; hyperlipidemia was protective (Table). Among patients with HCC, N-HCC patients were more likely than A-HCC patients to be female (58% vs 4%;P&lt;0.0001) and have metabolic syndrome (27% vs 9%;P=0.025). On pathology, N-HCC patients were also more likely to have steatosis (76% vs 34%;P&lt;0.001), steatohepatitis (67% vs 19%;P&lt;0.0001), or nuclear grade 1 or 2 (89% vs 67%;P=0.03). Five-year survival was similar in N-HCC and A-HCC (67% vs 68%;P=1).
Conclusions: We report the largest series of liver transplantation for HCC in steatohepatitis. Metabolic factors such as diabetes and hyperlipidemia appear to play large and independent promoting and protective roles in hepatocarcinogenesis. Modulation of causative factors may be important in management of this increasingly common obesity-related disease.
Table. Multivariate Predictors of HCC Presence in Explant
Table. Multivariate Predictors of HCC Presence in Explant HR P Age &gt; 60 y 2.07 0.002 Diabetes 1.64 0.04 Male gender 1.47 0.18 Hypertension 1.31 0.26 NASH etiology 0.93 0.77 Smoking 0.90 0.64 BMI &gt; 35 kg/m2 0.71 0.30 Hyperlipidemia 0.33 0.02
Citation Format: Ali Zarrinpar, Vatche Agopian, Jonathan Hiatt, Ronald Busuttil. Metabolic factors and hepatocarcinogenesis in steatohepatitis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4825. doi:10.1158/1538-7445.AM2013-4825
Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 4834: Interactions between smoking and DNA repair in breast cancer risk.
Authors: Hu Jennifer J. , Allen Glenn O. , Reis Isildinha M. , Gong Feng 
Published: August 2014

Abstract
Breast cancer risk has been associated with tobacco smoking or deficient DNA repair. However, limited previous studies have focused on genetic susceptibility-exposure interactions. Using T-lymphocytes collected in a breast cancer case-control study (357 controls and 360 cases), this study tested whether the association between smoking and breast cancer risk is modified by individual's nucleotide excision repair capacity (NERC) using a newly developed plasmid-based electroporation assay. There was a significant age-dependent decline of NERC in controls (p=0.01) but not in breast cancer cases (p=0.59). Controls with current smoking status had a significantly higher NERC (mean+SD, 5.72+3.30, n=38) than never smokers (4.61+2.76, n=206). There was a significant association between lower NERC and elevated breast cancer risk only among current smokers (odds ratio [OR]=4.44; 95% confidence interval [CI]=1.03-19.13) after adjustment for age, race, and family history. In contrast, there was a significant association between lower NERC and reduced breast cancer risk in never smokers (OR=0.39; 95%CI=0.20-0.76). In controls, smoking-related elevation of NERC may be related to adaptive response. In breast cancer cases, elevated cancer risk may be associated with: (1) deficient NER response to smoking-related DNA damages in smokers and (2) environmental exposures (e.g. ionizing radiation) in non-smokers, which induced NER but repaired by other repair pathways (e.g. base excision and double-strand repair). Our findings highlight the complex interplay between individual's NER capacity and smoking in breast cancer risk.
Citation Format: Jennifer J. Hu, Glenn O. Allen, Isildinha M. Reis, Feng Gong. Interactions between smoking and DNA repair in breast cancer risk. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4834. doi:10.1158/1538-7445.AM2013-4834