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Biliary tract cancers are rare but highly fatal with poorly understood etiology. Identifying potentially modifiable risk factors for these cancers is essential for prevention. Here we estimated the relationship between adiposity and cancer across the biliary tract, including cancers of the gallbladder (GBC), intrahepatic bile ducts (IHBDC), extrahepatic bile ducts (EHBDC), and the ampulla of Vater (AVC). We pooled data from 27 prospective cohorts with over 2.7 million adults. Adiposity was measured using baseline body mass index (BMI), waist circumference, hip circumference, waist-to-hip, and waist-to-height ratios. HRs and 95% confidence intervals (95% CI) were estimated using Cox proportional hazards models adjusted for sex, education, race, smoking, and alcohol consumption with age as the time metric and the baseline hazard stratified by study. During 37,883,648 person-years of follow-up, 1,343 GBC cases, 1,194 EHBDC cases, 784 IHBDC cases, and 623 AVC cases occurred. For each 5 kg/m2 increase in BMI, there were risk increases for GBC (HR = 1.27; 95% CI, 1.19–1.36), IHBDC (HR = 1.32; 95% CI, 1.21–1.45), and EHBDC (HR = 1.13; 95% CI, 1.03–1.23), but not AVC (HR = 0.99; 95% CI, 0.88–1.11). Increasing waist circumference, hip circumference, waist-to-hip ratio, and waist-to-height ratio were associated with GBC and IHBDC but not EHBDC or AVC. These results indicate that adult adiposity is associated with an increased risk of biliary tract cancer, particularly GBC and IHBDC. Moreover, they provide evidence for recommending weight maintenance programs to reduce the risk of developing these cancers. Significance: These findings identify a correlation between adiposity and biliary tract cancers, indicating that weight management programs may help minimize the risk of these diseases.

Pancreatic cancer (PC) is highly fatal, and its incidence is increasing in the United States. Population-based registry studies suggest associations between a few autoimmune conditions and PC risk, albeit based on a relatively small number of cases. We hypothesize that autoimmune conditions are associated with risk of PC. We conducted a population-based, nested case-control study to examine the association between autoimmune conditions and PC risk within the Surveillance, Epidemiology, and End Results Program (SEER)-Medicare population. Incident primary malignant PC cases (n=80,074) were adults > 66 years and diagnosed between 1992 and 2015. Controls (n=320,296) were alive at the time cases were diagnosed and frequency-matched to cases (4:1 ratio) by age, sex, and year of diagnosis. We used multivariable-adjusted, unconditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for 45 autoimmune conditions identified from Medicare claims. Eight autoimmune conditions including ankylosing spondylitis (OR = 1.45; 95% CI: 1.14-1.84), Graves’ disease (OR = 1.18; 95% CI: 1.03-1.34), localized scleroderma (OR = 1.27; 95% CI: 1.06-1.52), pernicious anemia (OR = 1.08; 95% CI: 1.02-1.14), primary sclerosing cholangitis (OR = 1.37; 95% CI: 1.18-1.59), pure red cell aplasia (OR = 1.31; 95% CI: 1.16-1.47), type 1 diabetes (OR = 1.11; 95% CI: 1.07-1.15), and ulcerative colitis (OR = 1.18; 95% CI: 1.07-1.31) were associated with increased PC risk (false discovery rate-adjusted P values < 0.10). In subtype analyses, these conditions were associated with pancreatic ductal adenocarcinoma, whereas only ulcerative colitis was associated with pancreatic neuroendocrine tumors. Our results support the hypothesis that autoimmune conditions may play a role in PC development. Citation Format: Fancheng Yuan, Ruth M. Pfeiffer, Sachelly Julian-Serrano, Simran Arjani, Michael J. Barrett, Jill Koshiol, Rachael Z. Stolzenberg-Solomon. Autoimmune conditions and pancreatic cancer risk in older American adults [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr B082.

Abstract Background: Laboratory and emerging epidemiologic data suggest that bile acids (BAs), major regulators of the gut microbiota, play an important role in liver disease and cancer etiology. However, few epidemiologic studies have comprehensively examined associations between BAs and either liver endpoints or biliary cancer. Methods: In the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, we designed 1:1 matched nested case-control studies of primary liver cancer (n=247 cases), fatal liver disease (n=261 cases), and primary biliary cancer (n=92 cases). Using baseline serum collected ≤30 years prior to diagnosis or death, we measured concentrations of 15 BAs with liquid chromatography tandem mass spectrometry. We used multivariable conditional logistic regression to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs) between BAs and each endpoint, accounting for multiple comparisons. Results: Comparing the highest to the lowest quartile, ten BAs were positively associated with liver cancer risk, including taurocholic (OR =4.70, 95% CI=2.51-8.78; Q-trend1. Conclusion: Conjugated BAs were strongly associated with increased risk of liver cancer and fatal liver disease, suggesting mechanistic links between the gut microbiota, BA signaling pathways, and liver cancer or death from liver disease. Citation Format: Zeinab Farhat, Neal D. Freedman, Joshua N. Sampson, Roni T. Falk, Jill Koshiol, Stephanie J. Weinstein, Demetrius Albanes, Rashmi Sinha, Erikka Loftfield. A prospective investigation of serum bile acids with risk of liver cancer, fatal liver disease, and biliary cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2385.

Background: Host immune response and chronic inflammation associated with chronic hepatitis C virus (HCV) infection play a key role in the progression of liver disease from cirrhosis to hepatocellular carcinoma (HCC). We evaluated a large panel of circulating immunologic markers to better understand the natural history of HCV-related liver disease. Methods: We sampled 94 HCC, 68 cirrhotic and 100 non-cirrhotic controls from a Taiwanese prospective cohort study of chronically HCV-infected individuals. Multivariable polytomous logistic regression and canonical discriminant analysis (CDA) were used to compare baseline plasma levels for 102 markers in individuals who developed cirrhosis as compared to controls and those who developed HCC. P-values for individual markers were corrected for multiple testing using a false discovery rate of 10%; a p-value Results: After adjusting for age, sex, years of follow-up, serum alanine aminotransferase level, alcohol and smoking, DEFA-1 (p-trend: Conclusion: To our knowledge, this is the first prospective study to assess immunologic markers in relation to liver disease progression in individuals chronically infected with HCV. While further validation is required, these findings highlight the importance of immunologic processes in HCV-related disease. Citation Format: Ilona Argirion, Ruth M. Pfeiffer, Zhiwei Liu, Allan Hildesheim, Ligia Pinto, Katherine A. McGlynn, Jessica L. Petrick, Tram Kim Lam, Thomas R. O'Brien, Kelly Yu, Chien-jen Chen, Hwai-I Yang, Mei-Hsuan Lee, Jill Koshiol. Immunologic markers and the progression of liver disease in HCV-positive individuals [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 836.

Incidence rates for liver cancer have increased 3-fold since the mid-1970s in the United States in parallel with increasing trends for obesity and type II diabetes mellitus. We conducted an analysis of baseline body mass index (BMI), waist circumference (WC), and type II diabetes mellitus with risk of liver cancer. The Liver Cancer Pooling Project maintains harmonized data from 1.57 million adults enrolled in 14 U.S.-based prospective studies. Cox regression estimated HRs and 95% confidence intervals (CI) adjusted for age, sex, study center, alcohol, smoking, race, and BMI (for WC and type II diabetes mellitus). Stratified analyses assessed whether the BMI–liver cancer associations differed by hepatitis sera-positivity in nested analyses for a subset of cases (n = 220) and controls (n = 547). After enrollment, 2,162 incident liver cancer diagnoses were identified. BMI, per 5 kg/m2, was associated with higher risks of liver cancer, more so for men (HR = 1.38; 95% CI, 1.30–1.46) than women (HR = 1.25; 95% CI, 1.17–1.35; Pinteraction = 0.02). WC, per 5 cm, was associated with higher risks of liver cancer, approximately equally by sex (overall, HR = 1.08; 95% CI, 1.04–1.13). Type II diabetes mellitus was associated with higher risk of liver cancer (HR = 2.61; 95% CI, 2.34–2.91). In stratified analyses, there was a null association between BMI and liver cancer risk for participants who were sera-positive for hepatitis. This study suggests that high BMI, high WC, and type II diabetes mellitus are associated with higher risks of liver cancer and that the association may differ by status of viral hepatitis infection. Cancer Res; 76(20); 6076–83. ©2016 AACR.

Background: Biliary tract cancers (BTCs) are rare, but lethal cancers with a median survival of Methods: All patients diagnosed with incident biliary tract cancer between 1990 to 2017 were selected from the population-based United Kingdom’s Clinical Practice Research Datalink. Site-specific associations between aspirin use after BTC diagnosis and overall survival was analyzed using Cox proportional hazards models with aspirin use modeled as time-dependent, adjusting for age at diagnosis, sex, comorbidities, history of aspirin use, and use of statins, using follow-up time as the time scale. Results: We identified 3,211 biliary tract cancer cases in which 2,694 (84%) deaths occurred after an overall median follow-up time of 5 months. The table presents the number of cases by cancer subtype, deaths, and median survival time. Aspirin use following a diagnosis of BTC was associated with a reduction in mortality for each of the BTC sites: gallbladder, HR 0.41 (95% CI: 0.28, 0.61); cholangiocarcinoma, HR 0.46 (95% CI: 0.36, 0.60); ampulla of Vater, HR 0.24 (95% CI: 0.11, 0.51); and mixed, HR: 0.51 (95% CI: 0.33, 0.78). Conclusions: The use of aspirin after BTC diagnosis was associated with a lower risk of overall mortality. These results warrant additional studies to understand the mechanisms underlying improved survival with aspirin use. Table.Association between post-BTC diagnosis aspirin use versus no use and survival in the UK CPRD datasetCancer siteBTC patients N (%)Mortality N (%)Median survival time in months (interquartile range)HR (95% CI)*Gallbladder668 (23)555 (83)3.9 (2 - 11)0.41 (0.28, 0.61)Cholangiocarcinoma1,560 (53)1321 (85)4.8 (2 - 12)0.46 (0.36, 0.60)Ampulla of Vater224 (8)142 (63)9 (4 - 21)0.24 (0.11, 0.51)Mixed484 (16)401 (83)5 (2 - 13)0.51 (0.33, 0.78)*Adjusted for age at diagnosis, comorbidities, prior aspirin use, and use of statins.Abbreviations: CPRD, Clinical Practice Research Datalink; CI, confidence interval; HR, hazard ratio; N, number; and UK, United Kingdom. Citation Format: Sarah S. Jackson, Bin Zhu, Ruth Pfeiffer, Zhiwei Liu, Shahinaz Gadalla, Jill Koshiol. Aspirin may extend biliary tract cancer survival: Results from population-based cohort [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2333.

Background: Aflatoxin, which is a risk factor for developing hepatocellular carcinoma, may also cause gallbladder cancer (GBC). We hypothesized that GBC patients have higher aflatoxin exposure than gallstone patients. Methods: We used samples and data from the Shanghai Biliary Tract Cancer Case-control Study conducted from 1997-2001. Of the 267 GBC and 730 gallstone participants with plasma available, 250 GBC patients and 250 controls with gallstones were randomly selected for measurement of aflatoxin B1 (AFB1)-lysine plasma adducts using isotope dilution mass spectrometry. In 54 GBC patients, tumor tissue was examined for the aflatoxin-related R249S TP53 mutation through targeted sequencing. Results: We calculated age- and sex-adjusted odds ratios (ORs) and 95% confidence intervals (CIs), as well as the population attributable fraction (PAF). AFB1-lysine adduct detection was nearly 3-fold higher in GBC patients (OR, 2.96; 95% CI, 1.90 to 4.61). Among the 85 GBC patients (34%) with detectable AFB1-lysine adduct levels, the median was 4.6 pg/mg, compared to 1.2 pg/mg among the 37 gallstone-patient controls (15%) with detectable levels, and the OR was 9.97(95% CI, 2.73 to 36.44) for quartile 4 versus 1 in GBC compared to gallstone patients. The PAF for cancer related to aflatoxin was 22% (95% CI: 17%-27%). In 54 GBC patients, tumor tissue was examined for the aflatoxin-related R249S TP53 mutation through targeted sequencing, however, all patients were negative for the mutation. Conclusions: Aflatoxin is significantly associated with GBC, although it does not appear to be correlated with the R249S TP53 mutation in the gallbladder. If aflatoxin is shown to cause GBC, it may have accounted for up to 22% of the gallbladder cancers in Shanghai during the study period and may account for an even higher proportion in high-risk areas. If verified, reducing aflatoxin exposure may reduce GBC incidence. Citation Format: Jill E. Koshiol, Yu-Tang Gao, Michael Dean, Patricia Egner, Chirag Nepal, Kristine Jones, Bingsheng Wang , Asif Rashid, Wen Lou, Alison Van Dyke, Catterina Ferreccio, Michael Malasky, Ming-Chang Shen, Bin zhu, Jesper Andersen, Allan Hildesheim, Ann W. Hsing, John Groopman. Association of aflatoxin and gallbladder cancer in Shanghai [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-157. doi:10.1158/1538-7445.AM2017-LB-157

Background: Since 1980, liver cancer has been among the most rapidly increasing cancer types in the United States (US), with 5-year survival rates of approximately 17%. While tobacco and alcohol are known to be associated with primary liver cancer, it is unclear whether they only increase the risk of hepatocellular carcinoma (HCC), the most common type of liver cancer, or whether they also increase risk of intrahepatic cholangiocarcinoma (ICC), second most common histologic type. Additionally, it is unclear what amount of alcohol consumption is associated with an increased risk of liver cancer. As liver cancer is a rare cancer type, we conducted a study of pooled data from the National Cancer Institute Cohort Consortium to examine the associations between smoking and alcohol use and liver cancer, stratified by histologic subtype. Methods: In the Liver Cancer Pooling Project, a consortium of US-based cohort studies, we pooled data from 1,518,741 individuals (HCC n=1,423, ICC n=410) in 14 cohorts. Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CI) were estimated using proportional hazards regression. Cubic splines were used to model the association between alcohol and liver cancer risk. Results: Compared to never smokers, both former and current smokers at study baseline had an increased risk of ICC (HR=1.32, 95% CI: 1.03-1.68 and HR=1.47, 95% CI: 1.07-2.02, respectively) and HCC (HR=1.24, 95% CI: 1.08-1.43 and HR=1.86, 95% CI: 1.57-2.20, respectively). This finding was consistent for heavier smoking intensity, longer duration of smoking, and more pack-years of smoking. Heavy alcohol consumption was associated with an 87% increased risk of HCC (HR≥7 drinks/day v. non-drinker=1.87, 95% CI: 1.41-2.47) and a non-significant 68% increased risk of ICC (HR≥5 drinks/day v. non-drinker=1.68, 95% CI: 0.99-2.86). Risk of HCC significantly increased at 4.5 alcoholic drinks per day, while risk of ICC was non-significantly increased with any amount of consumption. Conclusions: These findings suggest that, in a US population, cigarette smoking is associated with an increased risk of both histologic subtypes of primary liver cancer - HCC and ICC. In contrast, alcohol consumption was primarily associated with an increased risk of HCC. These results suggest that smoking cessation and alcohol reduction programs could be important intervention opportunities for these lethal cancer types. Citation Format: Jessica Leigh Petrick, Peter T. Campbell, Jill Koshiol, Jake E. Thistle, Gabriella Andreotti, Laura E. Beane-Freeman, Julie E. Buring, Andrew T. Chan, Dawn Q. Chong, Michele M. Doody, Susan M. Gapstur, John Michael Gaziano, Edward Giovannucci, Barry I. Graubard, I-Min Lee, Linda M. Liao, Martha S. Linet, Julie R. Palmer, Jenny N. Poynter, Mark P. Purdue, Kim Robien, Lynn Rosenberg, Catherine Schairer, Howard D. Sesso, Rashmi Sinha, Meir J. Stampfer, Marcia Stefanick, Jean Wactawski-Wende, Xuehong Zhang, Anne Zeleniuch-Jacquotte, Neal D. Freedman, Katherine A. McGlynn. Tobacco smoking, alcohol use and risk of hepatocellular carcinoma and intrahepatic cholangiocarcinoma: The Liver Cancer Pooling Project [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3007. doi:10.1158/1538-7445.AM2017-3007

Digestive system cancers include cancers of the oral cavity, esophagus, stomach, pancreas, liver, gallbladder, small intestine, colon and rectum, making it the second organ system most commonly affected by cancers in the world. These cancers are among the deadliest cancers worldwide. Gallstones (GS) can lead to inflammation and trauma (which are positively associated with cancer development) in digestive system organs adjacent to the gallbladder. However, the association between gallstones and digestive system cancers outside of the biliary tract has not been well established, especially in the presence of cofounders, such as obesity, physical activity, and alcohol consumption. Cholecystectomy (CH), the most common treatment for GS, can ameliorate inflammation, but has been shown to increase the exposure of the stomach the small intestine to bile. We hypothesized that GS and CH are differentially associated with cancers of the digestive system outside of the biliary tract. Within the National Institutes of Health-AARP Diet and Health Study (n=487,207) we used Cox proportional hazards regression models adjusted for age, gender, race, smoking, alcohol consumption, body mass index, caloric intake, physical activity, and non-steroidal anti-inflammatory drugs intake to investigate GS (n=30,674) and CH (n=25,457) in relation to cancers of the oral cavity (n=1,004), esophagus (adenocarcinoma n=392 and squamous cell carcinoma n=138), stomach (cardia n=264 and non-cardia n=292), small intestine (n=192), colon (n=3,865), rectum (n=1,410), pancreas (n=1,268), and liver (n=414). GS were associated with liver cancer [Hazard Ratio = 1.80 (95% confidence interval = 1.37, 2.37)], while CH was not [1.43 (0.83, 2.48)]. In contrast, CH was associated with non-cardia gastric cancer [2.67 (1.45, 4.90)], colon cancer [1.45 (1.29, 1.63)], and esophageal adenocarcinoma [1.74 (1.02, 2.97)] while GS were not [1.31 (0.90, 1.90), 1.06 (0.95, 1.18), and [1.16 (0.81, 1.65)], respectively]. CH was also associated with pancreatic [1.99 (1.49, 2.66)] and small intestine cancer [2.61 (1.61, 4.23), as was GS [1.19 (1.00, 1.43) and 1.61 (1.07, 2.42), respectively]. Neither GS nor CH was associated with oral cavity cancers, esophageal squamous cell carcinoma, or rectal cancer. A major strength of this large study was the ability to adjust for important cancer risk factors, including tobacco smoking, alcohol intake, and obesity. Nonetheless, future studies are needed to replicate our findings and establish the underlying mechanisms responsible for the identified associations. Citation Format: Leticia Nogueira, Amanda Cross, Neal Freedman, Gabriel Lai, Felipe Castro, Jill Koshiol. Gallstones, cholecystectomy, and risk of digestive system cancers. [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 4804. doi:10.1158/1538-7445.AM2013-4804 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.

BACKGROUND: Lung cancer is the leading cause of cancer mortality worldwide. Infections may contribute to lung carcinogenesis. Results from a few small studies have suggested that Helicobacter pylori (HP) may be a potential risk factor. However, these studies have been limited in size and in the evaluation of lung cancer histology and smoking. METHODS: We conducted a study of 350 lung adenocarcinoma cases, 350 squamous cell carcinoma cases, and 700 controls nested within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) cohort of male Finnish smokers. Controls were 1 to 1 matched by age (+/- 5 years) at and date (+/- 30 days) of baseline serum draw and had to be alive and cancer free at the date that the corresponding case was diagnosed. We used enzyme linked immunosorbent assays to detect immunoglobulin G antibodies against HP whole-cell and CagA antigens and calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for associations between HP seropositivity and lung cancer risk using conditional logistic regression. RESULTS: 79% of cases and 78% of controls were seropositive for whole cell HP, and 43% of cases and 44% of controls were seropositive for the cytotoxin-associated gene (cagA) antigen. Whole cell seropositivity was not associated with lung adenocarcinoma (OR: 1.2, 95% CI: 0.80-1.8) or squamous cell carcinoma (OR: 1.1, 95% CI: 0.73-1.6) after adjusting for age at serum draw, date of serum draw, age at smoking initiation, pack-years, and cigarettes smoked per day. Similarly, CagA seropositivity was not associated with lung adenocarcinoma (OR: 1.1, 95% CI: 0.78-1.5) or squamous cell carcinoma (OR: 0.88, 95% CI: 0.63-1.2). CONCLUSIONS: Despite earlier small studies suggesting that HP may contribute to lung carcinogenesis, HP seropositivity does not appear to be associated with lung cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1889. doi:10.1158/1538-7445.AM2011-1889

Background: Lung cancer kills over one million people worldwide each year. Human papillomavirus (HPV) has been proposed as a potential cause. Over 50 studies have evaluated HPV in lung tumor tissue over the last 20 years with mixed findings, but most were severely underpowered or had other methodological limitations. While several HPV-associated cancers have been identified (e.g., cervical, tonsillar), the role of HPV in lung carcinogenesis remains controversial. Methods: We tested 450 lung cancer cases in the Environment And Genetics in Lung cancer Etiology (EAGLE) Italian population-based, case control study for HPV DNA. DNA was extracted from ethanol or formalin-fixed, paraffin-embedded tumor tissue under strict PCR clean conditions and was evaluated for HPV16 and 18 by type-specific, real-time PCR targeted to the E6 or E7 gene. The number of cell equivalents evaluable in these reactions was estimated by real-time PCR targeted to the human ERV3 gene. DNA purity was assessed by standard spectrophotometry (260/280 ratio). Results: 79.6% (n=358) of the 450 cases were male, 48.9% (n=220) were current smokers, 44.0% (n=198) were former smokers, 6.7% (n=30) were never smokers, and 0.4% (n=2) had unknown smoking status. 399 of 450 cases (88.67%) met quality indices for DNA quantity (at least 100 evaluable cell equivalents) and quality (260/280 ratio of 1.5 to 2.2). Of these, 398 (99.75%, 95% confidence interval: 98.61%-99.99%) were negative for HPV16 and 18. One case, a female former smoker with adenocarcinoma, was positive for HPV16 at low copy number (0.4 per 1000 cell equivalents). We are currently evaluating a subset of cases (n=100) for a broad spectrum of HPV types by PCR with SPF10 primers and a cocktail of conservative probes recognizing at least 54 mucosal HPV genotypes in a microtiter plate format (DEIA). To date no HPV has been detected in the 30 cases tested. Conclusions: Using extensive laboratory efforts to avoid DNA contamination and sensitive HPV DNA detection assays, we found no evidence to support a role for HPV in lung cancer in a representative Western population. Our results provide the strongest evidence to date to rule out a role for HPV in lung carcinogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4824.