bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 13: Telomere length and pancreatic cancer in the alpha-tocopherol beta-carotene cancer prevention (ATBC) study.
Authors: Lynch Shannon M. , Major Jacqueline M. , Cawthon Richard , Weinstein Stephanie J. , Virtamo Jarmo , Lan Qing , Rothman Nathaniel , Albanes Demetrius , Stolzenberg-Solomon Rachael Z. 
Published: August 2013

Abstract
Genome-wide association studies have found an association between pancreatic cancer and the TERT or telomerase gene. Smoking and diabetes, consistent risk factors for pancreatic cancer, are also factors that influence telomere length maintenance. To test whether blood leukocyte telomere length is associated with pancreatic cancer risk, we conducted a nested case-control study in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study cohort of male smokers, aged 50-69 years at baseline. Between 1992 and 2004, 193 incident cases of pancreatic adenocarcinoma occurred (mean follow-up from blood draw: 6.3 years) among participants with whole blood samples available for telomere length assays. For these cases and 660 controls, we calculated odds ratios (OR) and 95% confidence intervals (CI) using unconditional logistic regression, adjusting for age, number of years smoked regularly, and history of diabetes mellitus. Telomere length was categorized into quartiles (shortest to longest) and analyzed as both a categorical and a continuous normal variable (reported per 0.2 unit increase in telomere length). All statistical tests were two-sided. Longer telomere length was significantly associated with increased pancreatic cancer risk (continuous OR=1.26 95% CI=1.09-1.46; highest quartile compared to lowest, OR=1.57, 95% CI=1.01-2.43, p-trend=0.007). This effect remained for subjects diagnosed within the first five years of blood draw (continuous OR=1.46, 95% CI=1.19-1.79 highest quartile OR=2.92, 95%CI=1.47-5.77, p-trend=0.002), but not subjects diagnosed greater than five years from blood draw (continuous OR=1.03, 95%CI=0.85-1.22; highest quartile OR=1.04, 95%CI=0.60-1.79). This is the first study to suggest an association between longer blood leukocyte telomere length and increased pancreatic cancer risk.
Citation Format: Shannon M. Lynch, Jacqueline M. Major, Richard Cawthon, Stephanie J. Weinstein, Jarmo Virtamo, Qing Lan, Nathaniel Rothman, Demetrius Albanes, Rachael Z. Stolzenberg-Solomon. Telomere length and pancreatic cancer in the alpha-tocopherol beta-carotene cancer prevention (ATBC) study. [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 13.
Abstract 17: Innate Immunity Pathways and Breast Cancer Risk in African American and European American Women in the Women's Circle of Health Study (WCHS).
Authors: Gong Zhihong , Quan Lei , Yao Song , Zirpoli Gary , Bandera Elisa , Hwang Helena , Roberts Michelle , Sucheston Lara , Ciupak Gregory , Davis Warren , Ambrosone Christine , Hong Chi-Chen 
Published: August 2013

Abstract
Although the incidence of breast cancer is highest in American women of European ancestry (EA), women of African ancestry (AA) are more likely to have early, aggressive breast cancer, characterized by negative estrogen receptor (ER) status. There are few explanations for these differences between ancestral groups. We hypothesized that differential distribution of genetic variants in innate immunity pathways could be related to these breast cancer disparities, and evaluated variant-breast cancer associations in a case-control study, the Women's Circle of Health Study (WCHS). In the first stage, 44 SNPs were genotyped among 1010 AA and 757 EA women who participated in the WCHS. For 38 of the 44 SNPs, genotype frequencies differed significantly between AA and EA women, and differential risk relationships were observed between groups for some SNPs. For example, in premenopausal women, CXCL5 (rs425535) was significantly associated with breast cancer risk for only AA women (P=0.008) and for EAs, associations were observed for CRP (rs1205) and TNFA (rs1799724) (P≤0.01). In post-menopausal women, two SNPs in IL1B (rs1143627, rs16944) and one SNP in NOD2 (rs2066842) were associated with risk in EAs (all P=0.01) but not AA women. The association was limited to ER positive cancers for TNFA-rs1799724 and to ER negative cancers for NOD2-rs2066842. In the second stage, with additional accruals in WCHS, we extended analysis for four SNPs with suggested associations from the first stage in a larger dataset of 1602 AA and 1542 EA women, which yielded similar results. Associations for CRP-rs1205 and CXCL5-rs425535 with breast cancer risk were strengthened in premenopausal women and were statistically different between AA and EA women (P for interaction=0.0009 and 0.002, respectively) in this larger dataset. In summary, AA and EA populations exhibited differential association patterns of these genetic variants with breast cancer risk. Our findings suggest that innate immune pathways may be differentially associated with breast cancer by ancestry, and that relationships vary according to menopausal and ER status.
Citation Format: Zhihong Gong, Lei Quan, Song Yao, Gary Zirpoli, Elisa Bandera, Helena Hwang, Michelle Roberts, Lara Sucheston, Gregory Ciupak, Warren Davis, Christine Ambrosone, Chi-Chen Hong. Innate Immunity Pathways and Breast Cancer Risk in African American and European American Women in the Women's Circle of Health Study (WCHS). [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 17.
Abstract 18: Association of polymorphisms in MCP-1 and CCR2 genes with the risk of cancer: A meta-analysis.
Authors: Kim Jeongseon , Cho Young Ae 
Published: August 2013

Abstract
Background: Chemokines and their receptors are known to play an important role in tumor progression, particularly as key mediators of tumor-stroma interactions. Studies have investigated the impact of monocyte chemotactic protein-1 (MCP-1) and CC chemokine receptor 2 (CCR2) polymorphisms on the susceptibility of cancer, but the results remain inconclusive.
Methods: We performed a meta-analysis using 20 eligible studies to summarize the data on the association between MCP-1 A2518G and CCR2 V64I polymorphisms and cancer risk. Q-statistics and I2 statistics were calculated to examine heterogeneity, and summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using a random effects model. Potential sources of heterogeneity were sought out via stratification and sensitivity analyses, and publication biases were estimated.
Results: In overall, MCP-1 and CCR2 polymorphisms showed no significant association with cancer risk (MCP-1 A2518G, GG + GA versus AA: OR = 0.94, 95% CI=0.76, 1.17; CCR2 V64I, AA + AG versus GG: OR= 1.30, 95% CI = 0.86, 1.95). The effect of these polymorphisms was further evaluated in stratification analyses. It was demonstrated that the increased risk of cancer was observed among Asian populations carrying at least one A allele of CCR2 V64I than those with GG homozygotes (AA + AG versus GG: OR=1.80; 95% CI=1.40, 2.33).
Conclusions: This meta-analysis demonstrates that gene polymorphism of CCR2 V64I may influence the susceptibility of cancer in Asian populations. Further well-designed studies with large sample size should be conducted.
Citation Format: Jeongseon Kim, Young Ae Cho. Association of polymorphisms in MCP-1 and CCR2 genes with the risk of cancer: A meta-analysis. [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 18.
Abstract 19: Soluble RAGE modestly inversely associated with liver cancer risk in male Finnish smokers.
Authors: Moy Kristin A. , Jiao Li , Freedman Neal D. , Weinstein Stephanie J. , Sinha Rashmi , Virtamo Jarmo , Albanes Demetrius , Stolzenberg-Solomon Rachael 
Published: August 2013

Abstract
Laboratory experiments suggest that activation of receptor for advanced glycation end products (RAGE) contributes to liver injury and blockade of RAGE with soluble RAGE (sRAGE) may mitigate the effects of RAGE activation. Epidemiologic studies examining sRAGE and advanced glycation end products (AGEs) in relation to liver cancer are sparse. Within a cohort of 29,133 Finnish male smokers who completed questionnaires and donated blood samples between 1985-1988, we conducted a case-cohort study examining the associations between serum concentrations of sRAGE or Nϵ-(carboxymethyl)-lysine (CML)-AGE, the most abundant AGE in humans, in association with liver cancer. During follow-up that began 5 years after enrollment through April 2006, 145 liver cancer cases occurred. Serum levels of sRAGE, CML-AGE, glucose and insulin were measured in cases and 485 randomly sampled cohort participants. Chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) were also measured. Weighted Cox proportional hazards regression was used to calculate relative risks (RR) and 95% confidence intervals (CI). Multivariate models were adjusted for age, years of smoking, and body mass index. Among subcohort participants, carbohydrate and sucrose intake increased across increasing tertiles of serum sRAGE (P-values ≤0.01). After adjusting for age, BMI and years of smoking, serum sRAGE concentration was inversely associated with liver cancer risk [continuous RR (95% CI): 0.86 (0.75-0.99), P-value=0.04]. Unexpectedly, serum CML concentration was also inversely associated with liver cancer risk [continuous RR (95% CI): 0.74(0.65-0.84), P-value &lt;0.0001]. Further adjustment for serum glucose and insulin did not change the associations. The prevalence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (anti-HBc) titers measured on 135 cases were 0.75% and 13%, respectively and 3% for hepatitis C exposure (anti-HCV). Exclusion of cases with chronic HBV or HCV did not change our results. Our results support the hypothesis that sRAGE is inversely associated with liver cancer. The findings need confirmation, particularly in populations that include women and non-smokers.
Citation Format: Kristin A. Moy, Li Jiao, Neal D. Freedman, Stephanie J. Weinstein, Rashmi Sinha, Jarmo Virtamo, Demetrius Albanes, Rachael Stolzenberg-Solomon. Soluble RAGE modestly inversely associated with liver cancer risk in male Finnish smokers. [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 19.
Abstract 20: Whole exome sequencing of aristolochic acid induced upper urothelial carcinomas.
Authors: Rosenquist Thomas A. , Hoang Margaret , Moriya Maasaki , Sidorenko Victoriya S. , Dickman Kathleen , Chen Chung-Hsin , Wu Lin , Papadopoulos Nickolas , Pu Yeong-Shiau , Kinzler Kenneth W. , Vogelstein Bert , Grollman Arthur P. 
Published: August 2013

Abstract
Aristolochic acid (AA), a human carcinogen and nephrotoxin, produced by Aristolochia plants and used extensively in traditional herbal medicines, was shown to be responsible for the clinical syndromes known as Chinese herb nephropathy and endemic (Balkan) nephropathy (EN), and to contribute to the high rate of upper urinary tract carcinoma (UUC) observed in certain Asian countries such as Taiwan. After bio-activation, AA gives rise to long-lived, pro-mutagenic aristolactam-DNA (AL-DNA) adducts that serve as specific biomarkers of exposure. Our studies of the TP53 gene in AA-induced UUC tumors detected a mutation spectrum that was dominated by A&gt;T transversions located almost exclusively on the non-transcribed DNA strand, reflecting a failure to excise AL-DNA adducts by global genomic nucleotide excision repair. In the present study we undertook the whole exome sequencing of a set of AAN/UUC tumors from Taiwanese patients, and matching normal DNAs, to establish the genome wide consequence of AA-exposure. To establish that AA was critical in tumor formation we selected patients who had: 1) detectable AL-DNA adducts in kidney cortex DNA, and 2) the TP53 gene in tumor DNA contained an A&gt;T mutation on the non-transcribed strand. The results indicate that these tumors indeed harbor a very high number of single base substitutions (SBS) in their coding exons (median of 545 SBS per tumor). Of these, 70% were A&gt;T mutations with the majority of the mutated adenines on the non-transcribed strand. We are currently completing whole exome sequencing of an additional set of AA-induced UUC tumors, and ten smoking-induced UUC tumors for comparison. We will present an analysis of the driver mutations found in these tumors and the pathways harboring oncogenic mutations. Our goal is to define a panel of AA-specific mutations useful for developing biomarker screens for early detection of UUC in at risk populations.
Citation Format: Thomas A. Rosenquist, Margaret Hoang, Maasaki Moriya, Victoriya S. Sidorenko, Kathleen Dickman, Chung-Hsin Chen, Lin Wu, Nickolas Papadopoulos, Yeong-Shiau Pu, Kenneth W. Kinzler, Bert Vogelstein, Arthur P. Grollman. Whole exome sequencing of aristolochic acid induced upper urothelial carcinomas. [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 20.
Abstract 21: Variations in DNA repair gene expression and breast cancer risk in the New York site of the Breast Cancer Family Registry.
Authors: Kappil Maya , Terry Mary Beth , Liao Yuyan , Santella Regina 
Published: August 2013

Abstract
Reduced DNA repair capacity contributes to genomic instability, a hallmark of carcinogenesis. The link between DNA repair capacity and cancer is especially relevant in breast cancer, where women with suboptimal repair capacity have been reported to have up to a five-fold increase in breast cancer risk compared to women with greater repair capacity. We investigated the expression level of several DNA repair-related genes and their association with breast cancer risk among participants of the New York site of the Breast Cancer Family Registry. We examined RNA from viable mononuclear cells in 213 sisters (N=511 women). A total of five genes, ATM, BRCA1, MSH2, MUTYH and XPC, were selected and assayed using Taqman gene expression kits from Applied Biosystems. With the exception of BRCA1, expression of these genes was lower, but not statistically significant, among sisters with breast cancer compared with their unaffected sisters. Using generalized estimating equations (GEE), we found that individuals in the lowest quartile of expression for MSH2, a gene involved in DNA mismatch repair, had significantly higher odds of breast cancer compared to individuals in the highest quartile of expression, adjusting for age at blood draw (OR=1.82, 95% CI=1.11, 2.99). These findings suggest that a reduction in MSH2 expression compromises mismatch repair capacity and, thereby, increases breast cancer susceptibility.
Citation Format: Maya Kappil, Mary Beth Terry, Yuyan Liao, Regina Santella. Variations in DNA repair gene expression and breast cancer risk in the New York site of the Breast Cancer Family Registry. [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 21.
Abstract 27: Telomere length in relation to the risk of Barrett's esophagus and esophageal adenocarcinoma.
Authors: Persson E. Christina , Liao Linda M. , Risques Rosana , Prunkard Donna , Giffen Carol , Chow Wong-Ho , Vaughan Thomas L. ,   on behalf of the Barrett's Esophagus, Adenocarcinoma Consortium (BEACON) Investigators
Published: August 2013

Abstract
Background: Repeated injury of the esophagus by chronic gastroesophageal reflux (GER) is associated with the development of Barrett's esophagus (BE), a condition in which the squamous epithelium is replaced by a metaplastic columnar epithelium. A proportion of individuals diagnosed with BE progress to esophageal adenocarcinoma (EAC), which has considerably increased in incidence in many Western countries over the past four decades. Major risk factors associated with BE and EAC, such as obesity, smoking and gastroesophageal reflux (GER), are all contributors to the presence of chronic inflammation and oxidative damage. Unlike other areas of the chromosome that have effective repair systems to deal with oxidative damage, telomeres are not as well maintained and telomere length may reflect the impact of chronic inflammation. We investigated whether leukocyte telomere length was associated with BE or EAC risk compared to population-based controls in a pooled analysis of seven studies from the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON).
Methods: Telomere length was measured by quantitative-PCR using leukocyte DNA samples. Participants included 1,198 cases (395 with EAC, 403 with BE, 400 with GER) and 749 population-based controls. The association of telomere length (in tertiles) along the continuum of disease progression from GER to BE to EAC was calculated using study-specific odds ratios (OR) and 95% confidence intervals (CI) from logistic regression models, adjusted for age, sex, smoking status, alcohol consumption, BMI and education. Summary risk estimates were obtained using a random effects meta-analysis models.
Results: Shorter telomeres were associated with decreased risks of EAC (OR 0.84; 95% CI 0.47-1.48) and BE (OR 0.68; 95% CI 0.46-1.01), when compared to population-based controls, though not statistically significant. In addition, subjects with shorter telomeres were associated with a decreased risk of GER (OR 0.43; 95% CI 0.18-1.01), compared to population-based controls.
Conclusion: Telomere length may play a role in the progression from chronic reflux to BE and EAC.
Citation Format: E. Christina Persson, Linda M. Liao, Rosana Risques, Donna Prunkard, Carol Giffen, Wong-Ho Chow, Thomas L. Vaughan, on behalf of the Barrett's Esophagus, Adenocarcinoma Consortium (BEACON) Investigators. Telomere length in relation to the risk of Barrett's esophagus and esophageal adenocarcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 27.
Abstract 28: Characterization of SNPs associated with prostate cancer in men of Ashkenazic descent from the set of GWAS identified SNPs: Impact of cancer family history.
Authors: Agalliu Ilir , Wang Zhaoming , Dunn Anne , Parikh Hemang , Myers Timothy , Burk Robert , Amundadottir Laufey 
Published: August 2013

Abstract
Background: Genome-wide association studies (GWAS) have identified several SNPs that are independently associated with prostate cancer (PrCa) in Caucasian men. Population isolates with unique allele frequencies are likely to have different sets of risk alleles for PrCa constituting personalized population risk stratification in addition to individual risk profiles.
Methods: To test this hypothesis, we examined associations between 31 GWAS SNPs and PrCa among 979 cases and 1,251 controls of Ashkenazic descent. Odds ratios (OR) and 95% confidence intervals (CIs) were estimated for each SNP using logistic regression models adjusted for age. We also investigated risk in strata by age at diagnosis, pathological features of PrCa, as well as family history of PrCa and other cancers.
Results: Of 31 SNPs, 19 (62%) were associated with PrCa at p&lt;0.05 in one or more genetic risk models. The strongest associations with PrCa were for rs6983267 at 8q24 (OR=1.78, p=5.7 x 10−7;comparison of GG vs. TT genotype), and rs1465618 at 2p21 (OR=2.19; p=0.003; AA vs. AG/GG). Six SNPs were associated with aggressive PrCa, while six others with less aggressive cancer. Four SNPs showed statistically significant interactions between PrCa and family history of PrCa (rs8102476 at 19q13), lung cancer (rs17021918 at 4q22), colorectal cancer (rs6983267 at 8q24), and breast cancer (rs10896449 at 11q13).
Conclusion: These data define a specific set of risk alleles associated with PrCa in Ashkenazic men. Results demonstrate differences between men of European and Ashkenazic ancestry in relation to genetic susceptibility of PrCa. Interactions of genetic variants with family history of specific cancers indicate a complex network of inherited cancer risk syndromes still to be defined. Use of genetic markers to identify men at higher risk of PrCa will provide an opportunity for personalized care of PrCa prevention through screening of high-risk individuals, independent of family history information.
Citation Format: Ilir Agalliu, Zhaoming Wang, Anne Dunn, Hemang Parikh, Timothy Myers, Robert Burk, Laufey Amundadottir. Characterization of SNPs associated with prostate cancer in men of Ashkenazic descent from the set of GWAS identified SNPs: Impact of cancer family history. [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 28.