bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B74: Prevention of breast cancer by withanolides
Authors: Singh Shivendra V. 
Published: May 2019

Abstract
Malignancy of the breast is a leading cause of cancer-related deaths among women globally. Feasibility of breast cancer prevention is illustrated by clinical success with SERMs and aromatase inhibitors for ER+ breast cancers. However, a clinically viable preventive intervention targeting ER-negative breast cancers is still lacking. Constituents of Ayurvedic medicine, which has been practiced in India for thousands of years, continue to draw attention for identification of novel small molecules potentially useful for prevention of chronic diseases including cancer. This presentation summarizes efficacy data, molecular targets, and biomarkers of mammary cancer prevention by a small-molecule steroidal lactone (withaferin A) derived from an Ayurvedic medicinal plant (Withania somnifera). This work was supported by the grant US PHS grant RO1 CA142694-05 from the National Cancer Institute.
Citation Format: Shivendra V. Singh. Prevention of breast cancer by withanolides [abstract]. In: Proceedings of the AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. Philadelphia (PA): AACR; Clin Cancer Res 2018;24(1_Suppl):Abstract nr B74.
Abstract A07: Risk of pancreatic cancer among individuals with hepatitis C or hepatitis B virus infection: A nationwide study in Sweden
Authors: Huang Jiaqi , Magnusson Måns , Törner Anna , Ye Weimin , Duberg Ann-Sofi 
Published: May 2019

Abstract
Background: A few studies indicated that hepatitis C and hepatitis B virus (HCV/HBV) might be associated with pancreatic cancer risk. The aim of this nationwide cohort study was to examine this possible association.
Methods: HCV and HBV-infected individuals were identified from the national surveillance database from 1990 to 2006, and followed to the end of 2008. The pancreatic cancer risk in the study population was compared with the general population by calculation of Standardized Incidence Ratios (SIR), and with a matched reference population (1:5 matching) using Cox proportional hazards regression model to calculate Hazard Ratios (HR).
Results: In total 340,819 person-years in the HCV-cohort and 102,295 in the HBV-cohort were accumulated, with 34 and 5 pancreatic cancers identified, respectively. The SIR was 2.1 (95% CI: 1.4, 2.9) for HCV infection and the SIR 1.4 (0.5, 3.3) for HBV infection. In the Cox model analysis, the HR for HCV infection was 1.9 (95% CI: 1.3, 2.7), diminishing to 1.6 (1.04, 2.4) after adjustment for potential confounders of chronic obstructive pulmonary disease, diabetes mellitus, chronic pancreatitis and diagnoses related to alcohol abuse.
Conclusion: This nationwide population-based cohort study demonstrated an increased risk of pancreatic cancer among HCV-infected individuals, although this excess risk was attenuated but still statistically significant after adjustment for other potential risk factors. Our results support the hypothesis that HCV infection might be associated with an increased risk of pancreatic cancer, but further studies, with more complete information about other potential confounding factors, are needed to verify the association and to explore the causality.
Citation Format: Jiaqi Huang, Måns Magnusson, Anna Törner, Weimin Ye, Ann-Sofi Duberg. Risk of pancreatic cancer among individuals with hepatitis C or hepatitis B virus infection: A nationwide study in Sweden. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A07.
Abstract A35: Associations between time spent sitting and cancer-related biomarkers: An exploration of effect modifiers
Authors: Jung Su Yon , Paxton Raheem J. , Hays-Grudo Jennifer , Paskett Electra , Hursting Stephen D. , Fenton Jenifer , Pollak Michael , Vitolins Mara , Chang Shine 
Published: May 2019

Abstract
Purpose: Despite convincing evidence that prolonged periods of sitting may influence critical biological mediators of cancer development, few studies assessed the relationship between time spent sitting and cancer-related biomarkers.
Methods: This cross-sectional study included 825 postmenopausal women who were enrolled in an ancillary study of the Women's Health Initiative Observational Study between February 1995 and July 1998. Plasma levels of biomarkers were measured at the third annual visit. The time spent sitting per day was categorized as quartiles (Qs) and analysis of covariance was used to assess the relationships between sedentary time and cancer biomarkers.
Results: No clear linear patterns were observed between the time spent sitting and levels of biomarkers; however, these relationships were modified by race, physical activity level, and exogenous estrogen use. Insulin-like growth factor-I (IGF-I) levels among black women were higher than those of white women across the Qs of time spent sitting. Likewise, IL-6 levels in black women were higher than those in white women at Q3 and Q4 of sedentary time. IGF binding protein-3 levels were higher and insulin levels were lower among women meeting guidelines for physical activity than women who were not across the Qs of sedentary time. Additionally, C-reactive protein levels were higher among estrogen users than nonusers at Q1, Q2, and Q4 of sedentary time.
Conclusions: Few meaningful associations were observed between the time spent sitting and the cancer-related biomarkers. More research is needed to characterize the relationship between time spent sitting and cancer-related biomarkers in the context of pertinent effect modifiers.
Citation Format: Su Yon Jung, Raheem J. Paxton, Jennifer Hays-Grudo, Electra Paskett, Stephen D. Hursting, Jenifer Fenton, Michael Pollak, Mara Vitolins, Shine Chang. Associations between time spent sitting and cancer-related biomarkers: An exploration of effect modifiers. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A35.
Abstract A39: Gene-environment interactions between SNPs in the renin-angiotensin-aldosterone system and hypertension, obesity, and blood pressure-related dietary exposures regarding renal cell cancer risk
Authors: Deckers Ivette AG , Brandt Piet A. van den , Engeland Manon van , Godschalk Roger , Schouten Leo J. 
Published: May 2019

Abstract
Background: Hypertension and obesity may increase renal cell cancer (RCC) risk, but the underlying mechanism is not well understood. Given that sodium, potassium and fluid intake influence blood pressure (BP), genetic variants in the renin-angiotensin-aldosterone system (RAAS) may constitute to RCC development, as RAAS regulates BP and sodium balance.
Methods: The Netherlands Cohort Study on diet and cancer with case-cohort design includes 120,852 participants aged 55-69 years. At baseline, diet and lifestyle factors were assessed using questionnaires and toenail clippings were collected. Genotyping of toenail DNA was performed using the iPLEX Gold system and MassARRAY software (Sequenom, Hamburg). After 20.3 years of follow-up, 13 candidate single nucleotide polymorphisms (SNPs) in seven RAAS genes known to be involved in BP regulation or sodium balance were available for Cox proportional hazards analyses for 3,583 subcohort members and 503 cases.
Results: Two SNPs, AGTR1_rs1492078 (AA vs. GG) and AGTR1_rs5186 (CC vs. AA), were associated with RCC risk in the total population [hazard ratio (95% confidence interval): 0.70 (0.49-1.00) and 1.49 (1.08-2.05), respectively] and in participants with hypertension. AGT_rs3889728 (AA + AG vs. GG) showed a lower RCC risk in participants with hypertension and a higher RCC risk in participants without hypertension (P-interaction = 0.039). Associations between sodium intake and RCC risk differed among genotypes of RAAS SNPs, but tests for these and other SNP-environment interactions were not significant.
Conclusion: SNPs in AGTR1 and the interplay between AGT_rs889728 and hypertension may influence RCC susceptibility. SNP-environment interactions with obesity, potassium intake and fluid intake were not significant. For sodium intake we can neither conclude nor exclude that such interactions may contribute to RCC risk.
Citation Format: Ivette AG Deckers, Piet A. van den Brandt, Manon van Engeland, Roger Godschalk, Leo J. Schouten. Gene-environment interactions between SNPs in the renin-angiotensin-aldosterone system and hypertension, obesity, and blood pressure-related dietary exposures regarding renal cell cancer risk. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A39.
Abstract A43: Circulating concentrations of serum 25-hydroxyvitamin D and colorectal adenoma
Authors: Choi Yoonji , Kim Young Ha , Cho Chang Ho , Kim Sung Hi , Lee Jung Eun 
Published: May 2019

Abstract
Introduction: Vitamin D has been suggested to decrease a risk of colorectal neoplasia. We examined the association between serum 25-hydroxyvitamin D (25(OH)D) levels and colorectal adenoma in Korea adults.
Methods: We conducted a case-control study among 364 patients (112 cases and 252 controls). Participants who underwent colonoscopy completed questionnaires and provided blood samples. Serum 25(OH)D were measured using the radioimmunoassay (RIA). We used multivariable logistic regression models to obtain odds ratios (ORs) and 95% confidence intervals (CIs) of colorectal adenoma.
Results: The mean values of serum 25(OH)D among controls were 16.8 ± 5.1 ng/ml for men and 16.6 ± 6.6 ng/ml for women. With adjustment for potential confounding variables, serum levels of 25(OH)D were not significant associated with adenoma in men (ORs = 0.94, 95% CIs = 0.26-3.40 compared the highest quartile with the lowest quartile). However, women in the highest quartile of serum 25(OH)D levels had a significant lower prevalence of colorectal adenoma compared to those in the lowest quartile (OR = 0.32, 95% CIs = 0.11-0.94).
Conclusion: Our results suggest that there is an inverse association between serum 25(OH)D levels and colorectal adenoma in Korea women.
Citation Format: Yoonji Choi, Young Ha Kim, Chang Ho Cho, Sung Hi Kim, Jung Eun Lee. Circulating concentrations of serum 25-hydroxyvitamin D and colorectal adenoma. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A43.
Abstract A45: Consumption of artificially and sugar-sweetened carbonated beverages and risk of non-Hodgkin lymphoid neoplasms: The Cancer Prevention Study-II Nutrition Cohort
Authors: McCullough Marjorie L. , Teras Lauren , Shah Roma , Diver Ryan , Gaudet Mia M. , Gapstur Susan M. 
Published: May 2019

Abstract
Background: The sweetener aspartame received regulatory approval for use in carbonated beverages 30 years ago, but debate continues over its safety. Only two prospective studies have examined the relationship between artificially-sweetened beverages and incidence of non-Hodgkin lymphoma (NHL), with one study finding no association and the other suggesting possible increased risk.
Objective: We examined the associations of consumption of artificially- and sugar- sweetened carbonated beverages and total aspartame intake with risk of incident NHL, overall and by major histologic subtypes in the Cancer Prevention Study-II (CPS-II) Nutrition Cohort.
Methods: Included in this analysis were 100,442 men and women, average age 69.2 (SD ± 6.1) years. Participants reported consumption of diet and regular soda in 1999 and 2003, in addition to information on medical history, lifestyle and anthropometric factors. During a 10 year follow-up, 1,196 self-reported NHL cases were verified through medical record or state cancer registry linkage. Cox proportional hazards regression was used to estimate multivariable-adjusted relative risks (RR) and 95% confidence intervals (CI).
Results: Average daily consumption of diet and regular soda at baseline was less than a half serving/day. In men and women combined, we observed no association between consumption of one or more servings/day of diet (RR=0.92, 95% CI 0.73, 1.17, p trend=0.14) or regular (RR=1.10, 95 % CI 0.77, 1.58, p trend=0.62) soda and total NHL risk, compared to no consumption (p heterogeneity by sex&gt;0.1); both models controlled for consumption of the other beverage. Aspartame intake was not associated with NHL risk (RR=1.02, 95% CI 0.84, 1.24 p trend=0.69, comparing top to bottom quintile of intake). Associations with NHL subtypes (multiple myeloma, DLBCL, CLL/SLL, follicular, other B cell lymphoma) were similarly null except for an inverse trend for consumption of artificially sweetened soda with risk of multiple myeloma (RR=0.70, 95% CI 0.42, 1.17 for 5+ servings/week vs. none, p trend=0.05).
Conclusion: In this cohort of older men and women, daily consumption of artificially- or sugar- sweetened sodas is not associated with increased risk of NHL. Further research in younger cohorts is needed to examine associations with higher amounts of consumption.
Citation Format: Marjorie L. McCullough, Lauren Teras, Roma Shah, Ryan Diver, Mia M. Gaudet, Susan M. Gapstur. Consumption of artificially and sugar-sweetened carbonated beverages and risk of non-Hodgkin lymphoid neoplasms: The Cancer Prevention Study-II Nutrition Cohort. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A45.
Abstract A52: ZIP11 and susceptibility to renal and bladder cancer
Authors: Wu Lang , Rabe Kari G. , Parker Alexander S. , Petersen Gloria M. 
Published: May 2019

Abstract
Introduction: Laboratory studies have demonstrated that zinc and zinc transporters play important roles in the development of urological cancers, including prostate, bladder, and renal cell cancer. To date however, there have been no efforts to evaluate whether germline variation in zinc transporter genes alter the risk of developing these cancers. Motivated by this, we evaluated associations of known variants in zinc transporter genes with risk of prostate, bladder, and renal cell cancer using three NCI Genome Wide Association Study (GWAS) data sets downloaded from dbGaP.
Methods: Data consisted of GWAS data from the PLCO Screening Trial (prostate; 1172 cases, 1157 controls); Bladder Cancer study (3527 cases, 5119 controls); and Renal Cancer study (1453 cases, 3531 controls). All genotyped variants in 10 ZNT family genes (ZNT1-ZNT10) and 14 ZIP family genes (ZIP1-ZIP14) in each data set were analyzed by logistic regression models to evaluate the association of each variant with risk of developing prostate, bladder, and renal cancer, respectively. We evaluated these associations in a univariable setting, after adjusting for available covariates, such as age and gender. Correction for multiple comparisons used Max T permutation tests.
Results: One variant in ZIP11, rs8081059, was associated with increased risk of renal cancer (OR=1.28, 95% CI= 1.13-1.45; corrected p= 0.049). Another ZIP11 variant, rs11871756, was associated with an increased risk of bladder cancer risk (OR=1.43, 95% CI 1.24-1.63; corrected p=0.0002). We also found three variants in ZIP11 associated with a decreased risk of bladder cancer: rs11077654 (OR=0.76, 95% CI 0.68-0.85; corrected p=0.001), rs9913017 (OR=0.76, 95% CI= 0.68-0.85; corrected p=0.002), and rs4969054 (OR=0.78, 95% CI 0.69-0.88; corrected p=0.02). Interestingly, these three protective variants are within the same LD block. There were no associations between zinc transporter variants and prostate cancer risk.
Conclusion: We report for the first time that specific genetic variants of a zinc transporter gene, ZIP11, are associated with risk of renal and bladder cancer. If validated in larger, more focused studies, further investigations are warranted to explore the functional significance of ZIP11 in these two cancers.
Citation Format: Lang Wu, Kari G. Rabe, Alexander S. Parker, Gloria M. Petersen. ZIP11 and susceptibility to renal and bladder cancer. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A52.
Abstract A54: Vitamin D and risk of colorectal cancer: The Melbourne Collaborative Cohort Study
Authors: English Dallas R. , Williamson Elizabeth J. , Heath Alicia K. , Ebeling Peter R. , Baglietto Laura , Hodge Allison M. , Giles Graham G. , Kvaskoff David , Eyles Darryl 
Published: May 2019

Abstract
Introduction: Several nested case-control studies have found that high serum or plasma levels of 25-hydroxy vitamin D (25OHD) are associated with decreased risk of colorectal cancer. Most of these studies were conducted in areas with lower UVB irradiance than Australia. To determine whether 25OHD was associated with reduced risk of colorectal cancer in Australia, we conducted a case-cohort study nested within a cohort study.
Methods: The Melbourne Collaborative Cohort recruited 41,514 participants from 1990-94. At baseline, blood samples were collected. This study was restricted to participants with dried blood spots from baseline blood samples. We included a random sample of 2996 people (i.e. subcohort), together with all incident cases of colorectal cancer during follow-up. 25OHD was measured using liquid chromatography tandem mass-spectrometry. The data were analysed with Cox regression, using Barlow's method to allow for the case-cohort design and adjusted for sex, education, physical activity, waist circumference, country of birth (southern Europe versus other), smoking, and intakes of alcohol, energy, margarine and processed meat.
Results: The method showed high reliability; the intra-class correlation from 500 repeat measurements was 0.78 (95% CI: 0.75, 0.82). In a separate calibration study, there was good agreement between 25OHD measurements from dried blood spots and plasma and for the subcohort, the predicted mean plasma concentrations were 55.5 nmol/L for males and 46.0 for females. During an average of 14 years of follow-up, we identified 563 cases. There was a weak, non-statistically significant inverse association between 25OHD and colorectal cancer; the hazard ratio for the highest versus lowest quartile was 0.82 (95% CI: 0.61, 1.10, p trend = 0.20).
Conclusions: In this Australian study, the association between 25OHD and risk of colorectal cancer was weaker than has been observed in studies from Europe and North America.
Citation Format: Dallas R. English, Elizabeth J. Williamson, Alicia K. Heath, Peter R. Ebeling, Laura Baglietto, Allison M. Hodge, Graham G. Giles, David Kvaskoff, Darryl Eyles. Vitamin D and risk of colorectal cancer: The Melbourne Collaborative Cohort Study. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A54.
Abstract A57: Alcohol consumption and plasma sex steroids in premenopausal women
Authors: Hirko Kelly A. , Hankinson Susan E. , Eliassen A. Heather 
Published: May 2019

Abstract
Purpose: Alcohol consumption is a consistent risk factor for breast cancer, and evidence suggests premenopausal plasma hormones are associated with breast cancer. In this study, we examined the association between alcohol consumption and plasma sex steroid hormones in premenopausal women.
Methods: We assessed the cross-sectional association between alcohol intake and circulating sex steroid concentrations among 2,034 premenopausal women in the Nurses' Health Study II (NHSII). Plasma concentrations of estradiol, estrone, estrone sulfate, testosterone, androstenedione, progesterone, prolactin, dehydroepiandrosterone (DHEA), and dehydroepiandrosterone sulphate (DHEAS) were measured in samples collected in 1996-99. Estrogens were measured in both the follicular and luteal phases of the menstrual cycle, while androgens were measured in the luteal phase as well as in random samples that were not timed in the menstrual cycle. Average alcohol intake was calculated from semi-quantitative food frequency questionnaires collected in 1995 and 1999.
Results: Alcohol consumption was positively association with concentrations of luteal estrone (p-trend&lt;0.0001) and luteal estradiol (p-trend=0.0001). Women who consumed more than 20 grams of alcohol per day, compared with non-drinkers, had higher concentrations of luteal estrone (geometric mean 98.0 vs. 79.9 pg/mL) and luteal estradiol (152.5 vs. 123.3 pg/mL). We did not observe statistically significant associations between alcohol and follicular estrogens, luteal estrone sulfate, testosterone, androstenedione, progesterone, prolactin, DHEA or DHEAS.
Conclusion: Alcohol consumption was significantly positively associated with luteal estrogen concentrations, but not with plasma androgen levels, nor estrogens measured in the follicular phase. Thus, luteal estrogen levels may mediate the association between alcohol and breast cancer.
Citation Format: Kelly A. Hirko, Susan E. Hankinson, A. Heather Eliassen. Alcohol consumption and plasma sex steroids in premenopausal women. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A57.