bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A90: The attribution of lifestyle related risk factors in middle age on breast cancer incidence in The Netherlands: Preliminary results
Authors: Gemert WAM van , Elias SG , Bausch-Goldbohm RA , Brandt PA van den , Grooters HG , Kampman E , Kiemeney LALM , Leeuwen FE van , Monninkhof EM , Vries E De , Peeters PHM 
Published: January 2014

Abstract
Background: Breast cancer, especially postmenopausal, is one of the most common cancers in Western women. Although therapeutic options have improved, there still is a high mortality rate. Several of the known risk factors for breast cancer are lifestyle related and modifiable, providing an opportunity for primary prevention. Middle-aged women still have the chance to modify these factors to lower nearby breast cancer risk. We estimated the fraction of postmenopausal breast cancer cases that is attributable to lifestyle factors as currently present in middle-aged Dutch women.
Methods: We estimated population attributable fractions (PAFs) of five potentially modifiable risk factors for Dutch women aged 45-54 years. Risk factors included overweight and obesity, alcohol use, physical inactivity, current use of hormone replacement therapy (HRT) and oral contraceptives.
We based relative risks on literature search including meta-analyses and expert group consensus. Current prevalence rates of the risk factors were derived from several Dutch registration databases and national surveys (2009-2011).
Results: Of all 45-54 year old contemporary Dutch women, 46% are estimated to be physically inactive, 43% to be overweight or obese, 42% to drink alcohol, 1% to use HRT and 17% to use contraceptives.
These risk factors jointly account for an estimated 20.2% of all future breast cancer cases in these women. Physical inactivity and alcohol use are responsible for the highest population attributable fraction (PAF of 7.0% and 6.8% respectively), followed by overweight and obesity (4.3%), oral contraceptive use (3.4%) and hormone replacement therapy (0.6%).
Conclusion: On a population level, lifestyle related factors play an important role in the development of postmenopausal breast cancer. Considering current prevalence rates in the Netherlands, our findings imply that modifiable risk factors present at middle-age are jointly responsible for 1 out of every 5 future breast cancer cases. This is in concordance with other studies in European countries.
Our findings thus suggest that incidence rates can be lowered substantially by changing lifestyle habits, even in a woman's later life.
Citation Format: WAM van Gemert, SG Elias, RA Bausch-Goldbohm, PA van den Brandt, HG Grooters, E Kampman, LALM Kiemeney, FE van Leeuwen, EM Monninkhof, E De Vries, PHM Peeters. The attribution of lifestyle related risk factors in middle age on breast cancer incidence in The Netherlands: Preliminary results. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr A90.
Abstract A93: Genetic variations in aging related genes/pathways and colorectal cancer risk
Authors: Zhang Fanmao , Eng Cathy , Lin Moubin , Hildebrandt Michelle A.T. , He Yonggang , Lin Jie , Huang Maosheng , Gu Jian , Wu Xifeng 
Published: January 2014

Abstract
Advanced age is arguably the most important risk factor for developing cancer. About 77% of all cancers are diagnosed in individuals 55 years of age and older. Aging is especially a dominant risk factor for colorectal cancer (CRC), with 91% of cases diagnosed in individuals 50 years of age and older. A number of genes and signaling pathways have been indicated in the aging process in model organisms including mammals, e.g. the insulin/IGF-1 signaling pathway, mTOR pathway and telomere and telomerase pathway. Recently, genome-wide association studies also identified several single nucleotide polymorphisms (SNPs) associated with longevity. Therefore, we hypothesized that genetic variations of the genes and pathways related to aging might be associated with CRC risk. We systematically identified 189 putative functional SNPs in 109 aging-related genes and 20 longevity-associated SNPs from GWAS. In the discovery phase, we genotyped these SNPs in 797 Caucasian CRC cases and 797 matched healthy control subjects. In main effect analysis, 10 SNPs were significantly associated with altered CRC risk. When evaluating combined effects of these SNPs, we found a significant gene dosage effect for increased CRC risk with increasing number of unfavorable genotypes. Compared with individuals carrying fewer than three unfavorable genotypes, individuals with six and more than six of these unfavorable genotypes exhibited a 2.06-fold (95% CI: 1.24-3.43, P = 0.006) and a 2.44-fold (95% CI: 1.76-3.38, P = 7.56×10−8) increased risk of CRC, respectively (P for trend 1.25×10−9). Higher order gene-gene interaction analysis also revealed potential relationships among SNPs in TP53, ERCC2, GPR133, PRKAG3, TEP1, TSC1 and LMNA that further defined risk groups for CRC. Our results suggest that genetic polymorphisms in aging-related genes and pathways may modify CRC susceptibility both individually and jointly. Replication is currently underway to validate these findings.
Citation Format: Fanmao Zhang, Cathy Eng, Moubin Lin, Michelle A.T. Hildebrandt, Yonggang He, Jie Lin, Maosheng Huang, Jian Gu, Xifeng Wu. Genetic variations in aging-related genes/pathways and colorectal cancer risk. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr A93.
Abstract A94: Missed opportunities: Racial and socioeconomic disparities in emergency presentation of colorectal cancer
Authors: Pruitt Sandi L. , Davidson Nicholas O. , Gupta Samir , Yan Yan , Schootman Mario 
Published: January 2014

Abstract
Background: Emergency presentation for colorectal cancer (CRC) is common and associated with high morbidity and mortality. African Americans and those with lower socioeconomic status (SES) experience higher CRC morbidity and mortality, and higher rates of emergency CRC presentation may, in part, account for these disparities. We hypothesized that African Americans and individuals with low SES have higher rates of emergency CRC presentation.
Methods: We examined disparities in emergency CRC presentation using nationally representative 1992-2005 SEER-Medicare data of U.S. adults aged ≥66 years with invasive CRC. Emergency CRC presentation (the primary outcome) was defined as a newly diagnosed CRC associated with: obstruction, perforation, or an inpatient admission requiring immediate medical intervention (e.g. for severe, life threatening conditions) identified using Medicare claims with ICD-9 and admission type codes. We used logistic regression to compare associations of race and census tract poverty rate with emergency CRC presentation, adjusting for sociodemographic (age, sex, Medicaid status, year of diagnosis, urban/rural residence at diagnosis), tumor (SEER historic stage, left/right side tumor location, grade, histology), and clinical (history of the following in the prior year: preventable hospitalizations, comorbidity, endoscopic testing) covariates.
Results: We identified 88,859 patients with CRC during the study period, 29.0% of whom presented emergently (of these, 81.3% had an emergency admission, 31.6% obstruction, and 4.2% perforation). In unadjusted analyses, CRC patients more likely to present emergently included African Americans (vs. whites OR: 1.64 95% CI: 1.57-1.72) and those living in census tracts with the highest poverty rate (≥20% vs. &lt;10% poverty OR: 1.31 95% CI: 1.26-1.37). In a single multivariable model, after adjusting for all covariates including tumor stage, African Americans (vs. whites AOR: 1.29 95% CI: 1.21-1.37) and those living in census tracts with the highest poverty rate (≥20% vs. &lt;10% poverty AOR: 1.10 95% CI: 1.04-1.16) continued to be more likely to present emergently.
Discussion: In this population-based study, racial and socioeconomic disparities are evident in emergency presentation of CRC, which may account for some of the observed disparities in morbidity and mortality. Targeted efforts to increase CRC screening in these populations would reduce this preventable disparity.
Citation Format: Sandi L. Pruitt, Nicholas O. Davidson, Samir Gupta, Yan Yan, Mario Schootman. Missed opportunities: Racial and socioeconomic disparities in emergency presentation of colorectal cancer. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr A94.
Abstract A99: Dietary N-nitroso compounds, endogenous nitrosation and the risk of esophageal and gastric cancer subtypes in the Netherlands Cohort Study
Authors: Keszei András P. , Goldbohm R Alexandra , Schouten Leo J. , Jakszyn Paula , Brandt Piet A. van den 
Published: January 2014

Abstract
Background: Dietary N-nitroso compounds and endogenous nitrosation are important carcinogenic factors, but evidence for their role from population studies is scarce for esophageal, and inconsistent for gastric cancer.
Objective: We studied the relationship between the risk of esophageal and gastric cancer subtypes and dietary intake of N-nitrosodimethylamine, heme iron, nitrite and nitrate in The Netherlands Cohort Study.
Methods: 120 852 men and women aged 55-69 years were recruited in 1986, and diet, based on a 150-item food frequency questionnaire, as well as other risk factors were assessed. The cohort was followed for 16.3 years, and 110 esophageal squamous cell carcinomas, 151 esophageal adenocarcinomas, 166 gastric cardia adenocarcinomas, and 497 gastric non-cardia adenocarcinoma cases were analyzed along with 4032 subcohort members in a case-cohort analysis.
Results: There were positive associations between N-nitrosodimethylamine intake and esophageal squamous cell carcinoma and gastric non-cardia adenocarcinoma risk in men (hazard ratio (HR) for 0.1 μg/day increase in intake: 1.15 [95% confidence interval (CI): 1.05-1.25; P(trend): 0.01] and 1.06 [95%CI: 1.01-1.10; P(trend): 0.09], respectively). Esophageal squamous cell carcinoma risk was associated with nitrite and heme iron intake (HR for 0.1 mg/day increase in nitrite intake: 1.19 [95%CI: 1.05-1.36; P(trend): 0.06] and for 1 mg/day heme iron intake: 1.83 [95%CI: 0.98-3.39; P(trend): 0.03]). Among women, exposure levels were lower, and we found a positive association only between N-nitrosodimethylamine and esophageal squamous cell carcinoma risk (HR for 0.1 μg/day increase: 1.34 [95%CI: 1.04,1.71; P(trend):0.57]).
Conclusion: These results suggest that N-nitroso compounds and their precursors may influence the risk of esophageal squamous cell carcinoma.
Citation Format: András P. Keszei, R Alexandra Goldbohm, Leo J. Schouten, Paula Jakszyn, Piet A. van den Brandt. Dietary N-nitroso compounds, endogenous nitrosation, and the risk of esophageal and gastric cancer subtypes in the Netherlands Cohort Study. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr A99.
Abstract B08: Effectiveness of team-based financial incentives for smoking cessation in the workplace
Authors: Haak Lee Sang , Dong Yeo Chang , Kyoung Kim In , Sun Kang Hye , Young Lee Hwa , Kwon Park Chan , Sook Kim Myung 
Published: January 2014

Abstract
Objective: Workplace offers a promising venue for encouraging smoking cessation. Worksite smoking cessation programs offer a number of advantages, including the accessibility of the target population, the availability of occupational health support and the potential for peer pressure and peer support. Financial incentives given to teams rather than individual participants could create team based effort to support and reinforce smoking cessation within the workplace. The purpose of this study is to identify the effectiveness of team-based financial incentives in improving long-term rates of smoking cessation among employees.
Methods: Total 28 smokers who were healthcare workers from St. Paul's Hospital, were enrolled. The financial incentives were ₩50,000 for smoking cessation at 1 week and 1 month after the initial cessation and ₩100,000 for abstinence at 3 and 6 months after the initial cessation.
Results: Abstinence rate at 3, 6 and 12 months after the initial cessation were 61%, 54% and 50%, respectively. There were no differences in age, body mass indexes and spirometric indexes between the success and failure group. Nicotine dependence scores were significantly higher in the failure group at 3 months, but not at 6 and 12 months. Smokers who participated within 1 month of enrollment had a higher abstinence rate at 3 months than those who participated after 1 month (p=0.007).
Conclusion: Team based financial incentives resulted in high abstinence rates, which was maintained through 12 months. These results suggest that the financial incentives given to teams could make use of the potential for peer pressure and peer support over a longer period. In addition, more intensive management is needed to members who participate after 1 month and have higher nicotine dependence scores, which results in a lower abstinence rate.
Citation Format: Lee Sang Haak, Yeo Chang Dong, Kim In Kyoung, Kang Hye Sun, Lee Hwa Young, Park Chan Kwon, Kim Myung Sook. Effectiveness of team-based financial incentives for smoking cessation in the workplace. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B08.
Abstract B09: PROMOTER CPG ISLAND METHYLATION DURING PROGRESSION OF ATYPICAL HYPERPLASIA TO BREAST CANCER
Authors: Martinez-Galan Joaquina , Delgado Juan Ramon , Moral Rosario Del , Torres-Torres Blanca 
Published: January 2014

Abstract
DNA methylation is the main epigenetic modification in cancer. The pathological features of breast cancer follow a sequential progression from transition of a normal cell to benign proliferative hyperplasia, hyperplasia with atypia, in situ carcinoma and, eventually, to invasive and metastatic disease. Purpose: This study was designed to evaluate the changes in promoter CpG islands hypermethylation during breast cancer progression from pre-invasive lesions to invasive ductal carcinoma and different methylation patron with benign breast disease. Material and Methods: We performed analysis for the methylation status of 5 promoter CpG island (ESR1, E-Cad, APC, RARB and 14-3-3-σ promoters) in a group with women with normal breast tissue n=74; other group with epithelial atypia/ atypical ductal hyperplasia (n=20), ductal carcinoma in situ (DCIS, n=14) and invasive ductal carcinoma (IDC, n=107). Results:Relative serum levels of methylated gene promoters ESR1 and 14-3-3-σ showed significant differences between IDC y normal breast tissue (were significantly higher in IDC than normal breast tissue) and between normal breast tissue and epithelial atypia/ atypical ductal hyperplasia/ ductal carcinoma in situ. There are no differences between IDC and epithelial atypia/ atypical ductal hyperplasia/ ductal carcinoma in situ when 14-3-3-σ and ESR1 mean values are compared. In fact, the present findings showed a frequent presence of methylated 14-3-3-σ in sera from women with breast benign disease, which could be considered the result of a proliferative alteration of epithelial and stromal components of the breast. Which may indicate presence of occult benign breast disease, although other possible sources of this DNA include normal tissues, which show higher methylation values with increasing age; which might undergo lysis during tumour growth; or premalignant lesion during tumour growth; or premalignant lesion.
Conclusions: These findings showed that promoter CpG island methylation changed significantly in pre-invasive lesions, and breast cancer, suggesting that CpG island methylation of tumor-related genes is an early event in breast cancer progression.
Citation Format: Joaquina Martinez-Galan, Juan Ramon Delgado, Rosario Del Moral, Blanca Torres-Torres. Promoter CpG island methylation during progression of atypical hyperplasia to breast cancer. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B09.
Abstract B10: Design of the DENSE trial: MRI as an additional screening modality to detect breast cancer in women aged 50-75 years with extremely dense breasts
Authors: Emaus Marleen , Veldhuis Wouter , Bakker Marije , Monninkhof Evelyn , Karssemeijer Nico , Bosch Maurice van den , Peeters Petra , Mali Willem , Gils Carla van 
Published: January 2014

Abstract
Background: Women with high mammographic density have an increased breast cancer risk and also a lower mammographic tumor detectability. Nevertheless, these women are currently screened with mammography only. MRI could lead to earlier tumor detection, because of its higher sensitivity. To study the additional value of MRI, a parallel-group randomized controlled trial design is needed with one group receiving mammography and the other group receiving mammography and MRI. With this design it is possible to determine the proportion of interval tumors within each arm. A reduction in interval tumors is a precondition of effectiveness, because this represents clinically relevant cancer detection, rather than overdiagnosis.
Study design: DENSE is a multicenter randomized trial, carried out in the Dutch biennial screening program (age range 50-75 years). Mammographic density is measured using a fully-automated volumetric method (Volpara™). Participants with extremely dense breasts (ACR4) and a negative mammogram are randomized to ‘additional MRI’ (n=7,237) versus ‘current practice’ (n=28,948). After randomization, only the intervention arm is asked for consent (single-consent prerandomized design). The intervention consists of a dynamic breast MRI with gadolinium-based contrast medium (Gadovist®) and is carried out for 3 screening rounds. The primary outcome is the difference in proportion of interval tumors between the arms. Secondary outcomes are the number of MRI screen-detected tumors, proportion false-positives, quality of life, breast cancer mortality and costs.
Conclusion: DENSE investigates the (cost-)effectiveness of screening with mammography and MRI compared to mammography alone in women with extremely dense breasts aged 50-75 years. Inclusion started in December 2011.
Citation Format: Marleen Emaus, Wouter Veldhuis, Marije Bakker, Evelyn Monninkhof, Nico Karssemeijer, Maurice van den Bosch, Petra Peeters, Willem Mali, Carla van Gils. Design of the DENSE trial: MRI as an additional screening modality to detect breast cancer in women aged 50-75 years with extremely dense breasts. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B10.
Abstract B104: Expressions of PCNA in triple negative breast cancers and Their clinical significance
Authors: Jiaping Peng , qun meng 
Published: January 2014

Abstract
Objective: To study expressions of matrix metalloproteinase-13 (PCNA) in triple negative (ER-, PR-, HER2-) breast cancers and evaluate their clinical significance.
Methods: The immunohistochemistry SP method was used to evaluate the expressions of PCNA in 32 cases of triple negative breast cancers, 24 cases of HR breast cancer (ER+/PR+, HER-2-), 12 cases of HER2 breast cancer (ER-, PR-, HER2+) and 12 cases of breast fibroadenoma and their correlations to clinicopathologic features were analyzed.
Results: The expressions of PCNA were significantly higher in the triple negative breast cancers than in breast fibroadenoma and HR breast cancers (P&lt;0.05). Furthermore, the expression of PCNA was significantly higher in the triple negative breast cancers than in HER2 breast cancers (P &lt;0.05). In the triple negative breast cancers, PCNA expression was associated with axillary lymph node metastasis and TNM stage (P &lt;0.05), but it was not correlated with patients age (P &gt;0.05). Correlation analysis showed that PCNA expression was positively correlated in the triple negative breast can cers, HR breast cancers and HER2 breast cancers (P &lt;0.05).
Conclusion: There is a close relationship between PCNA the occurrence and development of triple negative breast cancers, and PCNA could serve as important indexes in the aspect of invasiveness and metastasis in triple negative breast cancers.
Citation Format: Peng Jiaping, meng qun. Expressions of PCNA in triple-negative breast cancers and their clinical significance. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B104.
Abstract B113: High Fat Diet Accelerates Development of Precancerous Lesions and Fibrosis in Mice Expressing mutant K-Ras in Pancreatic Acinar Cells
Authors: Cruz-Monserrate Zobeida , Philips Bincy , Ji Baoan , Daniluk Jaroslaw , Logsdon Craig D. 
Published: January 2014

Abstract
Background: Obesity is postulated to be a major risk factor for pancreatic ductal carcinoma (PDAC), which is the fourth deadliest cancer in the US. Although the association between obesity and pancreatic cancer has been reported, the molecular mechanisms are not yet known. Since K-Ras mutations are almost universal in PDAC, and we have recently shown that endogenous levels of oncogenic K-Ras make cells susceptible to otherwise benign levels of inflammation, we hypothesize that high fat intake can act as a persistent low level inflammatory mechanism capable of inducing PDAC in cells expressing a single copy of oncogenic K-Ras. In the current study, we examined the effects of high dietary fat on the development of precancerous lesions and fibrosis, as well as the activation of K-Ras signaling pathways in mice expressing mutant K-Ras in pancreatic acinar cells.
Methods: Transgenic mice LSL-K-Ras were cross with Ela-CreER (Pancreatic-Ras) and treated with tamoxifen to “knock-in” oncogenic K-Ras in adult pancreatic acinar cells. Pancreatic-Ras and littermate control mice were administered a low fat diet with 10.2% kcal fat or a high fat diet with 61.6% kcal fat for 30 days starting at 50 days of age. Mice were then sacrificed and analyzed histologically for fibrosis development, presence of precancerous lesions, and activation of K-Ras signaling pathways.
Results: Mice expressing endogenous levels of oncogenic K-Ras and fed a high fat diet developed abundant fibrosis, low grade precancerous lesions throughout the pancreas and had higher levels of phospho-ERK when compared to littermate controls and mice fed a low fat diet.
Conclusions: These findings suggest that consumption of high dietary fat acts as an inflammatory stimulus that enhances the activation of oncogenic K-Ras downstream signaling pathways, leading to the early development of precancerous lesions and fibrosis in the pancreas. Therefore, efforts aimed at inhibiting inflammation and K-Ras activation would be expected to prevent cancer development.
Citation Format: Zobeida Cruz-Monserrate, Bincy Philips, Baoan Ji, Jaroslaw Daniluk, Craig D. Logsdon. High-fat diet accelerates development of precancerous lesions and fibrosis in mice expressing mutant K-Ras in pancreatic acinar cells. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B113.