bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A62: Alcohol consumption, genetic variation in alcohol dehydrogenase genes, and risk of clear cell renal cell carcinoma
Authors: Parker Alexander Scott , Diehl Nancy , Arnold Michelle L. , Rivera Shauna , Cannon Ashley , Custer Kaitlynn , Leibovich Bradley 
Published: May 2019

Abstract
Introduction: An inverse association between alcohol consumption and risk of renal cell carcinoma (RCC) is well reported in the literature. Despite this, no investigators have explored the potential for effect modification of this association by genetic variations in enzymes that metabolize alcohol. Motivated by this, we conducted a pilot investigation of the role of genetic variation in the alcohol dehydrogenase genes (ADH) as an effect modifier of the association of alcohol and RCC risk.
Methods: We analyzed data on 121 RCC cases and 121 controls. Cases were prospectively collected as part of our Renal Registry in the Department of Urology. Controls were recruited through the Family Medicine and frequency matched to cases on age, gender and state of residence. We collected detailed risk factor data (self-report questionnaire) as well as a DNA sample on cases and controls. We utilized Sequenome analysis to determine presence of published SNPs in the ADH gene cluster (ADH1-7). We employed logistic regression with interaction terms as well as stratified analyses to evaluate effect modification by genetic variants in the ADH gene cluster on the association of alcohol consumption and RCC risk.
Results: Compared to non-drinkers, those that consumed alcohol above the median experienced a lowering in RCC risk (OR=0.80; 95% CI 0.5 to 1.43). We observed evidence of interactions with 6 SNPs in the ADH gene (p-values from 0.05-0.2). As an example, in stratified analysis, the inverse association strengthened in those without the minor allele present at rs1154454 in ADH7 (OR=0.56; 95% CI 0.3 to 1.0; p=0.08) while evidence of an increased in RCC risk was noted among those with the minor allele (OR=2.14; 95CI 0.8 – 5.7; p=0.1). Adjustment for age and gender did not alter our results.
Conclusion: Our pilot data suggest that specific variants in the ADH gene cluster may modify the reported protective effect of alcohol consumption on RCC risk. Given the possible implications for improving our understanding of the biology of this association and informing prevention, future investigations that analyze a larger sample size and examine additional variants are warranted.
Citation Format: Alexander Scott Parker, Nancy Diehl, Michelle L. Arnold, Shauna Rivera, Ashley Cannon, Kaitlynn Custer, Bradley Leibovich. Alcohol consumption, genetic variation in alcohol dehydrogenase genes, and risk of clear cell renal cell carcinoma. [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 A62.
Abstract B45: Obesity, diabetes, other comorbidities and survival in a cohort of women with ovarian cancer
Authors: Protani Melinda M. , Nagle Christina M. , deFazio Anna , Blomfield Penelope , Jobling Thomas , Leung Yee , Nicklin James L. , Perrin Lewis C. , Wain Gerard , Webb Penelope M. 
Published: May 2019

Abstract
Purpose: To determine the relationship between obesity, diabetes, other major comorbidities and survival following a diagnosis of ovarian cancer.
Methods: We examined the association between obesity, as measured by body mass index (BMI), diabetes and other comorbidities and survival from ovarian cancer in a large (n=1404), population-based cohort of women diagnosed with epithelial ovarian cancer between 2002-2006. Information about pre-diagnostic BMI and medical history was obtained via a self-administered questionnaire. BMI at the commencement of primary chemotherapy and clinicopathologic data were abstracted from medical records and deaths were ascertained up to October 2011 via linkage with the Australian National Death Index. We also examined short- (≥5 years) and long-term (&gt;5 years) survival, as well as survival differences by histological subtype. Adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were obtained using Cox regression.
Results: After adjustment, a survival disadvantage was observed for women who were obese prior to diagnosis compared to women in the normal BMI range (BMI 30-34.9:HR 1.21, 95%CI 0.99-1.48; BMI≥35:HR 1.19, 95%CI 0.92-1.55). The association was similar for BMI at the commencement of primary chemotherapy. There was a suggestion that the adverse association between obesity and survival time was restricted to women with serous or endometrioid histological subtypes. Obesity conferred a survival disadvantage for both short- and long-term survival, with a stronger association in long-term survivors. Diabetes and other comorbidities did not appear to influence survival overall; however appeared to be important in the sub-group of women surviving longer than 5 years (HR1.44 and HR1.64, respectively).
Conclusion: This is the first study to show that obesity is important in both short- and long-term survival following a diagnosis of ovarian cancer. More research examining diabetes, comorbidities and ovarian cancer survival should be conducted.
Citation Format: Melinda M. Protani, Christina M. Nagle, Anna deFazio, Penelope Blomfield, Thomas Jobling, Yee Leung, James L. Nicklin, Lewis C. Perrin, Gerard Wain, Penelope M. Webb. Obesity, diabetes, other comorbidities and survival in a cohort of women with ovarian 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 B45.
Abstract C16: Effects of cessation counseling types on quit attempts and intentions
Authors: Cornelius Monica E. , Cummings K. Michael 
Published: May 2019

Abstract
Smoking cessation assistance programs aid smokers in quitting. While cessation programs have shown some effectiveness, many smokers do not utilize them. The combination of nicotine addiction, access to cheaper products and a general lack of access to smoking cessation tools present difficulties to smokers. Direct counseling from a healthcare provider has been shown to aid in smokers thinking about quitting their smoking; however greater assistance is often needed beyond the recommendation to quit. The purpose of this study was to examine the effect different types of cessation counseling on (1) quit attempts and (2) intention to quit within the next month. We hypothesized that advice + quit assistance from a healthcare provider would be associated with making a quit attempt and intending to quit within the next month when compared with advice alone. This paper presents data from the first eight waves of the International Tobacco Control (ITC) US adult smoker survey from 2002-2011 (N=6669). Participants who visited a healthcare provider within the past year of survey were eligible for inclusion. The levels of healthcare provider counseling included no advice, advice only, and advice + quit assistance. Repeated measures logistic regression, using generalized estimating equations (GEE) was used to model (1) whether participants made a quit attempt and (2) intention to quit within the next month. Models were controlled for age, sex, daily smoking, time-in-sample, wave, education, income, and region, as well as cessation counseling. Over 60% of participants indicated having seen a healthcare provider, with over 60% receiving advice to quit. Among those who reported receiving advice to quit, less than one third received a referral or quit prescription and less than one half received a pamphlet from their healthcare provider. Those receiving advice + quit assistance were almost twice as likely to have attempted to quit as those who received advice only. Participants receiving assistance were more likely to intend to quit within the next month. Not all smokers get advice to stop smoking when seen by their doctor and even fewer get offered assistance beyond the recommendation to stop smoking. This study shows that those who received both advice and assistance were more likely to report making a quit attempt or at least report a greater intention to stop smoking in the future.
Citation Format: Monica E. Cornelius, K. Michael Cummings. Effects of cessation counseling types on quit attempts and intentions. [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 C16.
Abstract C22: Telomere length variation and frequency of short telomeres in blood lymphocytes: Novel biomarkers for lung cancer risk
Authors: Sun Bing , Wang Ying , Kota Krishna , Shi Yaru , Motlek Salaam , Makambi Kepher , Loffredo Christopher A. , Shields Peter G. , Yang Qin , Harris Curtis C. , Zheng Yun-Ling 
Published: May 2019

Abstract
Background: Although it is widely recognized that telomere dysfunction plays an important role in cancer, the relationship between telomere function in somatic cells and lung cancer risk is not well defined. In a case-control study of non-small cell lung cancer, we examined relationship between several key telomere features and lung cancer risk. Method: Telomere fluorescent in situ hybridization was used to measure telomere features using short-term cultured blood lymphocytes. Logistic regression was used to estimate the strength of association between telomere features and lung cancer risk. Results: Telomere length variation across all chromosomal ends was significantly associated with lung cancer risk, with adjusted odds ratios of 4.67 [95% confidence interval (CI) = 1.46 – 14.9] and 0.46 (95% CI = 0.25 – 0.84) for young (age &lt; 60) and old (age &gt; 60) individuals, respectively. Similar strength and direction of associations between percentage of short telomeres and lung cancer risk were also observed. Telomere length variation and average telomere length jointly affect lung cancer risk. When comparing individuals with short telomere and high telomere length variation to those with long telomere and low telomere length variation, adjusted odd ratios were 8.21 (95% CI = 1.71 – 39.5) and 0.33 (95% CI = 0.15 – 0.72) for young and old individuals, respectively. Conclusion: Telomere length variation and percentage of short telomeres in blood lymphocytes are significantly associated with lung cancer risk and the associations are modulated by age. Telomere length variation in combination with average telomere length may be a promising tool for lung cancer risk assessment.
Citation Format: Bing Sun, Ying Wang, Krishna Kota, Yaru Shi, Salaam Motlek, Kepher Makambi, Christopher A. Loffredo, Peter G. Shields, Qin Yang, Curtis C. Harris, Yun-Ling Zheng. Telomere length variation and frequency of short telomeres in blood lymphocytes: Novel biomarkers for lung 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 C22.
Abstract C54: Mechanism and preclinical prevention of increased breast cancer risk caused by pregnancy
Authors: Li Yi 
Published: May 2019

Abstract
While a first pregnancy before age 22 lowers breast cancer risk, a pregnancy after age 35 significantly increases life-long breast cancer risk. Pregnancy causes several changes in the normal breast that raise barriers to transformation, but how pregnancy can also increase long-term cancer risk remains unclear. Precancerous lesions accumulate in the breast with age. We show in mice that pregnancy has different effects on the few early lesions that have already accumulated in the otherwise normal breast'it causes apoptosis evasion and accelerated progression to cancer. The apoptosis evasion is due to the normally tightly controlled STAT5 signaling going astray' in response to pregnancy/lactation hormones, these precancerous cells can activate STAT5; but during involution, the oncogenic signaling can prevent STAT5 deactivation. The resulting persistent STAT5 signaling prevents the apoptosis normally initiated by oncogene activation and involution. Short-term anti-STAT5 treatment of lactation-completed, early lesions-bearing mice eliminates the increased risk after a pregnancy. This chemoprevention strategy has important implications for preventing increased human breast cancer risk caused by pregnancy as it may lower long-term breast cancer risk in women who have had a late-age pregnancy and thus are more likely to harbor STAT5-activated progressing early lesions.
Citation Format: Yi Li. Mechanism and preclinical prevention of increased breast cancer risk caused by pregnancy. [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 C54.
Abstract CN01-03: Frameshift peptide vaccination: Towards cancer prevention in Lynch syndrome
Authors: Kloor Matthias , Reuschenbach Miriam , Karbach Julia , Rafiyan Reza , Al-Batran Salah-Eddin , Pauligk Claudia , Jaeger Elke , Doeberitz Magnus von Knebel 
Published: May 2019

Abstract
Lynch syndrome is one of the most common hereditary cancer syndromes. It is caused by germ line mutations of DNA mismatch repair genes and predisposes affected individuals to the development of colorectal cancer and extracolonic malignancies with a lifetime risk of over 50%. Lynch syndrome-associated cancers show the high-level microsatellite instability (MSI-H) phenotype and are characterized by signs of a pronounced local anti-tumoral immune response, suggesting that the immune system plays an active role in the surveillance and natural history of these cancers. The progression of MSI-H cancers is triggered by mutations in microsatellite sequences within gene-encoding regions, which can cause shifts of the translational reading frame and lead to the generation of immunogenic frameshift peptides (FSP) at the carboxy-terminal end of the respective proteins. FSP-specific immune responses have been observed frequently in MSI-H cancer patients and Lynch syndrome mutation carriers. We have therefore initiated a clinical phase I/IIa vaccination trial that evaluates vaccination with a combination of three FSP antigens in patients with MSI-H colorectal cancer, UICC stage III and IV. Preliminary data demonstrate that no treatment-associated severe adverse events have been observed after FSP vaccination. Moreover, significant T cell and humoral immune responses against FSP antigens were induced in the majority of vaccinated patients. The observation of strong FSP-specific immune responses in vaccinated patients suggests that FSP-based vaccination may represent a novel option for the treatment of MSI-H colorectal cancer patients. Moreover, FSP vaccination may be used for tumor prevention in Lynch syndrome mutation carriers in the future.
Citation Format: Matthias Kloor, Miriam Reuschenbach, Julia Karbach, Reza Rafiyan, Salah-Eddin Al-Batran, Claudia Pauligk, Elke Jaeger, Magnus von Knebel Doeberitz. Frameshift peptide vaccination: Towards cancer prevention in Lynch syndrome. [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 CN01-03.
Abstract CN05-01: Genomics and cancer management: Mind the gap!
Authors: Jankowski Janusz A. 
Published: May 2019

Abstract
All diseases are a combination of nature versus nurture. In the former understanding of the inherited genetics through genomics is vital to understanding the predisposition to diseases and in some cases prognosis and response to therapy. The application of genome wide analyses studies identify several diseases has been particularly helpful especially in Crohn's disease, Diabetes and Psoriasis. Outside autoimmune diseases genomics whilst improving the understanding of cancer and its etiology has not made a difference in the clinical management of diseases. As an exemplar the progression from oesophagitis to metaplasia to esophageal adenocarcinoma presents challenges which are generalizable to other cancers. These include delineating differential genomic drivers for premalignant intermediates from those for the subsequent neoplastic lesions. In addition developments in cancer genomics by Exome sequencing or whole genome sequencing don't readily match with inherited genomic changes from GWAS. Moreover genomics has yet to reveal robust pathways for the design of new targets.
When these issues are coupled with failure in many cases to assess other factors responsible for inherited variation including CNVs and methylation patterns, it seems likely progress will be slow and need very large sample sets.
Citation Format: Janusz A. Jankowski. Genomics and cancer management: Mind the gap! [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 CN05-01.
Abstract ED03-01: Using electronic health data in “real-world” studies: Examples and opportunities in the HMO Cancer Research Network
Authors: Doria-Rose Vincent Paul , Mazor Katherine 
Published: May 2019

Abstract
The HMO Cancer Research Network (CRN) is a National Cancer Institute-funded initiative to support and facilitate collaborative cancer research within non-profit integrated health care delivery systems. The CRN has several characteristics that result collectively in a unique, unparalleled resource for epidemiologic and health services research in cancer. These include scientists with expertise in conducting public-domain cancer research in these settings; defined populations with a combined membership of approximately 8.5 million individuals within 9 different integrated health care delivery systems; clinical and administrative data systems that capture most aspects of care; development and implementation of common data models in the Virtual Data Warehouse (VDW) to facilitate collaborative and multi-institutional research; and access to clinicians and administrators to facilitate translation of research findings to practice. The VDW includes demographic, utilization, diagnostic, procedure, and pharmacy data which can be used to study cancer epidemiology, cost effectiveness, practice patterns and more. Investigators can propose collaborative research projects via the CRN website (http://crn.cancer.gov/). The presentation will include examples of recent CRN-based research studies highlighting both study design and practical issues in conducting studies using electronic data from multiple sources. Strategies for successful collaborative research within and beyond the CRN will be discussed. Supported by U24 CA171524.
Citation Format: Vincent Paul Doria-Rose, Katherine Mazor. Using electronic health data in “real-world” studies: Examples and opportunities in the HMO Cancer Research Network. [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 ED03-01.
Abstract ED04-01: Untargeted metabolite profiling as a powerful new tool in the armamentarium of cancer researchers
Authors: Gross Steven S. , Chen Qiuying 
Published: May 2019

Abstract
Metabolomics, or global metabolite profiling, hails the lofty goal of establishing the identity and levels of all metabolites in a biological system, under a defined set of circumstances. A convergence of enabling technologies has recently made broad metabolite profiling a reality, providing a powerful new tool for defining disease mechanisms, identifying disease biomarkers and evaluating the efficacy of therapies. This overall goal of this educational session is to describe how global metabolite profiling technologies are being used to develop a systems-wide understanding of cancer cell metabolism and to discover the molecular basis for cancer chemopreventative drug therapies.
Citation Format: Steven S. Gross, Qiuying Chen. Untargeted metabolite profiling as a powerful new tool in the armamentarium of cancer researchers. [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 ED04-01.
Abstract FO02-02: Risk-based breast cancer screening
Authors: Kerlikowske Karla M. 
Published: May 2019

Abstract
Breast cancer screening guidelines are primarily based on age. The discussion and science is changing focus from what age to start screening mammography to how best to identify women most likely to benefit from screening mammography, such as those at increased risk of breast cancer and advanced stage disease. The Breast Cancer Surveillance Consortium (BCSC) and Cancer Intervention and Surveillance Modeling Network (CISNET) are evaluating risk-based screening approaches aimed at maximizing the benefit of screening and minimizing the harms. This session will discuss how risk-based screening could maximize the potential benefits of screening by identifying and screening women at high risk of breast cancer and minimize the potential harms of screening by identifying women at low risk of breast cancer that could begin screening at a later age and/or be screened less often.
Citation Format: Karla M. Kerlikowske. Risk-based breast cancer screening. [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 FO02-02.
Abstract PL01-01: The clinical and biologic effects of tobacco on cancer treatment
Authors: Warren Graham W. 
Published: May 2019

Abstract
Smoking and tobacco use are well-established risk factors for the development of cancer as well as other adverse health conditions. Whereas substantial work has been done to elucidate cancer risks from smoking as well as biologic mechanisms of tobacco induced carcinogenesis, proportionately little work has been done to understand the clinical and biologic effects of continued tobacco use after a cancer diagnosis. Tobacco use leads to the development of tumors that are usually diagnosed at a more advanced stage. A history of tobacco use may also lead to tumors that do not respond as well to conventional cancer treatments such as surgery, chemotherapy, or radiotherapy. However, current smoking at the time of diagnosis or during cancer treatment appears to confer a worse prognosis in cancer patients by increasing cancer treatment toxicity, recurrence, risk for developing a second primary cancer, and overall mortality. The adverse effects of smoking are further noted across both tobacco related and non-tobacco related cancers. This talk will review the effects of smoking on outcomes in cancer patients and will begin to discuss how tobacco products may alter cancer biology by promoting a more aggressive tumor phenotype. Importantly, data suggest that the adverse effects of current smoking on cancer treatment outcomes may be reversible. The implications of tobacco as a potentially reversible systemic agent that can affect cancer biology and treatment will be discussed.
Citation Format: Graham W. Warren. The clinical and biologic effects of tobacco on cancer treatment. [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 PL01-01.