bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A84: Red and processed meat-derived mutagen exposure and colorectal cancer risk in a population-based case-control study
Authors: Miller Paige E. , Lazarus Philip , Lesko Samuel M. , Muscat Joshua E. , Harper Gregory , Cross Amanda J. , Sinha Rashmi , Liao Jason , Ashmore Joseph H. , Hartman Terry J. 
Published: January 2011

Abstract
A recent report issued jointly by the World Cancer Research Fund (WCRF) and the American Institute for Cancer Research (AICR) concluded that the evidence to support a positive association between greater intakes of red and processed meat and colorectal cancer was convincing, but the evidence for specific meat components explaining these associations remained inconclusive. To explore potential underlying mechanisms for these observations, we examined associations of mutagens generated through meat cooking and meat processing methods with colorectal cancer in a large multisite population-based case-control study in a contiguous 19-county area in central and northeast Pennsylvania. Participants (863 healthy controls, 483 incident colon and 196 incident rectal cancer cases) completed a detailed lifestyle questionnaire and the 137-item National Cancer Institute's Diet History Questionnaire (DHQ). The DHQ included a detailed cooked and processed meat module to estimate intakes of heterocyclic amines (HCAs), polycyclic aromatic hydrocarbons (PAHs), nitrites, and nitrates. Odds ratios (ORs) and 95% confidence intervals (CIs) for associations between meat exposures and colorectal cancer stratified by sub-site of the large intestine were estimated from unconditional logistic regression models. After multivariate adjustment for age, total energy intake, sex, body mass index, energy-adjusted total fruit and vegetable intake, and past regular NSAID use, positive associations with HCAs and PAHs, as measured by total mutagenic activity, were stronger for rectal cancer (OR = 1.55, 95% CI: 0.97, 2.47; P for trend = 0.049) than colon cancer, whereas positive associations with nitrites plus nitrates were stronger for colon cancer (OR = 1.31, 95% CI: 0.91-1.87; P for trend = 0.031). Our findings support the hypothesis that greater exposure to HCAs, PAHs, nitrites, and nitrates is a plausible mechanism by which red and processed meat may increase colorectal cancer risk. Our sub-site analyses indicate that associations between meat-derived exposures and colon and rectal cancer may differ, which underscores the need for additional studies that examine dietary risk factors for colon and rectal cancer as separate endpoints. The investigation of interactions between genetic polymorphisms and meat exposures in relation to colorectal cancer risk is underway in our study population.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):A84.
Abstract A95: KCNK5 regulates proliferation of ER-negative breast cancer cells
Authors: Shen Qiang , Markaverich Jamie 
Published: January 2011

Abstract
Prevention and treatment of estrogen receptor (ER)-negative breast cancer are clinical challenges to reduce breast cancer incidence and mortality. All ER-negative breast cancer and a significant portion of ERpositive breast cancer are not preventable using currently available preventive drugs such as tamoxifen and raloxifene. Furthermore, ER-negative breast cancer does not respond to hormonal therapies and inclines to develop metastasis. Thus, novel targets are urgently needed to achieve effective prevention and treatment of ER-negative breast cancer. The ion channels for transporting potassium ions are deregulated in breast cancers. Specifically, the KCNK5 ion channel is differentially overexpressed at mRNA levels in ERnegative vs ER-positive breast cancers. Several lines of evidence suggest that KCNK5 may be a promising target for ER-negative breast cancer prevention and treatment. We hypothesize that KCNK5 is required for malignant transformation of breast cells and development of ER-negative breast cancer. In our studies, we found that majority of ER-negative breast cancer cells expressed moderate to high level of KCNK5 protein whereas minimal/low levels of KCNK5 in ER-positive cells. We also found that transient knockdown of KCNK5 mRNA with siRNA significantly inhibited proliferation of two ER-negative breast cancer cells (HCC1569 & BT20) that express high levels of KCNK5 protein. We are now testing whether gain of KCNK5 function by overexpressing KCNK5 in ER-negative breast cancer cells (HCC1937 & BT549, expressing relatively low level of KCNK5 protein) will promote cell growth. The proposed studies will provide useful pre-clinical information regarding the role of KCNK5 in ER-negative breast cancer development, which currently is poorly understood.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):A95.
Abstract A96: Trans-resveratrol decreases breast proliferation and alters mammary promoter hypermethylation in women at increased risk for breast cancer
Authors: Qin Wenyi , Zhu Weizhu , Rottinghaus George , Chen Yin-Chieh , Zhang Ke , Sauter Edward R. 
Published: January 2011

Abstract
Trans-resveratrol, present in high concentration in the skin of red grapes and red wine, has a dose-dependent antiproliferative effect in vitro, prevents the formation of mammary tumors, and has been touted as a chemopreventive agent. We conducted in vitro experiments in hormone sensitive breast cancer cells and observed that trans-resveratrol downregulated DNA methyltransferase gene expression in a dose dependent fashion. Based upon this preclinical observation, we determined if transresveratrol had dose related anti-proliferative and methylation effects in humans. 16 adult women at increased breast cancer risk were randomized in double-blind fashion to placebo, 5 or 50 mg trans-resveratrol twice daily for 12 weeks. We collected serum, breast nipple aspirate fluid (NAF) and mammary duct (MD) specimens from all participants at all time points. Breast specific and systemic antiproliferative effects were assessed measuring the cancer promoting prostaglandin (PG)E2 in NAF and serum as well as changes in MD cytology, while methylation assessment of three cancer related genes (p16, RASSF-1α, APC) was performed on MD specimens. Serum resveratrol increased after consuming both trans-resveratrol doses (p&lt;.001 for both). Cytology was not significantly changed by resveratrol treatment. RASSF-1α methylation significantly decreased after high (but not low) dose resveratrol, and the decrease correlated with increasing levels of serum resveratrol. RASSF-1α methylation also correlated with change in NAF levels of PGE2 (p=.0087). This work provides novel insights into the anticancer effects of trans-resveratrol in women at increased breast cancer risk, including prostaglandin inhibition and a decrease in methylation of the tumor suppressor gene RASSF-1α.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):A96.
Abstract A97: Quality assessment of colonoscopy reporting: Results from a statewide cancer screening program
Authors: Li Jun , Nadel Marion 
Published: January 2011

Abstract
Objectives: Appropriate documentation of the colonoscopy procedure is an important component of patient care and one measure of quality. However, direct evaluation of colonoscopy reporting has been minimal. The aim of this study was to assess the quality of colonoscopy reporting.
Methods: We retrospectively collected data from 110 colonoscopy reports, where at least one polyp was noted. These reports were completed by 110 endoscopists from 2005-2006 through a statewide colorectal cancer screening program in Maryland, representing a variety of reporting formats from endoscopists throughout the state. We evaluated 25 key data elements recommended by the Standardized Colonoscopy Reporting and Data System (CO-RADS), including procedure indications, risk and comorbidity assessments, procedure technical descriptions, colonoscopy findings, and specimen retrieval and submission for pathology.
Results: All 110 reports stated an indication for the endoscopy, 36% included patient's medical comorbidities, 73% documented the bowel preparation quality, and 82% documented specific cecal landmarks. For the 177 individual polyps identified, information on size and morphology was documented for 87% and 53%, respectively. For these key data elements, ambiguous descriptors were sometimes used.
Conclusions: There was considerable variation among these colonoscopy reports. The absence of key data elements may impact the ability to make recommendations for recall intervals for colorectal cancer screening. Measurement of quality indicators in colonoscopy practice can identify areas for quality improvement.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):A97.
Abstract B100: Rotating night shift work and risk of ovarian cancer
Authors: Poole Elizabeth M. , Schernhammer Eva S. , Tworoger Shelley S. 
Published: January 2011

Abstract
Introduction: Night shift work has been associated with higher risks of breast, endometrial, colorectal, prostate cancer and non-Hodgkin's lymphoma. These associations may be driven by a diminished ability of the pineal gland to produce melatonin among those exposed to light at night. Melatonin likely has multiple anti-cancer mechanisms, including down-regulation of the reproductive axis and direct actions of melatonin on estrogen receptors — both of note for ovarian cancer. Moreover, melatonin exhibits a growth-inhibitory effect on ovarian cancer cell lines. Few epidemiological studies have evaluated an association between night shift work and ovarian cancer risk. Within the NHS and NHSII cohorts, we prospectively assessed the association of rotating night shift work with ovarian cancer risk.
Methods: Total number of years of rotating night shift work (defined as at least 3 nights per month in addition to days and evenings during that month) was queried in 1988 for NHS and in 1989 for NHSII. Duration was updated in 1991, 1993, 2001, and 2005 for NHSII. We used Cox proportional hazards regression to model the incidence rate ratios (RR) and 95% confidence intervals (CI) of ovarian cancer for each shift work category (1-2 years, 3-5 years, 6-9 years, 10-14 years, 15-19 years, 20-29 years, and 30+ years), compared to those who never worked rotating shifts, adjusting for age in months, cohort, tubal ligation, duration of oral contraceptive use, parity, BMI, smoking status, menopausal status, family history of ovarian cancer, and duration of breastfeeding. In our analysis, we updated the values for these covariates when new data were available and otherwise carried forward the values from the previous cycle or the last cycle when each covariate was assessed.
Results: There were 666 cases of ovarian cancer among 2,856,537 person-years of follow-up time. Overall, rotating shift work was not associated with ovarian cancer risk: 15-19 years vs. none: OR: 1.21; 95% CI: 0.78-1.86; 20-29 years vs. none: OR: 0.65; 95% CI: 0.35-1.19; 30+ years vs. none: OR: 0.79; 95% CI: 0.40-1.54. Estimates were unchanged when adjusted for menstrual irregularity.
Conclusion: In this large prospective study, overall, there was no association between duration of rotating night shift work and risk of ovarian cancer. Additional analyses stratifying by hormonal receptor status. menopausal status and other potential effect modifiers are ongoing and may reveal subgroup associations.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B100.
Abstract B103: HPV vaccine adherence in urban youth
Authors: Tracy J. Kathleen , Terplan Mishka , Lydecker Alison D. , Schluterman Nicholas 
Published: January 2011

Abstract
This abstract is being presented as a short talk in Concurrent Session 15. A full abstract is printed in the Proferred Abstracts section (PR-11) of the Conference Proceedings.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B103.
Abstract B13: High-risk human papillomavirus prevalence in oral and oropharyngeal premalignant lesions: A critical literature review
Authors: Hatton Elizabeth R. , Jayaprakash Vijay , Reid Mary E. , Loree Thom R. , Rigual Nestor R. , Frustino Jennifer L. , Johnson Timothy R. , Sullivan Maureen A. 
Published: January 2011

Abstract
Introduction: During the past decade, there has been a significant increase in the incidence of human papillomavirus (HPV) related squamous cell cancer of the oropharynx, especially those of the tonsil and tongue base. HPV-16 and HPV-18 have been linked to these malignant neoplasms. Generally, oral epithelium undergoes a sequence of histopathological pre-malignant transformations before the development of invasive carcinoma. A study evaluating the prevalence of HPV-16/18 types in histopathologically diagnosed oral pre-malignant lesions (OPL) is lacking. Therefore, we conducted a comprehensive literature review to estimate the prevalence of HR HPV types in different grades of OPLs.
Study Design: A critical literature search was conducted using Pubmed and SCOPUS databases for the key terms human papillomavirus infection, head and neck cancer, oral cancer, oral hyperplasia, oral dysplasia, and oral leukoplakia. A total of 90 articles related to HPV in oral tissue and pre-malignant lesions were identified. Of these, 29 articles evaluated the prevalence of HPV in histopathological OPLs (hyperplasia and dysplasia). In addition, 11 out of these 29 articles determined the prevalence of HPV in histologically evaluated leukoplakic samples. Only research articles published from 1990 — 2009 were used for this review.
Results: Overall, the 29 articles evaluated high-risk (HR) HPV in 1,171 OPLs. This included 140 hyperplasias, 467 dysplasias, 425 leukoplakic lesions without dysplasia, and 139 leukoplakic lesions with dysplasia. The prevalence of any type of HPV in hyperplasia, dysplasia, leukoplakia without dysplasia, and leukoplakia with dysplasia was 24%, 25%, 28%, and 20% respectively. The prevalence of HR HPV-16/18 in these lesions was 24%, 21%, 26% and 26% respectively. The difference in prevalence of different grades of OPLs was not statistically significant. The prevalence of any HPV type in mild, moderate, and severe dysplastic lesions was 43%, 39%, and 33% respectively. The prevalence of HR HPV-16/18 in mild, moderate, and severe dysplastic lesions was 39%, 32%, and 28% respectively.
Conclusion: High-risk HPV infection has been noted even in early stage histopathological OPLs like hyperplasias and mild dysplasias, and their prevalence rate is very similar to high grade OPLs, and oral (OC) and oropharyngeal cancers (OPC). Larger studies are needed to obtain a more precise estimate of the prevalence and persistence of HR HPV in histopathologically diagnosed OPLs in order to better understand the etiopathogenesis of HPV related OC and OPC.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B13.
Abstract B18: Personalizing the frequency of mammography: Cost effectiveness of screening mammography for women age 40 to 80 by breast density and other risk factors
Authors: Cummings Steven R. , Schousboen John T. , Loh Andrew , Kerlikowske Karla 
Published: January 2011

Abstract
Background: Current guidelines recommend mammography starting at age 40 or 50 years regardless of individual risk of breast cancer and do not take into account a woman's risk of breast cancer or breast density.
Methods: We used Markov microsimulation models to estimate the most cost-effectiveness intervals for screening mammography. Data about Breast Imaging Reporting and Data System (Bi-Rads) breast density, age, risk factors and risk of breast cancer, the natural history of breast cancer, estimates of progression in stages of breast cancer between mammograms, the cost of mammograms and medical care for breast cancer came from the Surveillance Epidemiology and End Results program, Breast Cancer Surveillance Consortium, and the medical literature. Simulations were done for cohorts receiving subsequent mammography between ages 40 to 79 years. We considered a strategy to be cost-effective if it cost ≤ $100,000 per lifetime quality adjusted life year (QALY) gained.
Results: Between ages 50 to 79, mammography every 2 years is cost-effective (&lt;$100,000 per QALY) for women with Bi-Rads-3 or −4 breast density, or with BI-RADS 1 or 2 and a family history of breast cancer or history of breast biopsy. Mammography is cost-effective if done less often -every 3 or 4 years — for women with lower (Bi-Rads-1 or −2) breast density and no family history of breast cancer or history of breast biopsy. For women age 40-49, mammography every 2 years is cost-effective for those with Bi-Rads-3 or −4 breast density plus a family history of breast cancer and/or a history of breast biopsy, but it is not cost-effective for 40 to 49 year olds without these risk factors and with lower breast density. In general, the most cost-effective screening interval is longer if false positive results cause a loss of quality of life.
Conclusions: The frequency of mammography should be personalized based on woman's risk of breast cancer, estimated from her age, breast density, family history of breast cancer, history of breast biopsy and the potential effect of false positive mammograms on her quality of life.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B18.
Abstract B19: Evaluation of progression of cirrhosis to hepatocellular carcinoma using site-specific protein glycosylation analysis.
Authors: Kosti Ourania , Goldman Radoslav , Brnakova Zuzana , Shetty Kirti , Karger B. , Rejtar Tomas 
Published: January 2011

Abstract
Hepatocellular carcinoma (HCC) is a major worldwide health problem and a cancer with increasing incidence in the United States mainly due to hepatitis C viral (HCV) infections. Approximately 10-30% of HCV carriers develop cirrhosis; patients with cirrhosis have an annual risk of 1-2% for developing HCC and their prognosis is generally poor. The slow development and late detection of HCC suggest that the identification of biomarkers of disease progression and early detection are needed. Glycosylation is the most common post-translational modification of secreted proteins. Alterations in protein glycosylation are associated with different cancers, including HCC. We hypothesized that the site-specific glycosylation of proteins in HCC patients would differ from that of patients with liver cirrhosis and healthy people. Haptoglobin is a liver secreted glycoprotein with four N-glycosylation sites. Its main function is to bind free hemoglobin released by intravascular hemolysis; haptoglobin prevents the loss of iron and subsequent kidney damage. We used mass spectrometry to define site specific glycoforms of haptoglobin in the serum of 15 patients with HCC, 20 patients with liver cirrhosis due to HCV etiology and 15 disease free controls. We used selected reaction monitoring (SRM) quantification to quantify the changes in N-glycosylation. Quantification of 7-10 glycoforms per glycosylation site (approximately 30 glycoforms in total), revealed that site specific glycosylation of haptoglobin is altered in the diseased liver and is associated with liver damage and the presence of HCC. Results also indicated an increase of fucosylated glycans among patients with liver disease. In this pilot case-control study we demonstrated the development of site specific haptoglobin glycoform in the progression of liver disease. If confirmed by larger and prospective studies, site specific glycosylation of haptoglobin and other proteins, in general, could be used as a marker of HCC risk.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B19.
Abstract B21: Relationship of the global metabolome in blood to smoking behavior: A pilot study
Authors: Hsu Ping-Ching , Zhou Bin , Ressom Habtom , Cheema Amrita , Sheikh Kathryn , Pickworth Wallace , Shields Peter 
Published: January 2011

Abstract
Introduction: Better biomarkers of cancer risk are needed for smokers to enhance early detection and support the FDA as it considers cigarette performance standards and evaluate health claims for modified tobacco products. This study will identify new biomarkers through metabolomics, a powerful method to identify numerous metabolites and profiles.
Study Design: We utilized a previously conducted epidemiology study of well-characterized smokers. These subjects completed an extensive interview and smoked two cigarettes, one hour apart, in a smoking laboratory. Blood and CO measurements were collected before and after each cigarette. Plasma is available for metabolomic profiling. A pilot study was conducted on 5 light smokers and 5 heavy smokers’ plasma from the study and evaluated whether number of cigarettes per day mediates the influence of global metabolome.
Hypothesis: We hypothesized that the number of cigarettes per day exerts their influence on phenotype through global metabolome.
Methods: Using UPLC-TOFMS in our pilot study, we first analyzed global metabolomic profiles of 5 light smokers and 5 heavy smokers’ plasma and evaluated whether number of cigarettes per day mediate the influence of global metabolomic profiles. The data obtained for multivariate data analyses using Scripps’ XCMS. t-test, SVM (Support Vector Machine analysis), and Random Forest from the Metaboanalyst (www.metaboanalyst) were used for feature selection. The OOB (out-of-bag) error was used to measure the performance of Random Forest classification and the performance for SVMs was estimated using leave-one-out cross validation (LOOCV).
Results: In our results, 1199 peaks in the positive mode and 497 peaks in the negative mode were detected and after feature selection, 816 and 361 peaks were selected in the positive mode and negative mode, separately. Those significant features from all three methods (t-test, SVM and Random Forest) were pooled together for identification using Metlin, MMCD and HMDB databases to obtain the KEGG IDs, and the pooled KEGG IDs were used for Ingenuity Pathways Analysis (Ingenuity@ Systems, www.ingenuity.com). Our preliminary results suggest that smoking behavior is associated with several biological pathways such as cell death, gene expression, cell-cell interaction, and lipid metabolism. The Pathways Analysis also reveals several liver, heart and renal toxicity and altered bile acid biosynthesis, phospholipid degradation due to heavy smoking.
Future Studies: We will further evaluate whether smoking topography and inhalation, as measured by a nicotine boost and CO boost, and whether nicotine metabolism is associated with smokers’ global metabolome by level of smoking.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B21.