bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B90: Smoking prevalence among tobacco-related cancer survivors in the United States, BRFSS 2009
Authors: Underwood J. Michael , Fairley Temeika L. , Tai Eric 
Published: January 2011

Abstract
Introduction: Cancer survivors who continue to smoke are at increased risk for primary cancer recurrences or development of new malignancies. Risks may be even higher among Tobacco Related Cancer Survivors (TRCS). We provide a national report on smoking behavior among TRCS.
Methods: Tobacco-related cancers (lung/bronchial, pharyngeal, esophageal, stomach, pancreatic, kidney/renal, urinary bladder, cervical and leukemia) are defined according to the 2004 report of the Surgeon General on The Health Consequences of Smoking. Data from the 2009 Behavioral Risk Factor Surveillance System (BRFSS) were used to describe demographic characteristics and tobacco use behaviors reported by TRCS, other cancer survivors and the non cancer BRFSS cohort. Self reported prevalence percentages and confidence intervals were calculated using SAS version 9.2 (SAS Institute, Inc, Cary, North Carolina).
Results: Overall, 10% of BRFSS respondents reported being diagnosed with cancer. Approximately 17% of all cancer survivors were diagnosed with a tobacco related cancer. Survivors in this group were primarily white (85.4%) and female (71.9%). Approximately 8.8% of TRCS were Hispanic. TRCS report a substantially higher proportion of current and past tobacco use. Among TRCS, 68% (95%CI 66.0-69.0) reported a history of smoking and 27.1% (95%CI 25.4-28.9) reported currently smoking; among other cancer survivors, 45.7% (95%CI 45.4-45.9) reported a history of smoking and 27.6% (95%CI 27.3-27.9) reported currently smoking.
Conclusion: When compared to other cancer survivors, persons diagnosed with tobacco related cancers have higher past and current smoking rates. Smoking cessation interventions should target TRCS, and increased surveillance of smoking behaviors is needed in this population.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B90.
Abstract B95: Long-term use of cholesterol-lowering drugs and cancer incidence in a large United States cohort
Authors: Jacobs Eric J. , Newton Christina C. , Thun Michael J. , Gapstur Susan M. 
Published: January 2011

Abstract
Background: HMG-coA reductase inhibitors, commonly known as statins, account for the great majority of cholesterol-lowering drug use in the United States. Relatively little is known about the association between long-term statin use and incidence of most types of cancers.
Methods: We examined the association between use of cholesterol-lowering drugs, predominantly statins, and the incidence of 10 common cancers, as well as overall cancer incidence, among 133,255 participants (60,059 men and 73,196 women) in the Cancer Prevention Study II Nutrition Cohort during the period from 1997-2007. Multivariate Cox proportional hazards regression was used to estimate relative risks (RRs).
Results: Current use of cholesterol-lowering drugs for five or more years was not associated with overall cancer incidence (RR = 0.97, 95% CI = 0.92-1.03), or incidence of prostate, breast, colorectal, lung, bladder, renal cell, or pancreatic cancer, but was associated with lower risk of melanoma (RR = 0.81, 95% CI = 0.67-0.98), endometrial cancer (RR = 0.61, 95% CI = 0.42-0.90), and non-Hodgkin lymphoma (NHL) (RR = 0.73, 95% CI = 0.61-0.87).
Conclusion: These results suggest that long-term use of statins is unlikely to substantially increase or decrease overall cancer risk. However, associations between long-term statin use and risk of endometrial cancer, melanoma, and NHL deserve further investigation.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B95.
Abstract B98: Association between alcohol consumption and colorectal carcinogenesis: An ecologic study in Korea
Authors: Kim Jeongseon , Cho Young Ae 
Published: January 2011

Abstract
Background and Aim: The sharp increase in the incidence rate of colorectal cancer in Korea over the past decades may be partly attributed to the increase in alcohol consumption. An ecologic study was conducted in Korea to determine the association between alcohol consumption and the risk of colorectal cancer.
Methods: We obtained the colorectal cancer incidence rates (1999–2007) from the Korea National Statistics Office and data on national alcohol consumption (1998–2007) from the reports of the Korea National Health and Nutrition Examination Survey. Pearson's correlation coefficients were determined using the data of alcohol intakes and colorectal cancer incidence rate. People who consumed more than 45 g alcohol/day were defined as heavy drinkers.
Results: A significant correlation between alcohol consumption and the risk of colorectal cancer was observed in men; Pearson's correlation coefficients were statistically significant for men (r = 0.99; P = 0.001), but not for women (r = 0.82; P = 0.180). In the &lt;50-year age group, the age-specific incidence rate for men was comparable to that for women, but in the ≥50-year age group, it increased rapidly in men. The increase in alcohol consumption appears to be attributable to increase in the number of heavy drinkers among men aged 25–59 years, particularly among men aged 45–49 years.
Conclusion: Alcohol consumption may be positively related to the incidence of colorectal cancer. Our findings may aid in predicting future colorectal cancer incidence in Korea.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B98.
Abstract CN01-03: Immunotherapy of established lesions caused by high-risk HPV
Authors: Melief Cornelis J.M , Welters M. J.P. , Valentijn A. R.P.M. , Meer T. M.A. Berends-van der , Lowik M. J.G. , Vloon A. P.G. , Essahsah F. , Fathers L. M. , Offringa R. , Drifhout J. W. , Oostendorp J. , Fleuren G. J. , Burg S. H. van der , Kenter G. G. 
Published: January 2011

Abstract
Therapeutic vaccination with a synthetic long peptide (SLP@) vaccine mediated the eradication of established human papillomavirus type 16 (HPV16)-positive tumors in mice and controlled wart growth and latent virus infection in rabbits persistently infected with cottontail rabbit papillomavirus. Subsequent phase I/II studies with an HPV16 SLP@ vaccine, consisting of 13 long peptides covering the HPV16 E6 and E7 antigens, in patients with advanced HPV16-positive cervical cancer, revealed that this vaccine was safe and highly immunogenic. The purpose of the current study was to test the clinical efficacy of this HPV16 SLP@ vaccine in HPV16-induced high-grade vulvar intraepithelial neoplasia (VIN3), a premalignant epithelial disorder, spontaneous regression of which occurs in less than 2% of patients and in which recurrence after standard treatment is high.
In a phase 2 trial, 20 women with VIN3 were vaccinated three times sc in the limbs with a mix of the HPV16 E6 and E7 synthetic long peptides formulated in Montanide ISA-51. The endpoints were objective clinical responses, defined as reduction of at least 50% in lesion size (partial response) or complete regressions, and HPV16-specific T-cell responses, determined before and after vaccination.
The vaccine was safe, as no side effects exceeding CTC grade 2 were observed. At 3 and 12 months after the last vaccination an objective response was observed in 12/20 (60%) and 15/19 (79%) patients respectively. Nine of them showed a complete and durable regression of the lesions at 12 months and at 24 months. The strength of the vaccine-induced HPV16-specific T-cell response was significantly higher in the group of patients with a complete regression of their lesions as compared to nonresponders.
This study shows that in women with VIN3 objective clinical responses can be achieved by therapeutic vaccination with synthetic long peptides that is able to induce effective HVP16-specific T-cell responses.
Literature:
1. Kenter GG, Welters MJ, Valentijn AR, Lowik MJ, Berends-van der Meer DM, Vloon AP, Essahsah F, Fathers LM, Drijfhout JW, Offringa R,Wafelman AR, Oostendorp J, Fleuren GJ, Burg van der SH, Melief CJ. Vaccination against Human Papillomavirus 16 oncoproteins for vulvar intraepithelial neoplasia. N Engl J Med. 2009 Nov 5;361(19):1838-47.
2. Melief CJ, van der Burg SH. Immunotherapy of established (pre)malignant disease by synthetic long peptide vaccines. Nat Rev Cancer. 2008 May;8(5):351-60.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN01-03.
Abstract CN01-04: HBV vaccination to prevent hepatocellular carcinoma
Authors: Chang Mei-Hwei 
Published: January 2011

Abstract
Chronic HBV infection can lead to chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). HCC is one of the five major cancers in the world population. Hepatitis B virus (HBV) is the most important etiologic agent of liver cancer in the world population, particularly in areas highly prevalent for liver cancer.
Taiwan has launched the world's first universal HBV vaccination program in July 1984. The prevalence of HBV infection in vaccinated birth cohorts have been reduced remarkably to approximately one-tenth of the original prevalence. Furthermore, reduction of the HCC incidence in the vaccinated birth cohorts aged 6-14 years have been demonstrated. Recently, we have further provided evidence that the effect of HCC prevention by HBV vaccination has been extended from childhood to adolescent and gradually into early adulthood. The incidence of HCC was significantly lower among children and adolescents aged 6-19 years in the vaccinated than unvaccinated birth cohorts, showing an age- and sex-adjusted relative risk of 0.31 for the population vaccinated since birth.
Failure to prevent HCC results mostly from unsuccessful control of HBV infection by highly infectious mothers. The risk of developing HCC for vaccinated cohorts was statistically significantly associated with prenatal maternal HBsAg and HBeAg seropositivity; lack of administration of hepatitis B immunoglobulin at birth, and incomplete HBV vaccination. Future strategies to interrupt mother-to-infant transmission and to increase the global coverage rate of HBV immunization may enhance the cancer prevention effect of HBV immunization.
In conclusion, prevention of chronic HBV infection can successfully reduce the incidence of liver cancer. This is the first example of cancer preventive vaccine in human, which proves that prevention of the infection of an infectious agent can prevent its related cancer. This example has been extended to the prevention of cervical cancers, and hopefully into other infection-related cancers in the near future.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN01-04.
Abstract CN02-06: Phase IIB study to evaluate the safety and efficacy of topical difluoromethylornithine and topical diclofenac in the treatment of sun-damaged skin
Authors: Jeter Joanne M. , Stratton Steven , Einspahr Janine , Curiel Clara , Warneke James , Hu Chengcheng , Bartels Peter , Alberts David 
Published: January 2011

Abstract
Difluoromethylornithine (DFMO) and nonsteroidal anti-inflammatory drugs have been shown to have a synergistic protective effect against colon cancer. As single agents, both DFMO and diclofenac have demonstrated efficacy in the treatment of actinic keratoses, the cutaneous precursors to cutaneous squamous cell carcinomas. We designed a study investigating the effects of these two medications, alone and in combination, on sun-damaged skin of the forearm. The primary objective is to determine whether a three-month course of combination therapy increases the efficacy over either agent used alone in the treatment of moderately sun-damaged skin. The primary endpoint is the change in karyometric values from skin biopsies before and after treatment. A total of 156 subjects were enrolled in the study and randomized to A: topical DFMO applied BID × 90 days; B: topical diclofenac applied QD × 90 days; or C: topical DFMO applied BID and topical diclofenac applied QD × 90 days. Planned sample size was 138 evaluable subjects to provide 80% power to detect the difference in response rate as measured by karyometric average nuclear abnormality (ANA) between the single-agent DFMO arm and the combination treatment arm at the 2.5% significance level. The results for efficacy and safety will be presented at the AACR Frontiers in Cancer Prevention meeting. Secondary biomarker and clinical endpoints will also be summarized. These findings will provide insight into the potential use of the combination of these medications as skin cancer chemopreventive agents.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN02-06.
Abstract CN08-03: Breast cancer prevention: Predictors and outcomes of patient decision making
Authors: O'Neill Suzanne 
Published: January 2011

Abstract
Several options exist for breast cancer risk-reduction in women at moderate to high risk for the disease. However, cancer risk management decisions can be difficult. This is partially due to the competing risks, benefits and limitations of each management option, as well as related cognitive and emotional factors. This presentation draws on behavioral and decision-making research to detail risk management decision outcomes in the literature to date, examining reasons women may choose certain management options over others and why some options, such as uptake of chemoprevention, have not have taken hold in this population at rates previously expected. Data demonstrating the decisions made by women who receive BRCA1/2 test results and other women at moderate to high risk of the disease, including risk-reducing surgeries, screening, chemoprevention, and diet and physical activity will be presented. Potential cognitive and emotional variables related to decision outcomes will be reviewed. The talk will conclude with discussion of future research needs regarding decision support for current risk management options, as well as consideration of cognitive and emotional factors that may impact new risk management options currently on the horizon.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN08-03.
Abstract CN12-04: The role of inflammation and stromal cells in gastrointestinal cancers
Authors: Wang Timothy C. , Worthley Daniel , Tu Shuiping Tu , Quante Michael 
Published: January 2011

Abstract
Most gastrointestinal cancers arise in the setting of chronic inflammation, but which leads to the recruitment of additional stromal cells, but the nature of these cells have not been well-defined. Carcinoma-associated fibroblasts (CAFs) that express alpha-smooth-muscle-actin (αSMA+) are thought to contribute to cancer progression but their precise origin has not been established. We have employed IL-1β transgenic mice and Helicobacter felis-infected mice that develop gastric dysplasia and cancer to investigate the origins and contributions of CAFs. These studies suggest that chronic inflammation of the GI tract, along with other carcinogenic stimuli, results in remodeling of the bone marrow and recruitment of bone marrow-derived cells to the incipient cancer site. At least 20% of CAFs originate from BM cells, and BM-derived CAFs promote tumor growth in organotypic and xenograft models. Thus, BM-derived fibroblastic cells create a new cancer niche that contributes to the progression of cancer, and as such represent a potential target for cancer prevention therapy.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN12-04.
Abstract CN14-02: Motivating individual behavior change through theory-driven community engagement
Authors: Logan Henrietta L. 
Published: January 2011

Abstract
Community-based interventions built on a strong theoretical framework are relatively rare in oral health disparity research. It is assumed that community-based research should engage the community but less frequently is it expected that the interventions are designed to expose and test the mechanisms through which behavior changes. A first step in such a paradigm is a thorough understanding of the target behavior and the associated physical and social environment and the interaction thereof. This presentation will discuss the use of the Theory of Planned Behavior and the Elaboration Likelihood Model to design and test community-based interventions aimed at changing behavior associated with late stage diagnosis of head and neck cancer. Consideration will be given to elucidating the pathways through which behavior change occurs.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN14-02.
Abstract CN14-04: Identifying the premalignant lesion at high risk for progression to cancer
Authors: Mao Li 
Published: January 2011

Abstract
Oral tumorigenesis is a multistep process requiring the accumulation of multiple molecular alterations such as mutations, genomic deletions and amplifications, as well as epigenetic modifications in oral epithelial cells. These alterations allow the affected cells gaining growth advantages over other cells and other malignant phenotypes.
In the past two decades, extensive studies have been conducted to understand molecular abnormalities in oral cancers and oral premalignant lesions (OPLs). Although promising, none of these has translated into a clinical test which can improve patient classification or cancer risk assessment. OPLs can exhibit a variety of histological features from hyperkeratosis, hyperplasia, and mild dysplasia to severe dysplasia. Together with other clinical features, our current practice has limited capability to accurately stratify cancer risk of patients with OPL. Such stratification is critical in our effort to develop surveillance measures for early cancer diagnosis and interventions to prevent or delay cancer development. In this presentation, I will focus on a series of biomarker discovery studies based on patients with OPL and enrolled in a prospective chemoprevention trial to illustrate some of the current efforts in oral cancer risk assessment based underlying molecular abnormalities in OPLs.
The chemoprevention trial randomized 167 patients with biopsies obtained at the time of enrollment and certain time points during follow-up. One hundred and sixty-two patients had oral cancer-free survival data with the median time of follow-up about 7.5 years. During the follow-up period, 38 patients developed oral cancer but no statistically significant difference was observed in any of the treatment arms. We examined podoplanin expression, deltaNp63 expression, EGFR expression, EFGR copy numbers, global gene expression, and histopathologic features in OPLs from the patients obtained at either baseline or at 3 months follow-up. Potential roles of these factors in progression of OPLs and oral cancer risk were evaluated. Results suggest that these alterations may outperform previously reported biomarkers and clinicopathologic parameters in stratifying oral cancer risk of patients with OPLs.
Development of oral cancer risk assessment strategies faces a number of challenges. Etiologies of OPLs and oral cancer may change over time, such as the emerging evidence of HPV infection in orapharyngeal cancers. Populations tested in many of our studies may be biased and not representative of the general population. Therefore, results may be difficult to validate in independent populations. We lack of systematic research networks at the national level to facilitate oral cancer risk assessment, early detection, and prevention. Efforts are lacking to integrate oral cancer risk assessment and chemoprevention programs. Some progresses and thoughts towards these limitations will be discussed.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN14-04.
Abstract ED03-03: The clinical and biological impact of aberrant DNA methylation patterning in human cancer
Authors: Melnick Ari M. 
Published: January 2011

Abstract
Heritable gene regulatory information can be imparted through cytosine methylation of DNA and posttranslational modifications of histones and other chromatin proteins. These epigenetic instructions play a fundamental role in determining the phenotype of normal cells during tissue differentiation. Disruption of normal epigenetic programming plays an equally fundamental role in determining the phenotype of tumor cells in concert with genetic lesions, and is a hallmark of cancer. Aberrant distribution of cytosine methylation occurs in specific biologically and clinically relevant patterns in acute myeloblastic and lymphoblastic leukemias, and is particularly widespread in advanced stages of myelodysplasia. Both aberrant hypomethylation and hypermethylation appear to contribute to these abnormal patterns. Genomic analysis of aberrantly methylated genes provides clues towards which transcription factors direct gene expression in epigenetically defined leukemia subtypes. One difference between epigenetic and genetic lesions is that the former can be therapeutically erased or reprogrammed. Along these lines efforts to identify epigenetic biomarkers to guide epigenetic therapy has become of great interest, as has the development of novel drugs that target the various chromatin-modifying complexes. This presentation will explore state of the art data from various sources and discuss the biological and clinical significance, as well as therapeutic targeting of aberrant epigenetic programming in these diseases.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):ED03-03.