bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B85: Role of the TASK2 in regulating breast cancer cell proliferation
Authors: Yin Tao , Shepherd Jonathan , Poage Graham , Yang Zhengduo , Chu Lili , Hartman Zachary , Shen Qiang 
Published: June 2012

Abstract
Selective estrogen receptor (ER) modulators (SERMs) such as tamoxifen and raloxifene, and aromatase inhibitors are able to partially reduce incidence in high-risk women to develop ER-positive breast cancer but not all ER-positive neither ER-negative breast cancers. Thus, effective targets and agents for the prevention of both ER-positive and ER-negative breast cancer are urgently needed. Potassium ion channels are essential in maintaining cellular homeostasis in terms of transmitting signal molecules, regulating cell volume and secreting ions and hormones. A family of potassium channels, TASKs, is differentially expressed in normal breast tissue and breast cancer tissues. In particular, TASK2 mRNA was found upregulated in human breast carcinoma but not in normal mammary gland tissue, and TASK2 is significantly up-regulated in ER-negative vs ER-positive breast cancers across multiple studies among the Oncomine databases. We hypothesized that TASK2 plays an important role in regulating growth of breast cancer cells. We then knocked down the TASK2 gene expression using siRNA in ER-positive and ER-negative breast cancer cells. Transient knockdown of TASK2 suppressed cell proliferation significantly in 7/8 ER-negative and moderately in 3/5 ER-positive breast cancer cell lines. However, proliferation of an immortal breast epithelial cell line, MCF-10A, was not affected. We are now investigating the phenotypic alterations in normal and malignant breast cells after overexpressing or knocking down the TASK2 gene. Current results suggest that TASK2 plays an important role in breast cell growth. Thus, TASK2 is a potential novel target for future breast cancer prevention and treatment.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B85.
Abstract B91: Self-reported prior lung disease as risk factors for non-small cell lung cancer in Mexican Americans
Authors: McHugh Michelle K. , Schabath Matthew B. , Ho Chung-Han , Liu Mei , D'Amelio Anthony M. , Greisinger Anthony J. , Delclos George L. , Spitz Margaret R. , Etzel Carol J. 
Published: June 2012

Abstract
Background: Although cigarette smoking is the primary risk factor for lung cancer, other risk factors have been shown to be associated with lung cancer including prior history of respiratory diseases. The purpose of this analysis was to assess the association between prior history of respiratory disease (i.e., asthma, chronic obstructive pulmonary disease (COPD), hay fever, and pneumonia) and lung cancer among Mexican Americans using data from a multi-racial/ethnic lung cancer case-control study.
Methods: The data were collected between 1991 and 2010. Cases (n = 217) were patients who presented with newly diagnosed, histopathologically confirmed and previously untreated lung cancer. Healthy control participants (n = 339) were recruited from a large multispecialty physician group practice. Demographics, cigarette use, and history of respiratory disease were collected by personal interview using a validated questionnaire. Multivariable logistic regression models were used to estimate relative risk. All analyses were restricted to self-report Mexican Americans.
Results: Prior history of COPD (OR = 2.33; 95% CI = 1.14–4.79) and pneumonia (OR = 2.88; 95% CI = 1.47–5.63) were associated with a statistically significant increased risk of lung cancer. Conversely, self-reported history of asthma (OR = 0.71, 95% CI = 0.20–2.45) or hay fever (OR = 0.59, 95% CI = 0.29–1.21) were inversely associated with lung cancer risk but the odds ratios were not statistically significant.
Conclusions: These findings illustrate that COPD and pneumonia are associated with an increased for lung cancer among Mexican Americans. Identifying risk factors such as C. pneumonia infections and COPD may induce targeted treatments to help attenuate progression to lung cancer. At present this study is one of largest case-control analyses assessing respiratory disease and lung cancer risk among Mexican-Americans.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B91.
Abstract B97: Soy and green tea intake protect against cervical cancer among Singapore Chinese
Authors: Butler Lesley M. , Wu Anna H. , Montague Julia A. , Koh Woon-Puay , Wang Renwei , Yuan Jian-Min , Yu Mimi C. 
Published: June 2012

Abstract
Background: Cervical cancer incidence is highest in developing countries in Asia and South America and is associated with relatively poor survival in these high-risk populations. Diet may influence susceptibility to and/or persistence of human papillomavirus infection, a necessary cause of cervical cancer. Soy isoflavones and green tea catechins have immunomodulating properties that may protect against cervical cancer.
Methods: We investigated the relationship between soy, green tea and black tea intake and risk of cervical cancer in the well-established prospective population-based Singapore Chinese Health Study. Soy and tea consumption data were collected at baseline using a validated food frequency questionnaire. Cervical cancer cases (n=257) were identified from 34,028 women followed for an average of 11.7 years. Proportional hazards regression methods were used to assess the associations between soy and tea intake and cervical cancer risk. Hazard ratios (HRs) and 95% confidence intervals (CIs) were adjusted for Papanicolaou (Pap) test history, education level, parity, use of oral contraceptives, and other potential confounders.
Results: A statistically significant inverse association was observed for highest versus lowest soy intake and cervical cancer risk (HR=0.71; 95% CI:0.53, 0.96; p for trend=0.03). Consumption of green tea on a weekly or more frequent basis, compared to no tea intake was inversely associated with cervical cancer risk (HR=0.80; 95% CI:0.56, 1.14; p for trend=0.2). There was no association with black tea. We observed interacting effects for soy and green tea intake on risk of cervical cancer. The inverse association with soy intake was stronger among women who drank green tea (HR=0.42; 95% CI:0.25, 0.69; p for trend=0.001). No association was observed for soy intake among non-tea drinkers (p for interaction=0.01).
Conclusions: We provide the first human evidence for individual, as well as synergistic protective effects of soy and green tea intake on risk of cervical cancer. These findings were independent of self-reported frequency of Pap testing and education level. Our findings support experimental evidence for immunomodulating effects of green tea catechins and soy isoflavones as a possible mechanism underlying the protective effect of these dietary factors on cervical cancer risk.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B97.
Abstract CN01-02: Glycoproteomic discovery of liver cancer biomarkers: Be careful how you use it!
Authors: Block Timothy M. 
Published: June 2012

Abstract
This presentation will describe the discovery and use of the new serum biomarkers of HCC, called GP73 and its fucosylated glycoforms, identified, in part, by comparative glycoproteomics. We will also provide an explanation as to why fucosylated glycoforms are elevated in people with HCC. There are now more than 25 publications reporting that these markers are elevated in the serum of people with HCC, but there are also several papers suggesting they are no better in distinguishing between people with HCC and liver cirrhosis than are other markers such as AFP. We will also provide a theory, supported with data, as to why these differences in observations have occurred. Briefly, the etiology of the HCC, the specific linkage of the glycoform on the putative cancer biomarker as well as the ability of the cancer cells to re-fucosylate the circulating biomarkers, all play roles in how the markers are sorted and the extent to which they can be used as risk and diagnostic markers of cancer. Failure to take these variables into consideration can result in their underperformance as biomarkers of disease.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):CN01-02.
Abstract CN06-03: Randomized double-blinded phase II trial of esomeprazole versus esomeprazole + two doses of aspirin in Barrett's esophagus patients
Authors: Falk Gary W. , Sontag Steven , Cruz-Correa Marica , Weinberg David , Chak Amitabh , Hur Chin , Fleischer David , Smyrk Thomas , Butar Navtej , Foster Nathan , Romero Yvonne , Corley Douglas , DeVault Kenneth , Marcon Norman , Schnell Thomas 
Published: June 2012

Abstract
Background and Aims: In patients with Barrett's esophagus (BE), reflux-induced injury promotes esophageal adenocarcinoma, presumably through cyclooxygenase 2 (COX-2) related pathways. Proton pump inhibitors (PPIs) and nonsteroidal anti-inflammatory drugs (NSAIDs) may interrupt reflux-associated carcinogenesis by reducing acid exposure and subsequent inflammation. However, clinical trial data regarding the chemopreventive efficacy of a PPI + NSAID combination are limited. The aim of this multi-center, randomized, phase II trial was to assess the effects of a 28-day intervention with esomeprazole 40 mg bid and aspirin 81 mg qd, 325 mg qd, or placebo qd on tissue prostaglandin E2 (PGE2) concentrations in BE patients.
Methods: Using the infrastructure of the Cancer Prevention Network, participants (&gt; 18 years) with histologically confirmed non dysplastic BE were randomly assigned to receive one of three interventions for 28 days: (arm A) esomeprazole 40 mg bid+ aspirin 81 mg placebo qd + aspirin 325 mg placebo qd (n=42); (arm B) esomeprazole 40 mg bid+ aspirin 81 mg qd + aspirin placebo 325 qd (n=63); (arm C) esomeprazole 40 mg bid + aspirin 81 mg qd placebo + aspirin 325 mg qd (n=63). Esophageal biopsies were obtained pre- and post-intervention to assess change in PGE2 concentration as the primary endpoint.
Results: In total, 122 participants were randomized, 121 (99%) completed the trial per protocol, and 115 (94%) were evaluated for the primary endpoint. Baseline characteristics were similar across intervention arms. The absolute change (mean + SD) in tissue PGE2 concentration was −67.6 (229.68) in Arm A, −120.9 (281.28) in Arm B (p = 0.10 vs Arm A) and −174.9 (263.62) in Arm C (p = 0.02 vs Arm A).
Conclusions: In combination with esomeprazole 40 mg twice per day, aspirin 325 mg per day significantly reduced tissue PGE2 concentration in BE patients after a 28-day intervention, as compared to aspirin placebo. Given the relevance of PGE2 pathways in BE-associated carcinogenesis, further evaluation of this chemoprevention strategy in larger, more definitive phase III trials is warranted.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):CN06-03.
Abstract ED02-03: Role of diet, energy balance, nutrition, and the risk for recurrence
Authors: Pierce John P. 
Published: June 2012

Abstract
As the risk for recurrence following breast cancer remains elevated for the majority of women for at least 15–20 years, there is considerable interest in whether the way someone lives their life can improve prognosis. There are now numerous cohort studies that have post diagnoses measures of dietary and physical activity patterns as well as body weight and have reported on associations with recurrence. Two large randomized dietary trials have also reported both primary and secondary analyses. However, there is a degree of inconsistency in the published findings.
This presentation will discuss the evidence for a role of dietary patterns, physical activity and body weight in recurrence. Dietary patterns will include those that are plant based and those with a high animal fat intake, as well as considering the impact of nutritional supplements. It will compare physical activity patterns that include half or multiple times the recommended daily pattern. With respect to obesity, the question is whether the overweight are at increased risk as well as those who are obese, and whether there are any obese women who are not at increased risk. Finally, the presentation will consider whether the real issue is not a particular lifestyle pattern but a cluster of behavioral patterns that are linked to increased risk of recurrence.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):ED02-03.
Abstract ED03-03: Analysis of DNA methylation arrays in population studies: Issues and opportunities
Authors: Houseman E. Andres , Accomando William P. , Kelsey Karl T. , Wiencke John K. 
Published: June 2012

Abstract
Epigenetics is the study of heritable changes in gene function unexplained by changes in DNA sequence, and is one of the modes by which environment is thought to interact with genetics. As such, epigenetic alterations constitute an important type of genome-scale variable mediating between environment and disease, and present unique opportunities for conducting epidemiological research. The most commonly studied type of epigenetic alteration in population studies is cytosine methylation, which is a well recognized mechanism of gene silencing that often becomes dysregulated in cancer, and is also thought to be implicated in other diseases. Arrays are now being used to study DNA methylation at a large number of loci; for example, the older Illumina Infinium platform assesses DNA methylation at 27,000 loci, while the newer Infinium array measures DNA methylation at over 470,000 sites. In this talk, we introduce the biology of DNA methylation and survey recent methods for statistical analysis of DNA methylation array data. Finally, we introduce a novel use of DNA methylation arrays to interrogate the distribution of white blood cells, an advancement in the use of DNA methylation to study immunological response as a function of disease status.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):ED03-03.
Abstract ED05-04: Harnessing the power of social media in cancer control communication
Authors: Chou Wen-Ying Sylvia 
Published: June 2012

Abstract
The presentation will review current social media-based health communication programs applied in a variety of health areas, including cancer addition, obesity and sexual health. Beginning with a broad description of the public's health-related social media use, I will summarize types of interventions and illustrate them with specific exemplary projects. Special attention will be given to issues of measurement and evaluation; in particular I will discuss how social media utilization, reach, and impact are measured with respect to health-related attitudes and behaviors.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):ED05-04.
Abstract PL01-01: Advances in functional cancer genomics
Authors: Hahn William C. 
Published: June 2012

Abstract
Recent advances in genomics now make it possible to consider enumerating all of the genetic lesions in specific cancers. While these approaches will yield critical information regarding the identify, number, and types of alterations found in human tumors, a complementary approach to decipher the molecular basis of malignant transformation depends upon the application of genome scale tools to annotate the function of genes involved in cancer initiation and progression. Over the past several years, we have developed genome scale RNAi libraries and open reading frame expression libraries that permit a systematic evaluation of genes involved in cancer initiation and maintenance. Using these libraries, we have now performed screens in a panel of human cancer cell lines to systematically identify cancer vulnerabilities. By combining these functional approaches with information derived from mapping the structural abnormalities present in cancer genomes, we have identified several new oncogenes that contribute to cancer development. The ability to systematically manipulate gene expression at genome scale now provides opportunities to investigate the function of genes involved in cancer initiation and maintenance, which will provide a framework for therapeutic and prevention strategies.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):PL01-01.
Abstract PL01-03: Quantitative biology and biomarker discovery without immunoassays
Authors: Carr Steven A. 
Published: June 2012

Abstract
Lack of antibody reagents and robust quantitative methods with sufficient sensitivity, specificity, reproducibility and throughput has significantly hampered our ability to understand dynamic, protein-based biological processes. My laboratory is addressing this serious barrier by developing targeted mass spectrometry-based technologies to screen and quantify low abundance proteins in a variety of biological contexts including human tissue and plasma. These assays are highly multiplexed, sensitive and specific and do not suffer from interferences that plague immunoassays. Targeted MS-based approaches are helping to usher in a new era of quantitative biology where proteins of interest and their modifications can be robustly measured in any biological context. We are applying these quantitative approaches in the context of a generalizable proteomics-based discovery-through-verification pipeline to identify early biomarkers of cardiovascular injury, breast cancer and infectious disease. These studies are beginning to demonstrate that modern proteomic technologies when coherently integrated can yield novel, credentialed protein biomarker candidates of sufficient merit to warrant real clinical evaluation.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):PL01-03.
Abstract SS01-01: Using genomic technologies to improve cancer risk assessment
Authors: Offit Kenneth 
Published: June 2012

Abstract
The heritable fraction of human cancers, estimated from genetic and epidemiologic approaches, is 21–42%. Heritable cancers include common adult onset malignancies (e.g. prostate, colon, breast cancers) as well as rarer cancers. During past decades, genetic approaches (e.g. linkage analysis and positional cloning) identified rare genetic mutations associated with markedly elevated cancer risk, with subsequent translation of these findings into effective preventive interventions. Recently genomic approaches (e.g. genome wide association studies [GWAS] exploiting linkage disequilibrium between single nucleotide polymorphisms in the human genome) have identified common variants of lower disease risk, as well as common variants which modify the risk of high-penetrance rare alleles. Ongoing studies are utilizing next-generation massively parallel sequencing (NGS) of whole exomes and genomes to identify the “missing heritability” of human cancer. The status GWAS and NGS approaches to cancer risk assessment will be reviewed. The large sample sizes required for GWAS will be emphasized; a case example of our recent consortium effort to identify genomic modifiers of BRCA2 penetrance will be cited. While the methods of identification of genomic variants are distinct, the principles of biomarker identification and clinical translation to preventive oncology are shared. These similarities include: the use of clinically validated variants that may not be functionally characterized; the segregation of these variants in non-Mendelian as well as Mendelian patterns; the role of gene–environment interactions; the dependence on evidence for clinical utility; the critical translational role of behavioral science; and common ethical considerations. It will be emphasized that during the current period of transition from investigation to practice, consumers must also be protected from harms of premature translation of research findings, while encouraging the innovative and cost-effective application of genomic discoveries that improve personalized oncologic care.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):SS01-01.
Nonlinear Effects on Convectively Forced Two-Dimensional Mesoscale Flows
Authors: Han Ji-Young , Baik Jong-Jin 
Published: June 2012

Abstract
One of the important problems in mesoscale atmospheric dynamics is how the atmosphere responds to convective heating or cooling. Here, the authors examine nonlinear effects on convectively forced mesoscale flows in the context of the nonlinear response of a stably stratified flow to elevated steady heating in two dimensions using a nondimensional numerical model. Results of two-dimensional numerical experiments in a uniform flow show that even without vertical wind shear, a separation of an upwind cellular updraft from the steady heating-induced main updraft occurs in a highly nonlinear flow system. This separation occurs as the compensating cellular downdraft associated with a secondary maximum in the main updraft develops. As the nonlinearity of the flow system increases, the upwind cellular updraft is separated earlier and becomes stronger. Smaller viscous terms result in the separation of more cellular updrafts, which become stronger and move farther away from the main updraft region. In particular, in an inviscid flow, cellular updrafts are periodically separated from the main updraft, and the first cellular updraft and downdraft have intensities comparable to the intensity of the main updraft. In a viscid flow with a constant vertical wind shear up to a certain height, the propagating cellular updraft and downdraft are produced when the nonlinearity is large, as in a uniform flow. Stronger vertical wind shear leads to the earlier formation of the cellular updraft and its stronger intensity, faster propagating speed, and longer lifetime. Results of numerical experiments with squall line–type forcing imply that the highly nonlinear state is necessary for the development of cellular updrafts.
Symmetric and Asymmetric Structures of Hurricane Boundary Layer in Coupled Atmosphere–Wave–Ocean Models and Observations
Authors: Lee Chia-Ying , Chen Shuyi S. 
Published: June 2012

Abstract
It is widely accepted that air–sea interaction is one of the key factors in controlling tropical cyclone (TC) intensity. However, the physical mechanisms for connecting the upper ocean and air–sea interface with storm structure through the atmospheric boundary layer in TCs are not well understood. This study investigates the air–sea coupling processes using a fully coupled atmosphere–wave–ocean model, especially the coupling-induced asymmetry in surface winds, sea surface temperature, air–sea fluxes, and their impacts on the structure of the hurricane boundary layer (HBL). Numerical experiments of Hurricane Frances (2004) with and without coupling to an ocean model and/or a surface wave model are used to examine the impacts of the ocean and wave coupling, respectively. Model results are compared with the airborne dropsonde and surface wind measurements on board the NOAA WP-3D aircraft. The atmosphere–ocean coupling reduces the mixed-layer depth in the rear-right quadrant due to storm-induced ocean cooling, whereas the wind–wave coupling enhances boundary inflow outside the radius of maximum wind. Storm motion and deep tropospheric inflow create a significant front-to-back asymmetry in the depth of the inflow layer. These results are consistent with the dropsonde observations. The azimuthally averaged inflow layer and the mixed layer, as documented in previous studies, are not representative of the asymmetric HBL. The complex, three-dimensional asymmetric structure in both thermodynamic and dynamic properties of the HBL indicates that it would be difficult to parameterize the effects of air–sea coupling without a fully coupled model.