bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract CN05-01: An overview of biomarker discovery and development
Authors: Srivastava Sudhir 
Published: June 2012

Abstract
Two great challenges in cancer diagnosis and prevention are 1) the detection of specific preinvasive neoplastic lesions that give origin to malignant tumors and 2) the identification of those markers that predict the outcome of individual cancer patients. Neoplastic lesions may derive from epithelial or nonepithelial cellular populations. Often, preinvasive neoplastic lesions are small, multiple and may display wide ranges of diversity. Morphological alterations characterizing preinvasive neoplastic lesions include nuclear pleomorphism consisting of increased variation in nuclear size, shape, and hyperchromatism, abnormal mitoses, abnormal nucleolar patterns and altered or absent differentiation. The evolution of these types of lesions may take three directions: spontaneous regression, progression toward a fully malignant phenotype, or stasis, remaining as a preinvasive neoplastic lesion. Although there are discrepancies in terminology used by pathologists to describe these types of early neoplastic lesions, they are most frequently referred to as preinvasive neoplasia, dysplasia, carcinoma in situ, intraepithelial neoplasia, or as incipient cancer.
Carcinogenesis is an indivisible continuum of molecular and morphological changes that may culminate in the development of invasive tumors. Studies in which the molecular features of preinvasive neoplastic lesions are correlated with molecular features of matching invasive lesions, for example, a colorectal cancer with an adenomatous polyp forming its edge, should be useful in identifying molecular features associated with greater risks of progression. Similarly, studies of prognostic factors in specific cancers may identify molecular features associated with aggressive behavior.
In this session we will discuss the molecular aspects of early preinvasive neoplastic lesions; specifically, alterations in genes regulating proliferation, differentiation, apoptosis and invasiveness as well as chromosomal aberrations and microsatellite instability will be addressed. We will argue that the identification of molecular changes associated with neoplastic transformation will lead to the development of new molecular markers for the early detection of preinvasive neoplastic and malignant lesions, assessment of cancer risk, assessment of responses to preventive or therapeutic interventions, and separation of less aggressive neoplastic lesions from more aggressive lesions.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):CN05-01.
Abstract CN06-01: Phase IIa trial of sulindac in individuals at increased risk for melanoma
Authors: Curiel-Lewandrowski Clara , Alberts D.S. , Chow H-H.S. , Swetter S. , Einsphar J. , Hsu C.-H. , Hsu C.-H. , Nagle R. , Sagerman P. , Tangrea J. , Parnes H. 
Published: June 2012

Abstract
Some epidemiological studies and several experimental publications suggest that regular use of non-steroidal anti-inflammatory drugs (NSAIDs) may reduce the risk of melanoma. However, specific information on the ability of NSAIDs to reach melanocytes in vivo and to modulate key biomarkers in pre-neoplastic lesions such as dysplastic nevi have not been evaluated to date. Methods: We conducted a randomized, double-blind, placebo controlled trial of sulindac in individuals at risk for melanoma to determine whether sulindac and related metabolites are bioavailable in the nevi and whether sulindac intervention has an effect on apoptosis and vascular endothelial growth factor (VEGF) expression in atypical nevi (AN). Fifty healthy subjects with ≥ 4 large (≥5 mm and &lt; 15 mm) AN and one benign nevus (BN) were enrolled between 2/09 and 7/10. Subjects underwent clinical and dermoscopic evaluation of their melanocytic lesions with 2 AN randomized to be excised at baseline for biomarker evaluation and 2 AN to post-intervention evaluation. Subsequently, participants were randomized to receive sulindac (150 mg BID) or placebo for 8 weeks. Upon completion of the intervention the residual 2 AN and the BN were surgically removed. Results: The study intervention was well tolerated with some mild or moderate gastrointestinal adverse events that were possibly or probably related to the intervention. Sulindac, sulindac sulfone, sulindac sulfide concentrations were 0.31 ± 0.36, 1.56 ± 1.35, 2.25 ± 2.24 μg/ml, respectively, in post-intervention plasma samples from the sulindac group. Sulindac, sulindac sulfone, sulindac sulfide concentrations were 0.51 ± 1.05, 1.38 ± 2.86, 0.12 ± 0.12 μg/g tissue, respectively, in post-intervention nevi samples. Eight weeks of sulindac intervention did not result in significant changes in VEGF expression. Sulindac intervention increased the expression of a marker of apoptosis, cleaved caspase 3 (an increase of 3 ± 33 in the sulindac arm vs. a decrease of 25 ± 45 in the placebo arm, p = 0.0056) in dysplastic nevi. After adjusting for baseline expression, the significance of this finding is attenuated to a p-value of 0.1103 based on a linear regression model. Overall, these findings are consistent with the identification of high concentrations of sulindac sulfone, a pro-apoptotic metabolite in the nevi. Conclusion: The study showed that sulindac and sulindac metabolites can reach measurable levels in melanocytic nevi. Eight weeks of sulindac intervention induced the expression of a marker of apoptosis in dysplastic nevi but did not result in significant changes in VEGF expression. The study findings support the further evaluation of sulindac as a chemopreventive agent for melanoma.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):CN06-01.
Abstract CN07-02: Molecularly targeted cancer prevention: From discovery to medicine
Authors: Dong Zigang 
Published: June 2012

Abstract
Despite the intensive efforts and substantial advances that have occurred through focusing on improving treatment, cancer is still a leading cause of death worldwide. Many have argued that this could be avoided by focusing on cancer prevention, which has now entered the arena of targeted therapies. During the process of identifying preventive agents, dietary phytochemicals have emerged as modulators of key cellular pathways. By molecular modeling of the interactions of targeted proteins with these chemopreventive agents, we have provided knowledge for a better understanding of how these preventive agents work. Such knowledge will help the translation to new clinical practice of preventive medicine.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):CN07-02.
Abstract ED02-02: Second cancers among cancer survivors: High-risk populations to target for prevention
Authors: Oeffinger Kevin C. 
Published: June 2012

Abstract
There are now over 12 million cancer survivors in the United States. Given advances in early detection, supportive care, and therapy, the 5-year overall survival rate for all invasive cancer types exceeds 67%. For many common cancers, such as breast, prostate, testicular, thyroid, bladder, and endometrial cancer, melanoma, and Hodgkin lymphoma, the overall 5-year survival rate exceeds 80%. As the number of long-term survivors has increased, there has been a growing awareness that many will develop health conditions as a direct or an indirect consequence of their cancer therapy or lifestyle, environmental and genetic factors associated with the primary cancer. One of the most serious outcomes experienced by cancer survivors is the diagnosis of a second cancer. The number of patients with multiple primary cancers is growing, with independent malignancies comprising about 16%. Second cancers are a major contributing factor to late mortality following the primary cancer for several high risk groups, including survivors of pediatric or young adult Hodgkin lymphoma. This presentation will describe the current estimates for second cancers, identify high risk populations, and discuss long-term screening strategies and risk-reducing interventions.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):ED02-02.
Abstract ED03-02: Issues in applications of genome-wide methylation data to epidemiology
Authors: Kelsey Karl T. 
Published: June 2012

Abstract
Epigenetic alterations are now well accepted as crucial changes in the development of cancer. Common epigenetic mechanisms affecting carcinogenesis ultimately phenotypically affect gene expression and genomic stability. This is effected through altered miRNAs, dysregulation of the histone code, changes in the chromatin structure and common changes in DNA methylation, again most commonly occurring at CpG dinucleotides, in specific gene regions and at well known DNA repeat regions. There is limited knowledge of the environmental or physiological factors that are associated with most of these somatic changes and epidemiologic investigation is poised to provide significant important information in human studies. In this presentation we will assess the types of epigenetic alterations amenable to epidemiologic investigation and discuss applications and interpretations of the data, including contrasting phenotypically driven candidate and discovery-based approaches, identifying appropriate cell types for different study designs and briefly touching upon the opportunities and limitations of various approaches.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):ED03-02.
Abstract ED04-03: Aspirin chemoprevention for Barrett's and esophageal cancer: The AspECT trial
Authors: Jankowski Janusz A. 
Published: June 2012

Abstract
Esophageal adenocarcinoma is increasing in the world. The premalignant lesion Barrett's esophagus is also being rapidly recognized. Unfortunately cost effective analyses has shown that the best strategy for prevention is chemoprevention of the premalignant lesion. Of the agents available for chemoprevention aspirin has arguably the best evidence. The efficacy of aspirin cancer prevention is probably now known and rests between 20–30% of the population. The big issues which remain are A. What is the percentage of serious side effects in aspirin takers? B. does concomitant medication abrogate or accentuate the risk benefit ratio? C. What biomarkers or genetic factors predict an optimal risk benefit ratio? The ASPirin Esomeprazole Chemoprevention Trial (ASPECT) is specifically designed to address these issues in patients with Barrett's esophagus.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):ED04-03.
Abstract ED05-01: Social media and cancer communications: Promises and perils
Authors: Viswanath K. Vish 
Published: June 2012

Abstract
The emergence of social media as a platform to communicate, network and mobilize is receiving considerable attention in mainstream media. For example, the use of social media has received both credit for the changes in the Middle East and blame for the recent riots in the United Kingdom. The potential to reach a networked and engaged “audience” in hundreds of millions offers significant promise to those in cancer communications to communicate risk and influence behaviors. Despite the promise, significant challenges need to be addressed to exploit the potential of the platform. These challenges include (a) varying characteristics of different social media platforms; (b) characterizing the nature of engagement and the interest of social media users, (c) multiple contesting interpretations of risk among message sponsors, (d) persistent problem of digital divide that social media could potentially bridge or exacerbate, and (e) measurement challenges including difficulty in assessing their impact. The overview will cover these challenges followed by speakers addressing specific cancer-related risk communication issues including tobacco use, communication inequalities and exemplar interventions that address different health risks.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):ED05-01.
Abstract ED05-03: Social media use, communication inequalities, and public health: Where we are and where we need to go
Authors: Kontos Emily Z. 
Published: June 2012

Abstract
Social media are emerging as an important platform for communication and health information exchange. Yet, despite the increase in popularity and use, only a limited number of empirical studies document which segments of the adult population are and are not using social media and with what, if any, affect on health. Preliminary studies highlight that while there are still significant inequalities by race and socioeconomic status in Internet access, once access is gained, use of social media such as social networking sites is equally prolific across socio-demographic groups. This ubiquity of use presents both significant opportunities and challenges for cancer communication efforts. With the new communication channel emerges a real need for refined measurement that adequately reflects the innate dynamism of the platform and a nuanced understanding of the links between computer/technology-mediated communication and health across populations to ensure that existing digital divides and health disparities are not exacerbated but rather narrowed.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):ED05-03.
Abstract PL01-02: Building the Texas Cancer Diagnostics Pipeline one biomarker at a time
Authors: McDevitt John T. 
Published: June 2012

Abstract
Diagnostic tools have not kept pace with medical knowledge. Fields of proteomics, genomics, and bioinformatics have enjoyed explosive growth, but precious few biomarkers found are translated into clinical practice. More than 20,000 scientific-discovery papers for cancer and 6,000 for cardiac disease have been published, yet only about one biomarker per year for ALL diagnostics areas received FDA each year. Unless biomarkers receive FDA approval they cannot move into widespread clinical practice in the US. Rich biomarker data combined with microfabrication techniques can provide means to deploy quick, affordable point-of-care diagnostics. This newfound wealth of information has strong potential to be used to build a “biomarker highway” and develop low-cost, advanced diagnostic tools that identify diseases early including various types of cancers, when they are less costly. This presentation features creation of programmable nano-bio-chip sensors that are capable of sophisticated measurements of strategic biomarkers from bio-fluid samples like blood, urine and saliva. This universal detection modality is now of a fast track to FDA approval through the simultaneous completion of 6 clinical trials in the area of HIV immune function (number one global humanitarian issue), cardiac heart disease (largest killer globally) and three types of cancers (oral, ovarian, prostate). These powerful devices have secured Popular Science Best of What's New (medical device category) as well as Science Coallition's Discovery of Year. The talk will highlight activities related to the recent launching of the Texas Cancer Diagnostics Pipeline.
Short Description: Programmable bio-nano-chip sensors are now in development with goal to diagnose cancer early while at the same time making healthcare more affordable and accessible globally.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):PL01-02.
Abstract PL04-01: Early Detection Research Network: Biomarker discovery and validation - A team approach
Authors: Thompson Ian M. 
Published: June 2012

Abstract
While the principle of early detection and treatment of cancer through the use of diagnostic tests including biomarkers may seem to be a straightforward process, the rate of registration of new cancer-related biomarkers (approximately one per year) illustrates the substantial challenges to this science. Essential elements of a successful biomarker include sensitivity in the face of cancer, specificity in the cancer-free state as well as in the face of disease which may clinically mimic cancer or which is associated with a higher cancer risk, a reproducible, accurate, and portable assay, and, more recently, evidence that the specifics of the cancer detected (stage and prognosis, for example) leads to reductions in morbidity, mortality, or, possibly, cost. There is possibly no greater opportunity for team science to merge discovery, validation, and clinical efficacy than in cancer biomarkers. The EDRN, now 11 years old, envisioned such a collaboration, including Biomarker Development Laboratories, Biomarker Reference Laboratories, Clinical Validation Centers, an Informatics Center, and a Data Management and Coordinating Center. EDRN member institutions participate in organ working groups including Breast and Ovarian, GI, Prostate and GU, and Lung. Organ working groups function as teams, all focused on collaborative science with the ultimate goal of validation of biomarkers for the purpose of improvements in clinical care. Cross-organ-site team collaborations also occur as biomarkers or concepts that are applicable to multiple organ sites are evaluated. Teams include biostatistical expertise that has developed new methods for biomarker evaluation and validation. Finally, the EDRN is an open organization that seeks to partner with non-EDRN investigators through sharing of biospecimens, clinical data, and new analysis techniques to further the goal of early cancer detection.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):PL04-01.
Abstract PR-01: Properties of adenomas in subjects treated with difluoromethylornithine and sulindac for reduction of colorectal adenomas
Authors: Carpenter Philip M. , Chen Wen-Pin , McLaren Christine E. , Gerner Eugene W. , Meyskens Frank L. 
Published: June 2012

Abstract
Difluoromethyl ornithine (DFMO), an ornithine decarboxylase inhibitor, and sulindac reduced the occurrence of colorectal adenomas by 70% in a phase III randomized placebo controlled clinical trial. The goal of the current study was to compare adenoma location in the colorectum and biomarker expression by immunohistochemistry of formalin fixed paraffin embedded adenomas from treatment and placebo groups in the trial. To take into account the relationship between the locations in the colorectum of multiple adenoma that were removed from individual subjects, the generalized estimation equation (GEE) method was applied for all analyses. The decrease in the reappearance of metachronous adenomas was similar throughout the colorectum in subjects treated with DFMO and sulindac (P = 0.44). For TP53, Ki67, and c-MYC there were no significant differences in the estimated mean percent of cells staining positive between treated and untreated subjects (P&gt;0.5 for all). For BCL-2, LC3B, CEA, sialy1-Tn, cleaved caspase 3 and apoptosis, the proportion of adenoma with expression levels 1+ to 3+ did not differ between subjects treated with DFMO plus sulindac versus those treated with double placebos. For hMSH2, hMSH6, hMLH1 and hPMS2, there was a loss of staining of a greater number of cells on average in adenomas from the control group compared to adenomas from the subjects treated with DFMO and sulindac. For hMSH2, this difference was statistically significant (P = 0.0004). This finding raises the possibility that DFMO and sulindac protect adenomas from loss of DNA mismatch repair protein expression and provides a rationale for further study of the possible role of DFMO and sulindac on DNA mismatch repair protein regulation and chemoprevention in patients at risk for colorectal carcinoma. In conclusion, DFMO decreases the occurrences of adenomas throughout the colorectum, including the right colon, and may have an effect on DNA mismatch repair enzyme expression. These findings provide further rationale for the use of DFMO as a chemopreventative agent for colorectal carcinoma.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):PR-01.
Abstract PR-02: The association between antioxidant intake and ovarian cancer risk: Results from a population-based case-control study in New Jersey
Authors: Gifkins Dina , Olson Sara , Paddock Lisa , King Melony , Demissie Kitaw , Lu Shou-En , Bandera Elisa 
Published: June 2012

Abstract
Ovarian cancer causes significant morbidity and is associated with the highest mortality among gynecologic cancers. Etiologic theories of ovarian cancer indicate that oxidative stress may have a role its development. It has been suggested that limiting oxidative stress to the ovarian epithelium could be considered a first-line defense against ovarian cancer. Although evidence for an association between individual dietary antioxidant intake and ovarian cancer risk is conflicting, the combined evidence suggests a modest inverse association with intake.
We evaluated the role of total dietary antioxidant capacity and intake of individual antioxidants (vitamin C, vitamin E, beta-carotene, selenium, lutein, and lycopene) on ovarian cancer risk in a population-based case-control study in New Jersey. Cases included women ages 21 years and older with newly diagnosed epithelial ovarian cancer who resided in six counties of New Jersey. Controls were women in the same age range who resided in the same geographic area. Women with a hysterectomy or bilateral oophorectomy were excluded. Dietary intake was assessed using the Block food frequency questionnaire (FFQ), and total antioxidant indices were constructed by linking FFQ-derived estimates to two standardized antioxidant capacity databases, the USDA Oxygen Radical Absorbance Capacity (ORAC) Database, and the University of Olso's Antioxidant Food Database. Multivariate logistic regression models were used to calculate odds ratios and 95% confidence intervals while controlling for major ovarian cancer risk factors.
Total antioxidant intake was not found to be associated with ovarian cancer risk. However, a strong protective effect was observed for the highest tertile of dietary selenium intake compared to the lowest (OR: 0.41; 95%CI: 0.20–0.85). In contrast, supplement use was associated with significant increased risks for all micronutrients. Vitamin C supplement use was associated with an increased risk of 1.63 (95%CI: 1.01–2.62), with similar results for vitamin E supplement use (OR: 1.63; 95%CI: 1.02–2.63), beta-carotene supplement use (OR: 1.69; 95%CI: 1.08–2.66) and selenium supplement use (OR: 1.64; 95%CI: 1.05–2.56).
In conclusion, we observed a strong decreased risk for ovarian cancer with dietary selenium intake. No associations were observed with total antioxidant intake or any other antioxidant micronutrients, while increased risks were observed with antioxidant supplement intake. Additional research is needed to confirm these findings.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):PR-02.