bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract DL01-01: Cancer Genomes and their Implications for Early Detection
Authors: Vogelstein Bert , Kinzler Kenneth W. 
Published: May 2019

Abstract
In the past five years, it has become possible to identify all of the mutations contributing to neoplasia in an individual cancer, leading to a deeper understanding of the pathogensis of neoplasia. The challenge now is to exploit this wealth information to reduce cancer deaths. Most current efforts towards this goal are focused on curing patients with advanced disease through “personalized” medicine approaches. However, the barriers to curing such patients are now being recognized, in part through the insights gained from cancer genome sequencing. Alternative strategies to reduce cancer deaths are therefore essential to achieving this goal. Fortunately, it is now clear that there are only ~150 genes, operating through ~12 well-recognized pathways, that drive the initiation and progress of the most common types of human cancers. These genes and pathways provide enormous opportunities for the early detection of neoplasia through sophisticated genomic, proteomic, and imaging-based technologies. Widespread implementation of early detection and prevention methods has the capacity to reduce cancer deaths by more than 75% in the foreseeable future.
Citation Format: Bert Vogelstein, Kenneth W. Kinzler. Cancer Genomes and their Implications for Early Detection. [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 DL01-01.
Abstract ED01-03: Forward and backward cell transformation induced by microenvironment factors: A tribute to Allan H. Conney
Authors: Dong Zigang 
Published: May 2019

Abstract
The cancer microenvironment affects cell proliferation and growth. By using JB6 cells and a melanoma cell culture system, we have studied forward and backward cell transformation by microenvironment factors. Embryonic stem (ES)-preconditioned 3-dimensional (3-D) culture of cancer cells induces cancer cell reprogramming and results in a change in cancer cell properties such as differentiation and migration in skin melanoma. Using the ES-preconditioned 3-D microenvironment model, we provided evidence showing that the ES microenvironment inhibits proliferation and anchorage-independent growth of SK-MEL-28 melanoma cells. We also found that the ES microenvironment suppresses telomerase activity and thereby induces senescence in SK-Mel-28 cells. Furthermore, we observed that gremlin, an antagonist of BMP4, is secreted from ES cells and plays an important role in cellular senescence. Knocking down gremlin in the ES microenvironment increases proliferation and anchorage-independent growth of SK-MEL-28 melanoma cells. Taken together, these results demonstrated that gremlin is a crucial factor responsible for abrogating melanoma properties in the ES-preconditioned 3-D microenvironment.
In a collaborative effort, Dr. Allan Conney's group demonstrated that an aqueous extract of the parametrial fat pads from SKH-1 mice enhanced the conversion of JB6 P+ cells from an epithelial-like morphology growing in liquid medium to cells with a fibroblast-like morphology with decreased E-cadherin and increased Twist, and these cells also formed colonies in soft agar. Mechanistic studies indicated that an extract of parametrial fat stimulated the formation of reactive oxygen species in JB6 P+ cells. These studies provide the first in vitro demonstration of a fat tissue-induced transformation of an epithelial cell. We also showed that several microenvironmental factors can induce JB6 cell neoplastic cell transformation.
Citation Format: Zigang Dong. Forward and backward cell transformation induced by microenvironment factors: A tribute to Allan H. Conney. [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 ED01-03.
Abstract ED02-01: Epigenetic variation as the missing link between aging and cancer
Authors: Issa Jean-Pierre 
Published: May 2019

Abstract
DNA methylation affects gene expression and genome stability in complex ways depending on the location of the CpG site in question. In humans, methylation patterns are highly regulated and generally conserved between different individuals with R2&gt;0.98 when comparing promoter DNA methylation genome wide among unrelated individuals of similar age. Despite this high degree of regulation, there are quantitative differences in methylation between individuals as well as evidence of methylation drift (increase at some loci, decrease at other loci) associated with aging in mammals. There is also a large degree of methylation drift in cancer cells (compared to normal tissues in the same individual) and a smaller but significant drift in other diseases such as atherosclerosis and neuro-degeneration.
Genome wide methylation drift associated with age in multiple species (humans, mice, monkeys) is tissue specific and affects up to a quarter of the methylome. The consequences of drift are twofold. First, it induces epigenetic diversity within a tissue that can serve as fodder for Darwinian selection to promote the development of proliferative diseases such as cancer and atherosclerosis. Second, given that some genes are affected more prominently due to genomic structural features, enough cells are affected in older tissues to potentially change gene expression and tissue function.
The determinants of age-related methylation drift remain largely unknown. There are diverse observations suggesting that the rate of drift can be modified by diet, chronic inflammation and exposures, and preliminary data suggesting a genetic component to the drift as well. Some of the outstanding questions in the field include the possibilities that methylation drift is modified by germline polymorphisms that influence DNA methylation genome wide, by prenatal exposures including diet and environmental toxins, and by lifestyle factors (including diet, exposures and exercise) that affect low level inflammation systemically. The model whereby methylation drift enables Darwinian selection at the tissue level also implies that possibility of preventing age-related development of pre-neoplasia and neoplasia through interventions targeting epigenetic processes.
Citation Format: Jean-Pierre Issa. Epigenetic variation as the missing link between aging and 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 ED02-01.
Abstract ED02-02: Interaction between genetics, epigenetics, and environment in cancer prevention
Authors: Tycko Benjamin 
Published: May 2019

Abstract
A recent convergence of genomic and epigenomic findings has brought the study of DNA methylation to the forefront of cancer research. In this session I will review our knowledge to date and suggest future directions for translational research and clinical applications in two key areas – (i) dietary methyl donors and DNA methylation in cancer prevention, (ii) allele-specific DNA methylation mapping as a tool for improving the yield of true-positive signals from genome-wide association studies (GWAS) for cancer susceptibility. These topics will highlight the importance of cis- and trans-acting influences of the genetic background on epigenetic patterns and cancer susceptibility.
References:
1. Kerkel K, Spadola A, Yuan E, Kosek J, Jiang L, Hod E, Li K, Murty VV, Schupf N, Vilain E, Morris M, Haghighi F, Tycko B (2008) Genomic surveys by methylation-sensitive SNP analysis identify sequence-dependent allele-specific DNA methylation. Nat Genet 40:904-908. PMID:18568024
2. Tycko B (2010). Allele-specific DNA methylation: beyond imprinting. Hum Mol Genet. 19:R210-220.
3. Gonda TA, Kim Y-I, Salas M, Gamble MV, Shibata W, Muthupalani S, Sohn K-J, Abram J, Fox JG, Wang TC, Tycko B (2012). Folic acid increases global DNA methylation and reduces inflammation to prevent Helicobacter-associated gastric cancer in mice. Gastroenterology. 142(4):824-833 PMID:22474448
4. Paliwal A, Temkin A, Kerkel K, Yale A, Yotova I , Drost N, Lax S, Nhan-Chang C-L, Powell C, Borczuk A, Aviv A, Wapner R, Chen X, Nagy P, Schork N, Do C, Torkamani A, Tycko B. (2013) Comparative anatomy of chromosomal domains with imprinted and non-imprinted allele-specific DNA methylation. PLoS Genet. 9(8):e1003622.
Citation Format: Benjamin Tycko. Interaction between genetics, epigenetics, and environment in cancer prevention. [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 ED02-02.
Abstract ED03-02: The era of big data informatics for clinical and translational research in cancer prevention
Authors: Pathak Jyotishman 
Published: May 2019

Abstract
Despite considerable progress in prevention and treatment, cancer remains the second leading cause of death in the United States. Cancer researchers around the world are generating massive amounts of clinical and genetic data, although due to its volume, complexity and lack of centralization, much is left unanalyzed. Big Data backed by powerful analytics holds the key to gain important insights from such high volume, variety and velocity data enabling a new understanding of cancer from molecular biology through clinical management. It provides opportunities to ask complex questions and identify novel knowledge from existing data including the study of genetics of an individual's cancer cells, on her response to treatment and sensitivity to side effects. In this session, we will understand the recent developments in Big Data Analytics platforms and how this transformative technology can be harnessed to leverage multidimensional data for developing new preventive measures, diagnostic tools and interventions in cancer research. We will also review success stories from early adopters of Big Data in cancer and highlight the challenges and opportunities for future research and development.
Learning objectives: By the end of this session, the participants should be able to:
1.) Understand the fundamental concepts and principles of Big Data technology
2.) Identify community-based open-source Big Data informatics resources and tools
3.) Recognize the importance of Big Data in cancer prevention research
Citation Format: Jyotishman Pathak. The era of big data informatics for clinical and translational research in cancer prevention. [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 ED03-02.
Abstract ED04-02: XCMS cloud-based metabolomics: A platform for the cancer biologist
Authors: Siuzdak Gary 
Published: May 2019

Abstract
Quantitative unbiased analysis of endogenous metabolites from cells, tissues, or fluids - metabolomics, has become an integral part of functional genomics efforts lending itself as a tool for clinical diagnostics, toxicology, agriculture, biofuels, and understanding fundamental biochemistry. Where the genome and proteome represent upstream biochemical events, the metabolites correlate with the most downstream biochemistry and therefore most closely represent the phenotype. This has been proven by the broad success of metabolite analysis in clinical diagnostics and pathogenesis. We have developed a platform to enable these analyses called XCMS, XCMS allows for alignment, statistical evaluation, and metabolite characterization from mass spectrometry data. In addition we have constructed METLIN currently the largest online metabolite MS/MS database. It is worth noting that XCMS, and related papers, enables the initial characterization of endogenous and exogenous metabolites, and has been cited in over a 1200 articles.
Citation Format: Gary Siuzdak. XCMS cloud-based metabolomics: A platform for the cancer biologist. [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 ED04-02.
Abstract ED05-01: Targeting nuclear hormone receptors for breast cancer prevention
Authors: Mazumdar Abhijit , Uray Ivan , Litzenburger Beate , Zhang Yun , Hill Jamal , Suh Nanjoo , Brown Powel 
Published: May 2019

Abstract
Nuclear receptors are key proteins that regulate cell proliferation, death, and differentiation. In breast cells, estrogen receptors (ERs) are critical for mammary gland development, differentiation, and tumorigenesis, and selective estrogen receptor modulators (SERMs) such as tamoxifen and raloxifene, and aromatase inhibitors can prevent the development of ER-positive breast cancer. Other nuclear transcription factors are critical regulators of proliferation and differentiation including retinoic acid receptors (RARs), vitamin D receptors (VDR), and peroxisome proliferator-activator receptors (PPARs). Each of these ligand activated nuclear hormone receptors bind the retinoid X receptors (RXRs) to regulate gene expression. Ligands of these nuclear hormone receptors have been shown to prevent many different types of cancer, including breast cancer. I will present results in preclinical and early clinical studies testing retinoids, rexinoids, Vitamin D analogs, and PPAR ligands for the prevention of breast cancer. Our results and the results of others have shown that ligands that bind and activate the rexinoid receptor are highly effective in preventing breast cancer in animals, particularly ER-negative breast cancer. These preclinical results supported the testing of the RXR ligand bexarotene in women at high risk of breast cancer. This early study demonstrated a biological effect of bexarotene on breast tissue in women. We and other have conducted preclinical studies testing combinations of nuclear hormone receptor ligands (RXR ligand + anti-estrogen SERMS)(RXR ligand + Vitamin D analog) and (RXR ligand + PPAR agonist). These results demonstrate that nuclear hormone receptor ligands can be used to prevent breast cancer and that rexinoids and other ligands provide an opportunity to prevent all forms of breast cancer.
Supported by RO1CA078480-11
Citation Format: Abhijit Mazumdar, Ivan Uray, Beate Litzenburger, Yun Zhang, Jamal Hill, Nanjoo Suh, Powel Brown. Targeting nuclear hormone receptors for breast cancer prevention. [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 ED05-01.
Abstract ED06-01: Detection and characterization of viable circulating tumor cells
Authors: Alix-Panabières Catherine 
Published: May 2019

Abstract
The enumeration and characterization of circulating tumor cells (CTCs) in the peripheral blood and disseminated tumor cells (DTCs) in bone marrow may provide important prognostic information and might help to monitor efficacy of therapy.
Since current assays cannot distinguish between apoptotic and viable DTCs/CTCs, it is now possible to apply a novel ELISPOT assay (designated ‘EPISPOT’) that detects proteins secreted/released/shed from single epithelial cancer cells. Cells are cultured for a short time on a membrane coated with antibodies that capture the secreted/released/shed proteins that are subsequently detected by secondary antibodies labeled with fluorochromes.
In breast cancer, we measured the release of cytokeratin-19 (CK19) and mucin-1 (MUC1) and demonstrated that many cancer patients harbored viable DTCs in their bone marrow, even in patients with apparently localized tumors (stage M0 : 54%). Preliminary clinical data (n=57) showed that patients with DTC-releasing CK19 have an unfavorable outcome. We also studied CTCs or CK19-releasing cells (CK19-RC) in the peripheral blood of 194 M1 breast cancer patients and showed that patients with CK19-RC had a worse clinical outcome.
In prostate cancer patients (n=48), we used prostate-specific antigen (PSA) secretion as marker to detect PSA-secreting cells and observed that 83% and 42% of M1 & M0 cancer patients, respectively, had CTCs with a difference in the CTC median (29 for M1 & 9 for M0) and found that a significant fraction of CTCs also secreted fibroblast growth factor-2 (FGF-2), a known stem cell growth factor.
More recently, in colon cancer, a considerable portion of viable CTCs detectable by the Epispot assay is trapped in the liver as the first filter organ in colon cancer patients. The enumeration of CK19-RC by the CK19-Epispot assay in 75 colorectal cancer patients revealed viable CTCs in 65.9% and 55.4% (p=0.04) patients in mesenteric and peripheral blood, respectively, whereas CellSearch detected CTCs in 55.9% and 29.0% (p=0.0046) patients. In mesenteric blood, the number of CTC was significantly higher than in the peripheral blood. Our clinical data showed that localized colon cancer patients with a high level of CTCs have an unfavorable outcome (n=60).
In conclusion, the EPISPOT assay offers a new opportunity to detect and characterize viable DTCs/CTCs in cancer patients and it can be extended to a multi-parameter analysis revealing a CTC/DTC protein fingerprint.
Citation Format: Catherine Alix-Panabières. Detection and characterization of viable circulating tumor cells. [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 ED06-01.
Abstract ED06-03: Circulating tumor cells versus circulating tumor cell products
Authors: Pantel Klaus 
Published: May 2019

Abstract
Metastasis is the main cause of cancer-related death and prevention of metastatic relapse is, therefore, the most important goal of cancer therapy. Distant metastases harbour unique genomic characteristics not detectable in the corresponding primary tumor of the same patient and metastases located at different sites show a considerable intra-patient heterogeneity. Thus, the mere analysis of the resected primary tumor alone (current standard practise in oncology) or, if possible, even re-evaluation of tumor characteristics based on the biopsy of the most accessible metastasis may not reveal sufficient information for treatment decisions. This dilemma can be solved by a new diagnostic concept: Liquid biopsy, i.e., analysis of therapeutic targets and drug resistance-conferring gene mutations on circulating tumor cells (CTCs) and cell-free circulating tumor DNA (ctDNA) released into the peripheral blood from metastatic deposits. In addition, cell-free microRNAs in the peripheral blood of cancer patients may provide real-time insights into the biology of cancer, including the effects of therapeutic interventions. MicroRNA levels in plasma, serum, urine and other body fluids have been used to detect cancer, predict the prognosis and response to therapy. Here the current challenges and future perspectives of CTCs and circulating nucleic acids as biomarkers in clinical oncology will be discussed. Both CTCs and circulating nucleic acids are interesting complementary technologies that can be used in parallel in future trials assessing new drugs or drug combinations. We postulate that the liquid biopsy concept will contribute to a better understanding and prevention of metastatic relapse and progression in cancer patients.
Citation Format: Klaus Pantel. Circulating tumor cells versus circulating tumor cell products. [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 ED06-03.
Abstract FO01-01: Global impact of HPV vaccination
Authors: Giuliano Anna R. 
Published: May 2019

Abstract
HPV causes multiple cancers in men and women, accounting for ~5% of all cancers worldwide. In 2006 a 4-valent HPV vaccine was licensed for use for cervical cancer prevention in the US and other countries. After completion of a male HPV vaccine efficacy trial, the 4-valent HPV vaccine was also licensed for the prevention of genital warts in 2009 and anal cancer in 2010. Since licensure, several countries have developed policies promoting national dissemination of the vaccine. Australia has led the way with a robust public health program that rapidly reached ~80% of the age eligible female population. With up to six full years of vaccine dissemination to adolescent females countries are now able to report population effectiveness, or the impact of the vaccine to prevent HPV-related diseases. There are three main outcome variables of interest: short-term (HPV infection and genital wart rates), intermediate-term (reduction in incident cervical lesions), and long-term (incidence and mortality from HPV-related cancers). Effectiveness data for short-term outcomes have recently been reported for Australia, New Zealand, Denmark, Sweden, Germany, Belgium, Canada, and the US. Significant declines in genital wart incidence in females have been reported from all countries to date that have evaluated effectiveness. In Australia, where there was early vaccine adoption nationally and high vaccine penetrance, concomitant declines in genital warts among unvaccinated males have also been documented. Intermediate-term endpoints, such as cervical pre-cancerous lesions have also significantly declined in Australia, Denmark, and the US. These results provide early evidence that routine vaccination significantly reduces HPV infection and early disease endpoints attributed to the 4 major disease causing types of HPV among young adult females at the population level. However, to achieve the full promise of eliminating HPV vaccine type-related disease, broad dissemination of the vaccine is required. Several strategies are under consideration to improve population coverage, including dissemination of vaccine to low resource countries through the GAVI program, alternative dose schedules, and two vs. three dose schedules. Ultimately, strong public health and physician recommendations, as well as population acceptability, are needed to eliminate HPV-related disease through a vaccine approach.
Citation Format: Anna R. Giuliano. Global impact of HPV vaccination. [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 FO01-01.