bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract CN01-03: Autoimmune rheumatic diseases and cancer: Not just chance?
Authors: Rosen Antony , Casciola-Rosen Livia 
Published: January 2014

Abstract
A relationship between cancer and autoimmune rheumatic diseases has been observed for many decades, although the relevance of, and mechanisms underlying this association remain unclear. Investigating this relationship has been extremely challenging, due to (i) the striking heterogeneity of the rheumatic diseases, (ii) the use of numerous pharmacologic agents which can be associated with cancer, (iii) the kinetic heterogeneity of cancer onset (some cancers precede the rheumatic disease; most follow diagnosis of cancer, but over a period which can vary from 0-25 years); and (iv) the large number of tumor types associated with rheumatic disease. Although &gt;80% of rheumatic disease patients do not have any associated cancer, a striking temporal clustering of the onset of cancer and autoimmune rheumatic disease has been observed. This is true for Dermatomyositis and Polymyositis, where most cancers are diagnosed -1 to +1 years around the onset of the rheumatic syndrome. Cancer is diagnosed in ∼15% of all patients with DM (mostly adenocarcinomas). Interestingly, myositis autoantigens are expressed at very low levels in most normal tissues, but at increased levels in both tumors and inflamed muscle, where autoantigen expression is localized to regenerating muscle cells. Similar observations have been made in other rheumatic diseases including scleroderma. The available data suggest a model where autoantigen expression and inflammation in the tumor initiates a humoral and cellular immune response to autoantigens. In the setting of injury to a normal tissue (e.g. muscle), the precursors which differentiate to repair the injury express the same antigens, and become the target of the ongoing immune response, and drive tissue damage in a feedforward loop.
Citation Format: Antony Rosen, Livia Casciola-Rosen. Autoimmune rheumatic diseases and cancer: Not just chance? [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN01-03.
Abstract CN03-02: Is newer better? Use of technology to encourage cancer screening among various populations
Authors: Skinner Celette Sugg 
Published: January 2014

Abstract
Several major technological breakthroughs have greatly expanded our options for health behavior interventions. In the 1980s, we started being able to record our own videos through hand-held cameras, mass produce tailored print on micro-computers, and develop interactive computer programs. Now, all these interventions can be web-based and accessed through smart phones that can collect data and deliver tailored feedback in real time. In our fascination with new media and their capabilities, we have rushed to employ latest technologies for interventions for all kinds of people. But, is newer necessarily better? To suggest some answers to this question, the presentation will use qualitative data as well as main and interaction effects from some large behavioral intervention trials among African Americans and other population subgroups.
Citation Format: Celette Sugg Skinner. Is newer better? Use of technology to encourage cancer screening among various populations. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN03-02.
Abstract CN03-04: The effect of the new screening guidelines on uptake of screening tests
Authors: Taplin Stephen H. 
Published: January 2014

Abstract
National organizations funded through public and private dollars have been setting cancer screening guidelines for more than a generation. While guidelines are a lightning rod for practitioners and people at risk for cancer, their actual effect on behavior is unclear. In this presentation I will review what we can expect regarding the association between guidelines and behavior based on conceptual models. I will also review what we know from published work about the association between guideline changes and screening for breast, colon, cervical, and prostate cancer. Finally I will summarize changes in the USPSTF in the last 10 years and examine their association with changes in screening rates for breast, colorectal, cervical, and prostate cancer. To do the latter I will compare rates of screening as reported in the National Health Interview Survey (NHIS) using survey data from the following years 2000, 2003, 2005, 2008, 2010, 2011 and comparing screeing rates before and after significant USPSTF guideline changes in 2002 (breast), 2003 (cervix), and 2009 (breast, colorectal cancer). Lively discussion, insight, but no lightning will be sought.
Citation Format: Stephen H. Taplin. The effect of the new screening guidelines on uptake of screening tests. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN03-04.
Abstract CN05-01: Viral and Dietary Factors in Declining Liver Cancer Mortality in Qidong, China
Authors: Kensler Thomas W. 
Published: January 2014

Abstract
Liver cancer is the third leading cause of cancer mortality globally. In endemic areas of sub-Saharan Africa and southeast Asia liver cancer largely arises from both chronic infection with hepatitis B virus (HBV) and the ingestion of aflatoxin-contaminated foods such as corn and groundnuts. While synergistic interactions between these viral and chemical carcinogens have been observed in prospective cohort studies in China, the effects of primary prevention against both of these factors has not been examined. Mortality rates from liver cancer by birth cohort in Qidong, China were compared to timelines in the region for the introduction of HBV vaccination and to mandated, wholesale changes in staple foodstuffs from corn to rice. Levels of aflatoxin-albumin adducts in archived serum samples collected in Qidong from 1989 to 2012 were quantified by isotope dilution mass spectrometry as measures of carcinogen exposure. Halving of mortality rates from liver cancer are seen between birth cohorts from the 1960s and 1980s for residents 34 years old and younger. However, prevalence of HBsAg positivity was unchanged in these cohorts as all were born prior to implementation of universal HBV vaccination of newborns. Changing agricultural policies from a planned to a market-oriented economy in the early 1980s led from corn to rice based diets and dramatic decreases in aflatoxin exposures in Qidong. Substantial declines in liver cancer morality in birth cohorts occurring prior to the introduction of a universal HBV vaccination program in Qidong highlight the importance of altered food policies as a means for rapid risk reduction, especially amongst the ∼350 million HBV carriers, many of whom reside in endemic areas. Supported by NIEHS ES 006052 and National Science and Technology of China 2008ZX10002-015.
Citation Format: Thomas W. Kensler. Viral and dietary factors in declining liver cancer mortality in Qidong, China. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN05-01.
Abstract CN06-01: Induction of oral cavity cancer in rats by (S)-N'-nitrosonornicotine, a constituent of smokeless tobacco
Authors: Hecht Stephen S. , James-Yi Sandra , O'Sullivan Gerard , Stepanov Irina , Wang Mingyao , Kassie Fekadu , Carmella Steven , Upadhyaya Pramod , Balbo Silvia 
Published: January 2014

Abstract
Smokeless tobacco products such as moist oral snuff are being promoted by the tobacco industry with a half billion dollars per year in advertising. It is likely that the prevalence of smokeless tobacco use will continue to increase in the U.S. Smokeless tobacco products are widely used in other parts of the world and are considered by the International Agency for Research on Cancer as causes of cancer of the oral cavity, esophagus and pancreas in humans. However, no previous study has reported the presence of a strong oral cavity carcinogen in these products.
N'-Nitrosonornicotine (NNN) occurs in significant amounts in smokeless tobacco products, generally being found at levels of 1 - 10 μg/g tobacco. Since NNN has a chiral center, it exists as (S)- and (R)- enantiomers. (S)-NNN is the major enantiomer in smokeless tobacco products. While racemic NNN (a 50:50 mixture of (S)- and (R)-NNN) has been previously shown to cause esophageal tumors in rats, the carcinogenicity of the individual enantiomers has not been reported. Based on our published metabolism and DNA binding studies of (S)-NNN, we hypothesized that it might be a more powerful carcinogen than (R)-NNN and, furthermore, that it might cause oral cancer.
Groups of 24 male F-344 rats were treated with either (S)-NNN (15 ppm), (R)-NNN (15 ppm), or racemic NNN (30 ppm) in the drinking water for 15-20 months. Necropsy of 20 rats treated with (S)-NNN demonstrated a 100% incidence of oral cavity tumors. More than 60 oral cavity tumors were observed, including benign and malignant tumors of the buccal mucosa, soft and hard palate, tongue, and pharynx. All rats also had esophageal tumors. (R)-NNN was significantly less carcinogenic than (S)-NNN. Racemic NNN also induced a high incidence of oral cavity and esophageal tumors.
The results of this study demonstrate for the first time the presence of a strong oral cavity carcinogen in smokeless tobacco. (S)-NNN is a prime target for elimination from these products as a positive step toward cancer prevention.
Citation Format: Stephen S. Hecht, Sandra James-Yi, Gerard O'Sullivan, Irina Stepanov, Mingyao Wang, Fekadu Kassie, Steven Carmella, Pramod Upadhyaya, Silvia Balbo. Induction of oral cavity cancer in rats by (S)-N'-nitrosonornicotine, a constituent of smokeless tobacco. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN06-01.
Abstract CN07-01: Understanding the role of stem-like tumor cells in proneural glioma
Authors: Barrett Lindy Elise , Nam Hyung-song , Benezra Robert 
Published: January 2014

Abstract
The ID (Inhibitor of DNA-binding) gene family regulates self-renewal in adult neural stem cells. Cells expressing high levels of Id1 in the neurogenic niches of the adult brain define the B1 stem cell populations and Id proteins are essential for self-renewal and the maintenance of multipotency. A decline in Id1 levels is associated with the progression to a progenitor-like cell type in which the bHLH marker Olig2 becomes highly expressed. Since the discovery of stem-like and progenitor-like cell populations within high-grade gliomas, there has been a great deal of interest in elucidating their contributions to tumorigenesis. However, analyses are complicated by the lack of reliable marker sets to definitively isolate and characterize these distinct cell lineages. Using a genetically relevant mouse model of high-grade proneural glioma, we show that high Id1 expression (Id1high) identifies self-renewing, multipotent tumor cells, while low Id1 expression (Id1low) identifies progenitor-like cells characterized by Olig2 expression and limited self-renewal capacity, thus recapitulating what is observed in the normal neurogenic niche. Id1high cells generate tumors upon orthotopic transplantation, but surprisingly, Id1low cells do so with shorter latency and higher penetrance, despite their limited self-renewal capacity. Both Id1high and Id1low cells generate tumors with high-grade features and histopathology similar to the parental tumors. Purified Id1high cells give rise to Id1low cells during tumor formation thereby possibly fueling the generation of the more tumorigenic progenitor-like population. Targeting the more progenitor-like cells via knockdown of Olig2 results in a dramatic survival benefit. These data highlight an important distinction between self-renewal capacity and tumor initiation potential, underscoring the importance of non-stem cell lineages in brain tumor disease progression.
Citation Format: Lindy Elise Barrett, Hyung-song Nam, Robert Benezra. Understanding the role of stem-like tumor cells in proneural glioma. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN07-01.
Abstract CN07-02: Targeting tumor-initiating cells in medulloblastoma
Authors: Markant Shirley , Esparza Lourdes Adriana , Barton Kelly , Sun Jesse , Wechsler-Reya Robert 
Published: January 2014

Abstract
The growth of many tumors has been suggested to depend on a subset of tumor cells with an extensive capacity for self-renewal, termed cancer stem cells or tumor-initiating cells (TICs). These cells are not necessarily abundant or proliferative, but because they are long-lived and often resistant to conventional therapies, they are thought to contribute to tumor resistance and recurrence. Therefore, identifying these cells and finding approaches to targeting them has become an important goal in cancer research. We recently identified a population of TICs in a mouse model of medulloblastoma, the most common malignant brain tumor in children. These cells, marked by expression of the cell surface antigen CD15, are capable of propagating tumors following transplantation, whereas CD15– cells from the same donors cannot. To gain insight into the molecular mechanisms underlying the increased tumorigenic potential of CD15+ cells, we compared their gene expression profile to that of CD15– cells. Among the genes most consistently elevated in CD15+ cells were regulators of the G2/M phases of the cell cycle. This observation led us to hypothesize that CD15+ cells display altered cell cycle regulation, and that these cells might be particularly vulnerable to inhibitors of cell cycle progression. Here we show that CD15+ cells move more quickly through the G1 and S phases of the cell cycle, and as a result contain an increased proportion of cells in G2/M. Consistent with this cell cycle skewing, CD15+ cells express higher levels of the G2/M regulators Aurora Kinase (Aurk) and Polo-like Kinase (Plk). Treatment of tumor cells with small molecule antagonists of Aurk or Plk inhibits cell cycle progression, promotes apoptosis and enhances sensitivity to other modes of chemotherapy. Treatment of tumor-bearing mice with these agents also significantly inhibits tumor progression. Importantly, cells from medulloblastoma patient-derived xenografts are also sensitive to Aurk and Plk inhibitors. These findings suggest that inhibitors of Aurk and Plk may be useful for targeting TICs and may represent a novel avenue for therapy of human medulloblastoma.
Citation Format: Shirley Markant, Lourdes Adriana Esparza, Kelly Barton, Jesse Sun, Robert Wechsler-Reya,. Targeting tumor-initiating cells in medulloblastoma. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN07-02.
Abstract CN08-01: Computerized approaches to molecularly-designed drugs and target identification for cancer prevention
Authors: Dong Zigang 
Published: January 2014

Abstract
In the post-genomic era, computational modeling, simulations and genomics play a critical role in the next revolution in cancer research. Computational biology is an interdisciplinary field that uses the techniques of computer science, applied mathematics, and statistics to address problems in biology. The supercomputer is widely used in computational biology. We have applied supercomputers in cancer prevention research and have made progress in the following areas:
1) Mapping protein interaction networks in cancer cells (e.g., to study protein kinase interactions with other protein kinases, transcription factors, or other proteins)
2) Computational screening of chemical libraries against target proteins, identification of available chemical libraries (NCI; natural compounds, etc.), crystal structures or homology screening
3) Reverse docking and screening of protein structures against a chemical to identify its molecular target(s)
4) Drug target discovery by supercomputer and in vitro and in vivo validation of computer-identified potential targets using:
a) kinase assays
b) site mutagenesis
c) animal studies
5) Identifying key protein/DNA interactions
6) Modeling cancer promotion and progression in order to study cancer promotion, progression, and therapeutic effectiveness to predict success (i.e. predicting drug resistance)
Citation Format: Zigang Dong. Computerized approaches to molecularly designed drugs and target identification for cancer prevention. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN08-01.
Abstract CN08-02: New strategies for cancer chemoprevention
Authors: Steele Vernon E. 
Published: January 2014

Abstract
Chemoprevention research in animals and humans has revealed that pathways in the cancer process are amenable to inhibition, reversal or retardation at various stages. We must therefore identify the key pathways in the evolution of cancer that can be blocked to prevent this carcinogenesis process. Current mechanistic approaches include administering agents which block the activation of carcinogens, promote the detoxification of carcinogens (Phase II enzyme inducers), enhance glutathione, block the production of reactive oxygen species, antioxidants, inhibit carcinogen uptake, promote repair processes, and block cell cycle progression. Some of the more promising strategies to prevent breast cancer include selective estrogen receptor antagonists and aromatase inhibitors, while for colon, skin and urinary bladder NSAIDs and polyamine synthesis inhibitors are highly preventive. Many of these strategies have been validated in human cancer prevention studies. Retinoids are differentiation and apoptosis inducers primarily, but act as agonists to the RAR and RXR receptors with many downstream effects. Newer safer rexinoids can prevent both ER positive and ER negative breast cancers. Targeted mechanistic approaches are currently being investigated, such as inhibition of lipoxygenase, PI3K/AKT/mTOR pathway inhibitors, EGF receptor tyrosine kinase inhibitors, histone acetylation/deacetylation and methylation/demethylation inhibitors. Most recently immunoprevention approaches have shown exciting promise and are being developed into the clinic. Future strategies include possible miRNA or antisense miRNA administration to prevent cancers. To conquer this diverse disease, multiple key pathways must be attacked at once for a predetermined period of time. It is becoming clear that each organ-specific cancer type may require a custom combination of prevention strategies to be successful.
Citation Format: Vernon E. Steele. New strategies for cancer chemoprevention. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN08-02.
Abstract CN08-04: Novel Gemini vitamin D compounds for prevention of breast cancer by targeting stem cells
Authors: Suh Nanjoo 
Published: January 2014

Abstract
Identification and characterization of cancer stem cells in cancer development offers a new promising strategy in cancer prevention. Targeting cancer stem cells by novel cancer preventive agents may provide a new approach to blocking the progression of premalignant tumors into invasive cancer. CD44, a transmembrane glycoprotein, is a major receptor for extracellular proteins involved in invasion and metastasis of human cancers. CD44 has been recognized as one of the key cell surface markers for tumor-initiating cells in breast cancer. Our laboratory has demonstrated that the novel Gemini vitamin D analog BXL0124 [1α,25-dihydroxy-20R-21(3-hydroxy-3-deuteromethyl-4,4,4-trideuterobutyl)-23-yne-26,27-hexafluro-cholecalciferol] represses CD44 expression in MCF10DCIS.com basal-like human breast cancer cells and inhibits MCF10DCIS xenograft tumor growth. We have investigated potential factors downstream of CD44 and the biological role of CD44 repression by BXL0124 in MCF10DCIS cells. CD44 forms a complex with STAT3 and Janus kinase 2 (JAK2) to activate STAT3 signaling, which was inhibited by BXL0124 in MCF10DCIS cells. The knockdown of CD44 by small hairpin RNA significantly decreased mRNA expression levels of invasion markers in MCF10DCIS cells and decreased tumor size and weight as well as invasion markers in MCF10DCIS xenograft tumors. Repression of CD44-STAT3 signaling by the Gemini vitamin D analog BXL0124 appears to be a key molecular mechanism in the inhibition of breast cancer invasion. Identification of new targets and pathways in specific populations of cancer stem cells, such as those expressing CD44, may open a new direction in cancer prevention research. (Supported by NIH grant R01 CA127645).
Citation Format: Nanjoo Suh. Novel Gemini vitamin D compounds for prevention of breast cancer by targeting stem cells. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr CN08-04.