bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract FO01-01: Estimating how many prostate cancers are overdiagnosed: Overcoming challenges and avoiding mistakes
Authors: Etzioni Ruth 
Published: January 2014

Abstract
Despite the promise of the PSA test for early detection of prostate cancer, it is now clear that PSA screening can be costly, generating harms alongside benefits. Overdiagnosis, or the detection of cancers that would never have been detected clinically, is perhaps the harm of greatest concern in PSA screening. However, different studies provide widely varying assessments of the magnitude of the overdiagnosis problem. A report from the European prostate screening trial estimated that 48 men would have to be overdiagnosed to prevent one prostate cancer death, and a report based on US incidence trends estimated that more than one million men had been overdiagnosed and overtreated by 2005. These statistics are alarming but dramatically overstate the problem. In this presentation I will demonstrate how different definitions, methods and even populations can produce very different, and sometimes inaccurate, assessments of the frequency of overdiagnosis associated with PSA screening. I will present results from two studies of the US population that showed that about one in four men over 50 detected by PSA screening prior to 2000 was overdiagnosed. I will also present personalized estimates of the likelihood of overdiagnosis that vary from from 3 to 80% depending on age, grade and PSA. These estimates can be used in designing population screening programs that reduce costs and harms while preserving benefit.
Citation Format: Ruth Etzioni. Estimating how many prostate cancers are overdiagnosed: Overcoming challenges and avoiding mistakes. [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 FO01-01.
Abstract FO03-02: Worldwide collaborations: The experience of EPIC
Authors: Key Timothy 
Published: January 2014

Abstract
Worldwide collaborations are essential for advancing cancer epidemiology. EPIC – the European Prospective Investigation into Cancer and Nutrition – was established in 1992 as a collaboration between epidemiologists in 10 European countries. Thus from the beginning EPIC has developed approaches to gain the maximum scientific benefit from international collaboration. Beyond Europe, EPIC now participates in several worldwide collaborations with the contribution of both scientific expertise and epidemiological data, including: the Breast and Prostate Cancer Cohort Consortium (BPC3) and the Pancreatic Cancer Cohort Consortium (PANSCAN) as part of the NCI Cohort Consortium; the Harvard Pooling Project of Prospective Studies of Diet and Cancer (Pooling Project); the Endogenous Hormones and Breast cancer Collaborative Group; and the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group. These worldwide collaborations provide the large numbers of cancer cases needed to produce definitive findings on risk factors for cancer.
Citation Format: Timothy Key. Worldwide collaborations: The experience of EPIC. [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 FO03-02.
Abstract OP-01: Global Initiatives in Cancer Prevention Research
Authors: Nelson William G. 
Published: January 2014

Abstract
As estimated by the World Health Organization in its 2010 Global Status Report, for 2008, some 36 million of the 57 million deaths worldwide could be attributed to non-communicable chronic diseases, such as cardiovascular diseases and cancer. The emergence of cancer as a global health threat has been particularly challenging for less developed nations- two thirds of cancer deaths occur in low- and middle-income countries, where poor people with cancer tend to suffer more and die younger than in more developed countries. With the increasing age of the world population and its tendencies for tobacco use, decreasing physical activity, and poor dietary habits, the global epidemic of cancer will get substantially worse unless concerted and coordinated efforts by researchers, medical care providers, governments, and commercial entities can deliver rational and practical strategies for cancer prevention, detection, diagnosis, and treatment that are truly effective, and with refinement can become cost-effective.
The AACR Frontiers in Cancer Prevention Conferences have attempted to bring together the broad collection of cancer research disciplines capable of contributing to the reduction of cancer and cancer mortality at a population scale, attracting experts in epidemiology, behavioral science, health services/economics, genetics, molecular biology, carcinogenesis, animal tumor modeling, imaging, clinical trials, and clinical care. Catalyzed in part by the Conferences, what started as increased dialog among these fields has started to yield productive scientific teams, with diverse members, poised to deliver solutions. Some of the teams have spontaneously organized around themes, such as infections and cancer, chronic or recurrent inflammatory processes and cancer, the epigenome as the genome record of life experience, etc., that have created a language and a logic that can transcend the perspectives of specific disciplines. Already, the power of technology drivers, including the progressive ease of genome-scale analyses and nearly vanishing costs of information storage and sharing, in support these teams has been balanced by significant limits, particularly in the consistent and quantitative collection of phenotypic and exposure data throughout the world.
The promise and problems of cancer prevention will be considered using the example of prostate cancer, a growing global health problem encompassing all of the foundational disciplines of cancer prevention and control.
Citation Format: William G. Nelson. Keynote Lecture: Global Initiatives in Cancer Prevention Research. [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 OP-01.
Abstract OP-02: Accelerating cancer prevention through individual behavior and public health approaches
Authors: Colditz Graham A. 
Published: January 2014

Abstract
We must overcome skepticism that cancer can be prevented, and harness current knowledge to translate and implement effective programs that will reduce the global cancer burden. More than half of cancer can be prevented through effective prevention strategies that are not routinely implemented. These include changes through health care providers, through regulations to reduce our cancer risk, and through community and individual behavior changes. Effective prevention programs require all components of a prevention strategy to work together to reinforce changes that reduce the burden of cancer. Yet we do not act to prevention more than half of all cancers in high income countries where smoking, obesity, lack of physical activity and poor diet are dominant causes of cancer. In low and middle income countries, infection causes 25% of all cancers.
We must align the time frame for research and outcomes to more directly relate to the time course of cancer development and the long time interval between successful interventions and reductions in cancer burden. Cancer incidence may be reduced 10 to 40 or more years after effective interventions. Accordingly, as prevention pays off over decades, we must communicate the time frame and align expectations for reducing the cancer burden with the underling knowledge of cancer etiology and prevention. Society must accept this time frame to commit resources to prevention.
Infrastructure for academic and public health units to effectively achieve prevention goals will be discussed. A great emphasis and reward for implementing effective prevention programs is urgently needed to arrest the global cancer epidemic.
Citation Format: Graham A. Colditz. Accelerating Cancer Prevention Through Individual Behavior and Public Health Approaches. [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 OP-02.
Abstract PL02-01: Inflammation, stem cells and cancer
Authors: Wang Timothy C. 
Published: January 2014

Abstract
Many if not most gastrointestinal cancers arise in the setting of chronic inflammation, and examples include gastroesophageal reflux-induced esophageal adenocarcinoma, H. pylori-associated gastric cancer and colitis-associated colorectal cancer. We have utilized murine models of esophagitis (L2-IL-1β transgenic mice), gastritis (H/K-ATPase-IL-1β and Helicobacter felis infection) and colitis (AOM/DSS) to investigate the role of chronic inflammation in the development of malignancy. In models of chronic gastrointestinal inflammation, there is an early expansion of immature myeloid cells (IMC) followed later by increases in αSMA+ stromal fibroblasts (CAFs). The increase in IMC results from in part from an expansion of splenic progenitors/HSC, while the increased CAFs reflects an increase in mesenchymal stem cells (MSCs) within the preneoplastic tissue. Together, the amplification of myeloid progenitors and MSC-derived stromal cells results in an evolving cancer niche that contributes to expansion of gut progenitors. In the colon, these inflammatory signals can results in crypt fission and monoclonal conversion of intestinal crypt units. Thus, an early amplification of epithelial stem or progenitor cells appears to be a requirement for the development of neoplasia. Eliminating the early cancer niche, which appears to be needed for the initiation of tumors, appears to represent a potential strategy for cancer prevention.
Citation Format: Timothy C. Wang. Inflammation, stem cells, and cancer. [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 PL02-01.
Abstract PL02-04: The obesity-inflammation connection: Implications for breast carcinogenesis
Authors: Dannenberg Andrew J. 
Published: January 2014

Abstract
Obesity is a risk factor for the development of several malignancies including hormone receptor–positive breast cancer in postmenopausal women and has been associated with an increased risk of recurrence and reduced survival. Chronic inflammation increases the risk of multiple tumor types. A link between obesity, breast inflammation and hormone receptor-positive breast cancer was previously unknown. Obesity causes subclinical inflammation in visceral and subcutaneous white adipose tissue, characterized by macrophages surrounding necrotic adipocytes forming crown-like structures (CLS). Estrogen synthesis is catalyzed by aromatase, which is encoded by CYP19. Recently, we found increased numbers of CLS, activation of the NF-κB transcription factor, increased levels of pro-inflammatory mediators and elevated aromatase levels and activity in the mammary glands of obese mice. These preclinical findings raised the possibility that the obesity→inflammation→aromatase axis is important for breast carcinogenesis. Importantly, these findings have now been translated to women. Breast tissue was obtained from women who underwent surgery. CLS of the breast (CLS-B) were found in nearly 50% of patient samples. The severity of breast inflammation, defined as the CLS-B index, correlated with both body mass index and adipocyte size. Consistent with our preclinical findings, increased NF-κB binding activity, increased levels of pro-inflammatory mediators and elevated aromatase expression and activity were found in the inflamed breast tissue of overweight and obese women. Collectively, our results suggest that the obesity→inflammation →aromatase axis is present in the breast tissue of most overweight and obese women and is likely to contribute to the increased risk of hormone receptor-positive breast cancer. The presence of CLS-B may be a biomarker of increased breast cancer risk or poor prognosis. The discovery of the connection between obesity, breast inflammation and changes in the expression of genes linked to breast cancer provides a mechanistic rationale for the development of behavioral, dietary and pharmacological strategies to reduce the risk of breast cancer. Recently conducted caloric restriction experiments provide proof-of-principle evidence that obesity-related mammary gland inflammation can be reversed.
Citation Format: Andrew J. Dannenberg. The obesity-inflammation connection: Implications for breast carcinogenesis. [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 PL02-04.
Abstract PL03-01: The nutrient-sensing mTOR pathway in cancer initiation and progression
Authors: Manning Brendan D. 
Published: January 2014

Abstract
The mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) has the ability to sense and integrate signals from a variety of sources, including intracellular nutrients and energy, growth factors, and cellular stresses. mTORC1 senses many of these signals through a small G protein switch involving the tuberous sclerosis complex (TSC) tumor suppressors, TSC1 and TSC2, and the Ras-related small G protein Rheb. Multi-site phosphorylation of the TSC2 protein downstream of distinct signaling pathways appears to account for much of mTORC1's signal-integrating capacity. Importantly, the two most commonly activated oncogenic signaling pathways in human cancers, the PI3K-Akt and Ras-Erk pathways, phosphorylate and inhibit TSC2 to activate mTORC1. Aberrant activation of mTORC1 through genetic and environmental effects on the upstream signaling network is a common molecular event in a large variety of pathological settings, including the majority of genetic tumor syndromes, sporadic cancers, and obesity. However, we are just beginning to understand the downstream consequences of mTORC1 activation in both normal and disease states. I will discuss our evidence suggesting that mTORC1 signaling might be a major molecular link between environmental influences, such as diet, and increased cancer risk. In addition, I will present our work on the role of mTORC1 as a key downstream effector of oncogenic signaling pathways that promotes anabolic cell growth and proliferation by altering the cellular metabolic program.
Citation Format: Brendan D. Manning. The nutrient-sensing mTOR pathway in cancer initiation and progression. [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 PL03-01.
Abstract PL04-01: The promise of GWAS studies to assess cancer prevention
Authors: Chanock Stephen J. 
Published: January 2014

Abstract
Genome-wide association studies (GWAS) have transformed the discovery of common susceptibility alleles for a wide spectrum of cancers. GWAS have been a highly successful approach for discovering common susceptibility alleles. Already, over 220 regions have been conclusively established (i.e., achieving genome-wide significance) in two-dozen cancers1. GWAS have uncovered new clues to biological insights as a consequence of collaboration between epidemiologists, statisticians, and geneticists. Since GWAS can be effectively scaled to accelerate discovery, the major challenge ahead is to determine how to establish the critical connection between the genetic markers and carcinogenic processes that underlie complex phenotypes, such as cancer. The rapid pace of discovery using the GWAS approach has not been matched by research to interpret and understand the functional significance of different alleles that are correlated with cancer phenotypes. The gap between the number of new independent markers and a biological understanding of the loci continues to widen, at an accelerated pace. The success of GWAS as a tool for discovery has raised a new series of questions. It is now possible to begin to estimate the underlying genetic architecture of genetic susceptibility alleles for specific cancers and explore both their main effect and interaction with either other genetic variants or environmental exposures. There are a few examples of GWAS findings that have lead to new insights into processes that could be targets for either prevention or treatment. Based on sound scientific insights, new approaches will begin to emerge and contribute to novel strategies for prevention and therapy.
Citation Format: Stephen J. Chanock. The promise of GWAS studies to assess 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 PL04-01.
Abstract PL04-02: Insights on cancer risk from normal breast tissue gene expression
Authors: Troester Melissa A. 
Published: January 2014

Abstract
Breast cancers evolve through interactions with the surrounding non-malignant tissue, with the non-malignant tissue providing a selective pressure during carcinogenesis. By conducting observational studies of non-malignant tissue, it is possible to identify pathways and phenotypes that contribute to cancer etiology and progression. Our gene expression profiling studies have demonstrated that cancer adjacent normal breast tissue is highly variable, with at least two distinct molecular subtypes. These subtypes are associated with histologic differences and distinct risk factor profiles, notably mammographic density. Given that mammographic density is the strongest, yet most poorly understood breast cancer risk factor, molecular studies to better understand this phenotype are important. We have also conducted studies of risk factor-associated gene expression in reduction mammoplasty tissue. Supervised analysis of gene expression in normal tissue is identifying novel biological phenotypes associated with established risk factors. For example, we have shown that aging is associated with specific gene expression changes in normal breast. Interestingly, the age-related pathways in non-diseased tissue are also dysregulated in the breast cancers that are more common in young women, providing a biological link between the aging process and tumor aggressiveness. Likewise, obesity causes alterations to the stromal milieu in normal breast tissue, with implications for the progression of basal-like breast cancers. Our results demonstrate that to study the evolution and outcome of breast cancers, it is important to consider the normal tissue microenvironment from which these cancers evolve.
Citation Format: Melissa A. Troester. Insights on cancer risk from normal breast tissue gene expression. [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 PL04-02.
Reactivating Memories during Sleep by Odors: Odor Specificity and Associated Changes in Sleep Oscillations
Authors: Rihm Julia S. , Diekelmann Susanne , Born Jan , Rasch Björn 
Published: January 2014

Abstract
Memories are reactivated during sleep. Re-exposure to olfactory cues during sleep triggers this reactivation and improves later recall performance. Here, we tested if the effects of odor-induced memory reactivations are odor-specific, that is, requiring the same odor during learning and subsequent sleep. We also tested whether odor-induced memory reactivation affects oscillatory EEG activity during sleep, as a putative mechanism underlying memory processing during sleep. Participants learned a visuospatial memory task under the presence of an odor. During subsequent SWS, the same odor, a different odor, or an odorless vehicle was presented. We found that odor re-exposure during sleep significantly improves memory only when the same odor was presented again, whereas exposure to a new odor or the odorless vehicle had no effect. The memory-enhancing effect of the congruent odor was accompanied by significant increases in frontal delta (1.5–4.5 Hz) and parietal fast spindle (13.0–15.0 Hz) power as well as by an increased negative-to-positive slope of the frontal slow oscillation. Our results indicate that odor-induced memory reactivations are odor specific and trigger changes in slow-wave and spindle power possibly reflecting a bottom–up influence of hippocampal memory replay on cortical slow oscillations as well as thalamo-cortical sleep spindles.
Individual Differences in Crossmodal Brain Activity Predict Arcuate Fasciculus Connectivity in Developing Readers
Authors: Gullick Margaret M. , Booth James R. 
Published: January 2014

AbstractCrossmodal integration of auditory and visual information, such as phonemes and graphemes, is a critical skill for fluent reading. Previous work has demonstrated that white matter connectivity along the arcuate fasciculus (AF) is predicted by reading skill and that crossmodal processing particularly activates the posterior STS (pSTS). However, the relationship between this crossmodal activation and white matter integrity has not been previously reported. We investigated the interrelationship of crossmodal integration, both in terms of behavioral performance and pSTS activity, with AF tract coherence using a rhyme judgment task in a group of 47 children with a range of reading abilities. We demonstrate that both response accuracy and pSTS activity for crossmodal (auditory–visual) rhyme judgments was predictive of fractional anisotropy along the left AF. Unimodal (auditory-only or visual-only) pSTS activity was not significantly related to AF connectivity. Furthermore, activity in other reading-related ROIs did not show the same AV-only AF coherence relationship, and AV pSTS activity was not related to connectivity along other language-related tracts. This study is the first to directly show that crossmodal brain activity is specifically related to connectivity in the AF, supporting its role in phoneme–grapheme integration ability. More generally, this study helps to define an interdependent neural network for reading-related integration.