bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract CN03-01: Dissemination and implementation of cancer prevention policies: The example of smoke-free public housing
Authors: Klassen Ann Carroll 
Published: October 2015

Abstract
Second and third hand smoke exposure increases risk for a number of cancers and other adverse health effects in smokers and non- smokers. Public health campaigns have reduced smoking in many types of public enclosed spaces, but the residential environment remains an important area for risk reduction. In multi-unit housing, significant exposure due to drift between units has led to market and policy efforts to promote smoke-free multi-unit housing options. Public housing authorities have implemented smoke-free policies in greater numbers since the 2009 HUD Healthy Homes Strategic Plan, but the implementation of smoke-free policies in public housing, which must serve diverse communities of low income families, disabled, and elderly residents, presents ethical and logistical challenges.
The Philadelphia Housing Authority is the fourth largest housing authority in the US, serving over 80,000 residents, and is among the largest to implement smoke-free policies. The Drexel School of Public Health, in partnership with the Philadelphia Department of Public Health and with funding from the Centers for Disease Control and Prevention, has conducted a longitudinal mixed methods evaluation of the implementation process.
Our formative evaluation began with in-depth interviews and focus groups with residents, including smokers and non-smokers, as well as PHA staff, policy leaders, and local tobacco control stakeholders, as well as ethnographic observations of the tobacco use culture in diverse housing communities in Philadelphia. We then conducted baseline interviews with a sample of residents in four communities, and conducted air nicotine monitoring in both residents' homes and in public areas, including elevators, laundry rooms, hallways, and lobbies. During implementation, we will continue to monitor resident knowledge, attitudes and tobacco related behaviors, as well as tobacco use in public and home environments.
Results will be discussed in the context of community behavior change, and tobacco control policies for high risk, low resource communities. As well, the Philadelphia example will be compared to other cities and communities, and to the broader theory of implementation science for public health.
Citation Format: Ann Carroll Klassen. Dissemination and implementation of cancer prevention policies: The example of smoke-free public housing. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN03-01.
Abstract CN10-01: Tumor surveillance strategies in pediatric hereditary cancer predisposition syndromes
Authors: Malkin David , Villani Anita , Wasserman Jonathan 
Published: October 2015

Abstract
Cancer is the most common cause of disease-related death in children beyond the neonatal period. Primary prevention has not been commonly considered in the management of childhood cancers as ‘environmental’ agents have not generally been associated with cancer risk. Evidence from genetic and genomic studies supports a rapidly increasing role for inherited or de novo genetic alterations in the etiology of many childhood cancers. Diverse phenotypes have been associated with many of these gene alterations, and genotype:phenotype correlations continue to be defined. Some cancer predisposition syndromes are associated with other non-neoplastic congenital or developmental anomalies, whereas other syndromes appear to be limited to occurrence of a few or many possible cancer types. In the past, the role of genetic testing of children was questioned based on the lack of evidence for effective intervention or improved outcomes. However, the creation and implementation of several comprehensive multi-modality surveillance protocols has offered means by which children at genetic risk of cancer may benefit from early tumor detection and treatment to reduce morbidity and mortality. Emerging discussion of potential opportunities for targeted chemoprevention have also begun. This talk will highlight some of these scenarios, present algorithms whereby such approaches can be used, and explore the complex medical, psychosocial, ethical and financial challenges and opportunities whereby biological/genetic understanding of childhood cancer risk, coupled with effective clinical surveillance can beneficially alter the natural course of hereditary cancer in children.
Citation Format: David Malkin, Anita Villani, Jonathan Wasserman. Tumor surveillance strategies in pediatric hereditary cancer predisposition syndromes. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN10-01.
Abstract CN11-03: SIRT3 is a mitochrondial tumor suppressor in breast cancer
Authors: Gius David 
Published: October 2015

Abstract
It is a well-established scientific observation that mammalian cells contain fidelity or watchdog proteins that maintain the correct function of cellular organelles. Over the past several years, the Sirtuin deacetylase family protein Sirt3 has emerged as a mitochondrial fidelity protein that directs energy generation and regulates reactive oxygen species (ROS) scavenging proteins. Genetic deletion of these fidelity proteins has been shown to create a cellular environment that is permissive for the development of cellular damage associated with processes such as aging and breast ductal cell carcinogenesis. In this regard, we have previously shown that mice lacking the mitochondrial Sirtuin-3 (Sirt3) gene develop estrogen receptor (ER+) positive, p53 wild-type, poorly differentiated invasive ductal carcinomas (IDC) (Kim et al., 2010, Cancer Cell), a subtype of malignancy similar to luminal B breast cancer that is predominantly observed in older women. Mice lacking Sirt3 also exhibit increased ROS, including superoxide due to the aberrant acetylation of manganese superoxide dismutase (MnSOD) resulting in decreased enzymatic ROS scavenging activity. In addition, over expressing a mutant deacetylated-mimic MnSOD isoform, which exhibits increased SOD enzymatic activity, reversed the tumor permissive phenotype (Tao et al, 2010, Molecular Cell) observed in breast tumor cells lacking Sirt3.
Finally, in collaboration with Dr. Joe Bass (Corresponding Author, Northwestern University) a link between SIRT3 and the clock proteins, in the form of mitochondrial NAD+ concentrations has been discovered. Specifically, a clock protein loop directs SIRT3, via NAD+ bioavailability, to regulate mitochondrial glycolytic and oxidative metabolism, as well as MnSOD lysine acetylation and detoxification activity. Furthermore, NAD+ supplementation decreased MnSOD acetylation and significantly restored mitochondrial function in circadian mutant mice by a mechanism involving SIRT3 activity (Peek et al., 2013, Science). These results suggest that circadian clock proteins coordinate mitochondrial metabolism, in part via the modulation of protein acetylation, to synchronize metabolic and oxidative pathways with circadian rhythms.
Citation Format: David Gius. SIRT3 is a mitochrondial tumor suppressor in breast cancer. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN11-03.
Abstract PL02-02: Tomatoes, lycopene, and prostate cancer
Authors: Clinton Steven K. 
Published: October 2015

Abstract
In 1995, the first large prospective cohort data emerged from the Health Professionals Follow-up Study (HPFS) demonstrating a protective association between the intake of tomatoes and processed tomato products and a lower risk of prostate cancer (PCa). By utilizing data-bases of food content of carotenoids it has been possible to demonstrate similar associations between the estimated intake of lycopene (LYC), the non-provitamin A carotenoid providing the familiar red color of tomatoes, and PCa risk. With an additional two decades of monitoring the associations originally identified in the HPFS remain consistent in the 2014 update, while other epidemiologic studies are less convincing. LYC and other carotenoids were documented in human prostate tissue supporting the hypothesis of a direct effect on prostate carcinogenesis. Studies employing various laboratory models from multiple investigators show that tomato components or pure LYC have a protective impact on experimental prostate carcinogenesis. Although an antioxidant mechanism is frequently imputed based upon the known capacity of LYC to quench reactive oxygen species, other potential mechanisms of action related to hormonal activity, cell signaling and growth control, angiogenesis, and metastasis have emerged. Yet, proof of a protective relationship remains elusive and there are many obstacles to defining the impact of specific plant derived phytochemicals for human prostate cancer risk. The importance of dose-response, host genetics, and the complexity of human prostate cancer are but a few of the challenges faced in establishing a causal relationship. The examination of a tomato, lycopene, and prostate cancer relationship provides an example for considering how we as a discipline will address the challenges of defining food or phytochemical based interventions for cancer risk.
Citation Format: Steven K. Clinton. Tomatoes, lycopene, and prostate cancer. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL02-02.
Abstract PL03-03: ER stress and TNF signaling control the progression from simple steatosis to non-alcoholic steatohepatitis (NASH)
Authors: Karin Michael 
Published: October 2015

Abstract
In addition to insulin resistance and type II diabetes, the obesity epidemic had resulted in a large increase in the incidence of non-alcoholic fatty liver disease (NAFLD), which ranges in its manifestations from simple steatosis without liver inflammation and fibrosis to NASH, which is accompanied by liver damage and fibrosis. The mechanisms that govern the progression from simple steatosis to NASH are obscure, but are thought to depend on secondary risk factors that act together with obesity. To study these mechanisms we have developed a new mouse model of NASH which closely mimics all of the features of human NASH. This model is based on the feeding of MUP-uPA mice, which specifically express urokinase plasminogen activator (uPA) in their hepatocytes. Unlike wild type mice, which only develop simple steatosis and insulin resistance after feeding with high fat diet (HFD), MUP-uPA mice on HFD exhibit pronounced liver damage, inflammation, fibrosis and all the classical signs of NASH. The key factors that drive NASH pathogenesis in MUP-uPA mice on HFD are ER stress and excessive TNF production. Interestingly, activation of type I TNF receptor (TNFR1) also controls lipogenesis and steatosis in MUP-uPA mice. Both ER stress and TNFR1 signaling appear to be suitable therapeutic targets for the prevention of NASH and inhibition of its progression to steatotic hepatocellular carcinoma.
Citation Format: Michael Karin. ER stress and TNF signaling control the progression from simple steatosis to non-alcoholic steatohepatitis (NASH). [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL03-03.
Abstract PL04-02: ATM: Bridging DNA damage responses and metabolic regulation
Authors: Kastan Michael B. , Valentin-Vega Yasmine , Brown Adam , Scarbrough Peter , Fleenor Donald 
Published: October 2015

Abstract
Much of our understanding of the mechanisms involved in cellular DNA damage response pathways have come from studies of human cancer susceptibility syndromes. ATM, the gene mutated in the cancer-prone, radiosensitive disorder, Ataxia-telangiectasia (A-T), is a protein kinase that is a central mediator of responses to DNA double strand breaks in cells. Once activated, ATM phosphorylates numerous substrates in the cell that modulate the cell's response to the DNA damage. p53, one of the many targets of the ATM kinase, is a critical mediator of cell cycle changes and cell death signaling following DNA damage and other stresses. Though ATM clearly plays a central role in mediating cellular responses to DNA breakage, some of the clinical abnormalities in A-T are difficult to attribute directly to alterations in DNA damage signaling. The broad-based symptoms in A-T and recently acquired data suggest that ATM has physiologic roles that extend beyond its regulation of DNA damage responses. In particular, ATM appears to affect insulin signaling pathways and to have a direct role in regulating mitochondrial function. Interestingly, we found in mouse models of A-T that these mitochondrial defects associated with ATM deficiency appear to be a contributing factor to cancer development in A-T. These new insights suggest that Ataxia-Telangiectasia should be considered, at least in part, as a mitochondrial dysfunction disease and provide links between cancer-related DNA damage signaling, general metabolic signaling pathways, and cancer development.
Citation Format: Michael B. Kastan, Yasmine Valentin-Vega, Adam Brown, Peter Scarbrough, Donald Fleenor. ATM: Bridging DNA damage responses and metabolic regulation. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL04-02.
Abstract PL04-03: Evidence for increased muscle breakdown associated with early pancreatic cancer
Authors: Heiden Matthew G. Vander 
Published: October 2015

Abstract
Most patients with pancreatic ductal adenocarcinoma (PDAC) are diagnosed with advanced disease and survive less than 12 months. PDAC has been linked with obesity and glucose intolerance, but whether changes in circulating metabolites are associated with early cancer progression had not been studied. To better understand metabolic derangements associated with early disease, we profiled metabolites in prediagnostic plasma from pancreatic cancer cases and matched controls from four prospective cohort studies. We found that elevated plasma levels of branched chain amino acids (BCAAs) are associated with a greater than 2–fold increased risk of future pancreatic cancer diagnosis. This elevated risk was independent of known predisposing factors, with the strongest association observed among subjects with samples collected 2 to 5 years prior to diagnosis when occult disease is likely present. Utilizing genetically engineered mouse models of PDAC, we have confirmed that these elevations represent a marker of early, sub-clinical disease. Furthermore, using these model systems, we demonstrate that the increase in plasma BCAAs reflects a breakdown of tissue protein that accompanies early stage disease. Together, these findings suggest that altered whole body amino acid metabolism is an early event in development of PDAC, and that elevations in BCAAs can be seen in patients years before their pancreatic cancer diagnosis.
Citation Format: Matthew G. Vander Heiden. Evidence for increased muscle breakdown associated with early pancreatic cancer. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL04-03.
Abstract PL06-02: The clock in the cell
Authors: Merrow Martha 
Published: October 2015

Abstract
The circadian clock is an endogenous, cell-based timing mechanism. It has apparently evolved as a response to the highly predictable and metabolically challenging light/dark cycle. Circadian clocks are characterized as having a free running, circa 24h rhythm in constant conditions, an entrainment mechanism whereby those rhythms become exactly 24h, robustness, precision and compensation towards environmental variability such as temperature. While most of our knowledge concerning molecular mechanisms of the daily clock comes from the free running state, the clock is always found in the entrained state in nature. It is this process, the biological oscillator finds its unique phase relationship with the environmental cycle, that leading to temporal compartmentation of various functions and activities. The clock controls gene expression, metabolism, physiology and complex behaviors by organizing them to specific times of day. Working ‘against the clock’ (e.g. in shift work) has been associated with increased incidence of cancers. I will review the molecular and genetic mechanisms that might be involved in this process.
Citation Format: Martha Merrow. The clock in the cell. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL06-02.
Abstract PR07: Calorie restriction normalizes global microRNA expression by preventing the loss of Dicer expression during mammary tumorigenesis
Authors: Devlin Kaylyn L. , Sanford Tiffany , Mambo Elizabeth , Hursting Stephen D. 
Published: October 2015

Abstract
MicroRNA (miRNAs) are small, post-transcriptional regulators that play an integral role in maintenance of cellular functions and whose dyregulation has been shown to promote many types of cancer, including breast cancer. Global downregulation of miRNAs has emerged as a common theme in human breast tumors and has been shown to contribute to oncogenesis. One of the primary mechanisms through which miRNAs are globally dysregulated is downregulation of enzymes involved in miRNA biogenesis. We aim to establish how calorie restriction (CR), which potently inhibits breast cancer progression, regulates global miRNA expression and miRNA biogenesis enzyme functionality in mammary tumors. To address these questions, 100 female Sprague Dawley rats were administered either dimethylbenz(a)anthracene (DMBA) or vehicle control at 50 days of age, then randomized to receive either control (AIN-76A) diet ad-libitum (n=40) or a 30% CR diet regiment (n=60). Resultant mammary tumors were allowed to develop for 12 weeks. Calorie restriction significantly increased survival to study endpoint relative to control diet (75% vs 35%, respectively) (p=0.0047). Furthermore, of the animals that developed tumors, CR significantly decreased median tumor area by 56% compared to control diet (109.4 mm2 vs 250.9 mm2, respectively) (p=0.0286). Global miRNA expression was analyzed through miRNA-specific sequencing. Calorie restriction had a broad effect on miRNA expression, illustrated by the fact that of all the miRNAs with a greater than two-fold expression difference between CR and control, 80% are overexpressed in CR tumors compared to control tumors. These results can be explained by the additional finding that CR was able to prevent the loss of Dicer expression, a key miRNA biogenesis enzyme, observed in control-fed mammary tumor tissue compared to normal tissue. This important finding suggests that global miRNA normalization through the retention of Dicer expression during cancer progression could be a contributing mechanism to CR's anticancer effects. We plan to further these investigations by exogenously manipulating Dicer expression in Rama25 cells, which were originally derived from a DMBA-induced mammary tumor from a Sprague Dawley rat, and analyzing the resultant tumorigenic potential in vitro and in vivo. The results obtained will provide insights into the mechanisms of breast cancer progression and how CR inhibits progression through microRNA modulation.
Citation Format: Kaylyn L. Devlin, Tiffany Sanford, Elizabeth Mambo, Stephen D. Hursting. Calorie restriction normalizes global microRNA expression by preventing the loss of Dicer expression during mammary tumorigenesis. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PR07.
Abstract PR12: Adolescent inflammation and body mass index in relation to colorectal cancer risk
Authors: Kantor Elizabeth D. , Udumyan Ruzan , Signorello Lisa B. , Giovannucci Edward L. , Montgomery Scott , Fall Katja 
Published: October 2015

Abstract
Inflammation and obesity in adulthood have been associated with risk of colorectal cancer (CRC); however, less is known about the role of early-life inflammation and body mass index (BMI) in relation to CRC risk. We therefore sought to evaluate these associations in a cohort of 239,464 Swedish men compulsorily enlisted in the military in late adolescence (ages 16-20 years). At the time of the conscription assessment (1969-1976), erythrocyte sedimentation rate (ESR) was assayed as a measure of inflammation and height and weight were measured. The conscription registry has been linked with national cancer and mortality registries, and men have been followed for CRC through January 1, 2010. Over an average of 35 years of follow-up, 885 cases of CRC occurred, including 501 colon cancers and 384 rectal cancers. Cox regression was used to estimate Hazard Ratios (HRs) and corresponding 95% Confidence Intervals (95% CIs) adjusted for covariates, including childhood socioeconomic status. Men with high inflammation (ESR ≥ 15 mm/hr) in late adolescence had 63% higher risk of CRC (HR: 1.63; 95% CI: 1.08, 2.46) than men with low inflammation (ESR &lt;10 mm/hr) (p-trend: 0.006). This association did not significantly differ by anatomic site (p-difference: 0.50), though the trend was statistically significant for cancers of the colon only (p-trend: 0.009). Late-adolescent BMI was also significantly associated with CRC risk (p-trend: &lt;0.001), with obese adolescents (BMI ≥ 30 kg/m2) experiencing a 2.37-fold higher risk of CRC (HR: 2.37; 95% CI: 1.50, 3.74) than their normal weight counterparts (BMI 18.5-&lt;25 kg/m2). Again, the association between BMI and cancer risk did not significantly vary by anatomic site (p-difference: 0.40), although the trend was statistically significant for cancers of the colon only (p-trend: &lt; 0.001). These analyses were mutually adjusted for BMI and ESR, suggesting that both adolescent inflammation and BMI may be independently associated with CRC risk. Future research is needed to better understand how life-course inflammation and BMI relate to colorectal cancer.
Citation Format: Elizabeth D. Kantor, Ruzan Udumyan, Lisa B. Signorello, Edward L. Giovannucci, Scott Montgomery, Katja Fall. Adolescent inflammation and body mass index in relation to colorectal cancer risk. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PR12.