bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B59: Epithelial ovarian cancer, comorbidity, and racial disparities
Authors: Fields Nicole Danielle , Whiteside Martin , Terry Paul Daniel 
Published: October 2015

Abstract
The purpose of our study was to determine if co-morbidities influenced survival among ovarian cancer patients and whether associations varied according to race. Ovarian cancer is one of the most deadly cancers among women in the United States, with an overall 5-year survival of 33%[1]. Tennessee ranks 14th highest in the United States for ovarian cancer incidence, with an age-adjusted rate of 11.8 per 100,000 cases. There have been few studies published addressing the relative contribution of comorbidity to the association between ovarian cancer and survival. Therefore, we identified epithelial ovarian cancer cases from the Tennessee Cancer Registry between 2004-2010, and linked these data to inpatient hospital discharge information from 2007 to 2009. Pre-diagnosis comorbid conditions were grouped into 7 broad categories: Heart Disease, Peripheral Vascular Disease, Gastrointestinal (GI) Disorders, Infectious Disease, Kidney Disease, Musculoskeletal Disease, and Non-Malignant Lung Disease. The median age of patients was 76.4 years and the median follow-up time was 103 days. We found that 53.8% of GI Disorder patients had Stage 4 ovarian cancer, with a relatively high median follow-up time of 130 days. 33.3% of Infectious Disease patients had Stage 4 cancer, and had the highest follow-up time of 196 days. In contrast, Kidney Disease patients had the lowest median follow-up time at 60 days, suggesting that this comorbidity was among the most predictive of poor survival. Median survival times of other comorbidities were within these latter two extremes. Race was not a substantial mediating factor in the associating among comorbidities and survival in ovarian cancer patients. Rather, the patient's age, stage at diagnosis, and the type of diagnosis had the greatest impact on survival.
Citation Format: Nicole Danielle Fields, Martin Whiteside, Paul Daniel Terry. Epithelial ovarian cancer, comorbidity, and racial disparities. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr B59.
Abstract IA01: Disparities in HPV infection
Authors: D'Souza Gypsyamber 
Published: October 2015

Abstract
Human papillomavirus (HPV) is a common sexually transmitted infection that can cause cervical, anal, vaginal, penile, and oropharyngeal cancers. There is heterogeneity in HPV prevalence across racial and socioeconomic groups as well as by age-cohort. These differences in HPV infection contribute to disparities observed in the rates of HPV-related cancer rates in these groups. This talk reviews what is known about genital, anal, and oral HPV infection, and how infection differs among groups. Reasons for disparities in HPV infection are discussed, including the roles of sexual behavior, sexual network, and co-factors (such as tobacco use). Common questions and answers about HPV infection will be discussed.
Citation Format: Gypsyamber D'Souza. Disparities in HPV infection. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr IA01.
Abstract IA05: Enhancing HIT platform design and employing novel analytic perspectives to reduce cancer
Authors: Gibbons M. Chris 
Published: October 2015

Abstract
The potential of Information and Communications technologies to help address cancer health disparities is significant. A growing body of evidence focuses on the efficacy of devices and tools. This literature suggests that both clinical and consumer oriented Health IT can positively impact health outcomes. Despite this literature, comparatively less work has been done detailing principles of effective Health IT design, particularly for underserved populations who may have unique physical, cultural and or environmental user characteristics that impact the usability of electronic tools, rendering them less useful, desirable or effective among these populations. If left unaddressed, sub optimal health IT design could contribute to increases in cancer disparities. In addition, little work has also been done focusing on the development of health technology platforms specifically for health coaches, navigators and health workers working with individuals from underserved population groups. Finally advances in Health IT are enabling the collection of vast amounts of data. This data may, in the future, be used to gain novel disparities insights not currently possible. This presentation will discuss evidence based design principles that can enhance the development of electronic health tools to address cancer disparities. The presentation will also provide examples of emerging platforms as well as novel analytic perspectives that could prove important in helping to effectively address and ultimately eliminate Cancer health disparities.
Citation Format: M. Chris Gibbons. Enhancing HIT platform design and employing novel analytic perspectives to reduce cancer. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr IA05.
Abstract IA13: Connecting science to law: Understanding the policymaking process
Authors: Berman Micah L. 
Published: October 2015

Abstract
Tobacco use remains the leading cause of preventable death in the U.S., killing 480,000 Americans a year. To address the death and disease caused by tobacco use, Congress enacted the Family Smoking Prevention and Tobacco Control Act (FSPTCA) in 2009, granting the U.S. Food and Drug Administration (FDA) broad authority to regulate the manufacture, marketing, and sale of tobacco products.
In order to help build the science base for tobacco regulation, the FDA has invested heavily in “tobacco regulatory science.” In partnership with the National Institutes of Health (NIH), it is investing $273 million over five years in the Tobacco Centers of Regulatory Science (TCORS) initiative. The TCORS program funds 14 centers at academic institutions (including Ohio State) that conduct research relevant to the FDA's regulation of tobacco. This initiative is a unique partnership between a regulatory agency and researchers, developed with the explicit expectation that the research will directly inform the FDA's regulatory actions.
To conduct research that will assist the FDA in fulfilling its regulatory mission, researchers must venture outside of their comfort zone and consider the relevant legal and policy environment. More specifically, scientists engaged in tobacco regulatory science must consider at least four different questions: (1) what FDA regulatory action(s) might my research inform?; (2) what types of evidence would the FDA need to consider in order to take such actions?; and (3) if such a regulation were reviewed in court, what questions would the courts ask about the available evidence? Failure to consider these questions may lead to research that, while scientifically valid, does not advance the FDA's ability to fulfill its regulatory mission. Thus, in order for the TCORS program to succeed, there must be a productive and ongoing dialogue between scientists and attorneys familiar with the regulatory landscape.
This presentation will discuss the need for better coordination between scientists and attorneys, particularly in the context of tobacco regulatory research. It will also discuss how law acts as a social determinant of health that has a significant impact (both positive and negative) on health disparities.
Citation Format: Micah L. Berman. Connecting science to law: Understanding the policymaking process. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr IA13.
Abstract IA34: Who benefits from patient navigation: Updates from the National Patient Navigation Research Program
Authors: Freund Karen M. 
Published: October 2015

Abstract
Patient navigation programs continue to proliferate across the country, as evidence of their effectiveness in addressing health disparities continues to grow. However, cancer centers are concerned about the sustainability of patient navigation programs, as they are usually not supported through insurance reimbursement of care. Therefore, it is useful to identify where patient navigation is the most effective, which patients benefit the most from navigation, and what aspects of patient navigation programs provide the greatest impact on patient care. This information is critical for programs to develop the most effective programs with limited resources.
e present new analyses from the National Patient Navigation Research Program, to address which patients benefit the most from patient navigation. Our findings indicate that a number of variables that can be collected at the time of referral to a cancer program are predictors of patients in need of navigation and patients who benefit from navigation. These include sociodemographic characteristics, such as education, employment, income and housing status, medical comorbidities, and social and logistic barriers to care. Systems with the greatest delays in care benefit the most from navigation. Navigators are most effective when their roles focus on direct interaction time with patients, their caregivers, and the health care team. Excess efforts by patient navigators to address limitations with electronic medical records detract from their clinical effectiveness.
These findings may help programs develop and refine their patient navigation programs to provide the greatest impact and support to patients.
Citation Format: Karen M. Freund. Who benefits from patient navigation: Updates from the National Patient Navigation Research Program. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr IA34.
Abstract PR06: Empowering Latina breast cancer patients to make informed decisions about clinical trials: A multicommunication approach
Authors: Chalela Patricia , Muñoz Edgar , Gallion Kipling J. , Karnad Anand , Ramirez Amelie G. 
Published: October 2015

Abstract
Background: Without adequate minority representation in clinical trials, researchers cannot assess differential effects in outcomes or ensure the safety of therapies across a range of biological and genetic characteristics among groups, nor can they ensure generalizability of trial results. In response, this theory-based educational intervention aims to empower Latinas to make informed decisions about breast cancer clinical trials (BCCTs) by enhancing their knowledge, attitudes, skills and self-efficacy required to support discussion of BCCTs as a treatment option with doctors and family members.
Methods: This is a cohort study with random assignment of 112 Latina breast cancer patients eligible to participate in a BCCT at the Cancer Therapy & Research Center at the University of Texas Health Science Center at San Antonio. The intervention includes: participation in a culturally sensitive, individually tailored, computer-based BCCTs video; a bilingual, low-literacy booklet; and assistance from a patient navigator. The control includes usual care clinical trial information materials for eligible patients.
Results: Preliminary analysis showed that participants exposed to the intervention had significant higher awareness of clinical trials, particularly understanding their purpose and requirements, benefits and risks and their potential as an appropriate treatment for a serious disease, than participants in the usual care control group. In addition, patients in the intervention group showed significant changes between baseline and post intervention on stages of change compared to the control group. In the intervention group the percentage of women in preparation increased from 26.4% at baseline to 62.3% at post-intervention and the proportion of those in action rose from 35.8% to 67.9% at post-intervention.
Conclusion: Computer-based videos if specifically tailored to Latinos may be a cost-effective strategy to effectively address awareness, cultural and attitudinal barriers and decision making skills needed to make informed decisions about clinical trial participation.
The study is funded by the Susan G. Komen for the Cure (Award No. SAB08-00005) and the Cancer Therapy & Research Center (Grant No. P30 CA054174).
This abstract was also presented as Poster A5.
Citation Format: Patricia Chalela, Edgar Muñoz, Kipling J. Gallion, Anand Karnad, Amelie G. Ramirez. Empowering Latina breast cancer patients to make informed decisions about clinical trials: A multicommunication approach. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr PR06.
Abstract PR11: Loss of imprinting: Tying prenatal diet to the aggressive biology of triple-negative breast cancer
Authors: Desai Shraddha R. , Dietze Eric C. , Skaar David , Jirtle Randy L. , Seewaldt Victoria L. 
Published: October 2015

Abstract
Background: Genomic imprinting is an inherited form of parent-of-origin specific epigenetic gene regulation that is dysregulated by poor prenatal nutrition and environmental toxins. Loss of normal imprinting results in a functional diploid state and overexpression of the imprinted gene. KCNK9 encodes for TASK3, a pH-regulated potassium channel membrane protein that is overexpressed in 40% of breast cancers; however, KCNK9 gene amplification accounts for increased expression in &lt;10% of these breast cancers.
Methods and Results: Using patient samples we showed that KCNK9 has imprinted expression in breast tissue, and identified the differentially methylated region (DMR) controlling its imprint status. We showed that loss of methylation (LOM) at the DMR, coupled with biallelic expression of KCNK9, occurred in 75% of triple-negative breast cancers (TNBC), and that association between LOM and TNBC status was highly significant in African-Americans, but not in Caucasians. Functional studies show that loss of KCNK9 imprinting leads to an increase in mitochondrial membrane potential and apoptosis resistance. Further, expression of a dominant-negative TASK3 in TASK3-overexpressing TNBC cells resulted in decreased mitochondrial membrane potential, decreased glucose uptake and apoptosis-sensitivity; conversely, overexpression of TASK3 in mammary epithelial cells with baseline TASK3 protein expression, increased mitochondrial membrane potential, increased glucose uptake and promoted apoptosis-resistance.
Significance: This is the first identification of the KCNK9 DMR, and demonstration that its LOM is associated with increases in mitochondrial membrane potential, glucose uptake and apoptosis resistance. Thus, patients with TNBC and KCNK9 overexpression may benefit from known low toxicity TASK3 inhibitors for the prevention and treatment of breast cancer.
This abstract was also presented as Poster A79.
Citation Format: Shraddha R. Desai, Eric C. Dietze, David Skaar, Randy L. Jirtle, Victoria L. Seewaldt. Loss of imprinting: Tying prenatal diet to the aggressive biology of triple-negative breast cancer. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr PR11.
Abstract A04: Characterization of VPS34-IN1, a specific inhibitor of Vps34 reveals that the phosphatidylinositol 3-phosphate binding SGK3 protein kinase is regulated by class III PI-3 kinase
Authors: Bago Ruzica , Sommer Eeva , Malik Nazma , Munson Michael J. , Prescott Alan R. , Davies Paul , Natalia Shpiro , Ganley Ian G. , Alessi Dario R. 
Published: October 2015

Abstract
The Vps34 Class III phosphoinositide 3-kinase (PI3K) phosphorylates phosphatidylinositol (PtdIns) at endosomal membranes to generate PtdIns(3)P that regulates membrane trafficking processes via its ability to recruit a subset of proteins possessing PtdIns(3)P-binding PX and FYVE domains. Here we describe a highly selective and potent inhibitor of Vps34, termed VPS34-IN1, that inhibits Vps34 with 25 nM IC50 in vitro but does not significantly inhibit the activity of 340 protein kinases or 25 lipid kinases tested that include all isoforms of Class I as well as Class II PI3K. Administration of VPS34-IN1 to cells, induces a rapid dose dependent dispersal of GFP-2xFYVEHrs , a specific PtdIns(3)P binding probe, from endosome membranes. Previous studies revealed that serum and glucocorticoid regulated kinase-3 (SGK3) possesses a PtdIns(3)P binding N-terminal PX domain. SGK3 was first identified as a novel isoform of SGK1 that played a role in enabling the IL-3-dependent survival of hematopoietic cells. We explored whether SGK3, the only protein kinase known to interact specifically with PtdIns(3)P, might be controlled by Vps34. We utilised U2OS Flp/In inducible cell line to find that the mutations disrupting PtdIns(3)P-binding, ablated SGK3 kinase activity by suppressing phosphorylation of the T-loop (PDK1 site) and hydrophobic motif (mTOR site) residues. Also, treatment of cells with VPS34-IN1 induced a rapid ∼50-60% loss of SGK3 phosphorylation and activity. Furthermore, a Class I PI3K inhibitor (GDC-0941) that does not inhibit Vps34, suppressed SGK3 activity by ∼30-40%. Combining VPS34-IN1 and GDC-0941 reduced SGK3 activity ∼80-90% similar to treatment with an mTOR inhibitor (AZD8055). This data suggest that SGK3 phosphorylation and hence activity is mainly controlled by the activity of PI3K Class I and Class III and the regulation of SGK3 activity through Vps34 may provide a prosurvival signal and a resistance mechanism during the treatment of cancer cells with PI3K Class I inhibitors.
Citation Format: Ruzica Bago, Eeva Sommer, Nazma Malik, Michael J. Munson, Alan R. Prescott, Paul Davies, Shpiro Natalia, Ian G. Ganley, Dario R. Alessi. Characterization of VPS34-IN1, a specific inhibitor of Vps34 reveals that the phosphatidylinositol 3-phosphate binding SGK3 protein kinase is regulated by class III PI-3 kinase. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A04.
Abstract A12: Genetic and pharmacologic inhibition of EPHA2 promotes apoptosis in NSCLC
Authors: Amato Katherine , Wang Shan , Hastings Andrew , Youngblood Victoria , Santapuram Pranav , Chen Haiying , Cates Justin , Colvin Daniel , Ye Fei , Brantley-Sieders Dana , Cook Rebecca , Tan Li , Gray Nathanael , Chen Jin 
Published: October 2015

Abstract
Genome-wide analyses determined previously that the receptor tyrosine kinase (RTK) EPHA2 is commonly overexpressed in non-small cell lung cancers (NSCLCs). EPHA2 overexpression is associated with poor clinical outcomes; therefore, EPHA2 may represent a promising therapeutic target for patients with NSCLC. In support of this hypothesis, we have shown that targeted disruption of EPHA2 in a murine model of aggressive KRAS-mutant NSCLC impairs tumor growth. Knockdown of EPHA2 in human NSCLC cell lines reduced cell growth and viability, confirming the epithelial cell autonomous requirements for EPHA2 in NSCLCs. Targeting EPHA2 in NSCLCs decreased S6K1-mediated phosphorylation of cell death agonist BAD and induced apoptosis. Furthermore, an ATP-competitive EPHA2 RTK inhibitor, ALW-II-41-27, reduced the number of viable NSCLC cells in a time-dependent and dose-dependent manner in vitro and induced tumor regression in human NSCLC xenografts in vivo. Collectively, these data demonstrate a role for EPHA2 in the maintenance and progression of NSCLCs and provide evidence that ALW-II-41-27 effectively inhibits EPHA2-mediated tumor growth in preclinical models of NSCLC.
Citation Format: Katherine Amato, Shan Wang, Andrew Hastings, Victoria Youngblood, Pranav Santapuram, Haiying Chen, Justin Cates, Daniel Colvin, Fei Ye, Dana Brantley-Sieders, Rebecca Cook, Li Tan, Nathanael Gray, Jin Chen. Genetic and pharmacologic inhibition of EPHA2 promotes apoptosis in NSCLC. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A12.
Abstract A20: Insulin receptor signaling in mammary epithelial cells
Authors: Poloz Yekaterina , Sheikh Mariam Z. El , Petschnigg Julia , Groisman Bella , Kotlyar Max , Jurisica Igor , Stagljar Igor , Stambolic Vuk 
Published: October 2015

Abstract
Obesity has recently emerged as a major adverse factor in the prevalence and severity of many types of cancers, including breast cancer (BC). Obesity is often accompanied by hyperinsulinemia and the development of type 2 diabetes. Elevated circulating insulin levels are thought to mediate some of the adverse prognostic effects of obesity in BC (Goodwin et al., 2002). Insulin receptor (IR) is expressed in many human BCs and the activation of the IR/receptor tyrosine kinase signaling pathway is characteristic of most BCs (Mulligan et al., 2007). We hypothesize that ectopic expression of IR in BCs sensitizes BC cells to the action of insulin, leading to signaling events specific to epithelial cells, functionally distinct from the insulin responses in physiological insulin-target tissues. To further understand the role of IR in BC we have implemented the recently developed Mammalian Membrane Two Hybrid (MaMTH) (Petschnigg et al., 2014) screen to identify IR interactors in human mammary epithelial MCF10A cells. The ongoing screen has to date identified 99 IR protein-protein interactions (PPIs), 51 of which are insulin-dependent. Coimmunoprecipitation and shRNA knockdown analyses are being used to validate the PPIs and provide insight into the functional significance of IR associations for growth and proliferation of MCF10A cells. Ultimately, the epithelial cell IR-interactome is meant to provide an insight into the insulin contribution to the activation of RTK signaling in BC, and provide a roadmap for further exploration of IR signaling in cancer.
Citation Format: Yekaterina Poloz, Mariam Z. El Sheikh, Julia Petschnigg, Bella Groisman, Max Kotlyar, Igor Jurisica, Igor Stagljar, Vuk Stambolic. Insulin receptor signaling in mammary epithelial cells. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A20.