bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A66: A population-based study of racial/ethnic differences in survival among patients with endometrial cancer
Authors: Do ThuyQuynh Ngoc , Rodriguez Ana R. , Perez Norma 
Published: October 2015

Abstract
Endometrial cancer is the fourth most common cancer in women in the United States with more minority women being diagnosed with more aggressive cancer than non-Hispanic Whites. Asians and Hispanics are two of the fastest growing racial/ethnic groups in the United States, but they remain one of the most poorly understood minorities in terms of endometrial cancer. Numerous studies have shown that racial/ethnic variation in endometrial cancer can be associated with socioeconomic status, reproductive history and use of exogenous estrogens, the basis for racial/ethnic differences in survival is not as clearly defined. Using public use data from population-based Surveillance, Epidemiology and End Results (SEER) Program, we investigated racial/ethnic differences in cancer-specific survival of women diagnosed with endometrial cancer from 2000-2010. A total of 81,645 women were diagnosed with endometrial cancer. Survival differences were examined using Kaplan-Meier and Cox proportional hazards models. The median cancer-specific survival was 40 months with survival worst among non-Hispanic Blacks. Compared to non-Hispanic Whites, cancer-specific survival was 33% less for non-Hispanic blacks, 10% less for Hispanics and 9% less for Asians after adjustment. About 29% of the racial/ethnic disparity is explained by the absence of any treatment. Racial/ethnic differences in survival may partially explained by differences in treatment and stage diagnosis.
Citation Format: ThuyQuynh Ngoc Do, Ana R. Rodriguez, Norma Perez. A population-based study of racial/ethnic differences in survival among patients with endometrial 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 A66.
Abstract A71: Metagenomic studies of bacterial agents in prostate cancer racial disparities
Authors: Porter Corey M. , Yu Shu-Han , Sfanos Karen 
Published: October 2015

Abstract
Prostate cancer is the most common type of noncutaneous cancer diagnosed in men in the United States and the second leading cause of cancer-related death. African American (AA) men are more likely to be diagnosed with and are more than twice as likely to die from prostate cancer compared to white men. The reasons for this difference are complex. While socio-economic factors and access to care may have some influence, they cannot fully explain this disparity. There is evidence of genetic factors as well as environmental, diet, and lifestyle factors being important contributors to the higher rate of prostate cancer and prostate cancer deaths in AA men. Inflammation has emerged as a potential contributory factor in both the initiation and progression of prostate cancer. Furthermore, previous studies indicate that inflammation and the overexpression of genes involved in inflammatory pathways may be more prevalent in the prostates of AA men versus white men. We hypothesize that prostatic inflammation may contribute to the increase in prostate cancer mortality rates in AA men and that the stimulus for the overexpression of genes involved in inflammatory pathways may be infectious agents. Infections, including sexually transmitted infections (STIs), can cause inflammation and, indeed, our previous studies have detected the presence of microorganisms in prostate tissue. Past infection with an STI as well as increased numbers of sexual partners are both associated with an increased risk of prostate cancer. With the advent of “metagenomic” sequencing technologies (i.e., the determination of all microbial species present in a sample using next-generation sequencing), we are now able to fully determine the variety of microbial species present in a prostate tissue sample. As an initial strategy, we are currently utilizing 16S ribosomal RNA (rRNA) sequencing to comprehensively evaluate the presence of bacterial rRNA in post-surgical prostatectomy tissue specimens from both AA and white men. The results of these analyses will be compared to presence, type, and extent of inflammation in the corresponding surgical tissue specimen and we will be developing strategies to localize microorganism(s) of interest in prostate tissues. The results of our studies stand to provide a wealth of information regarding the prostate tumor microenvironment in AA men and will begin to allow for a mechanistic understanding of the role of inflammation and infections in this prostate cancer racial disparity.
Citation Format: Corey M. Porter, Shu-Han Yu, Karen Sfanos. Metagenomic studies of bacterial agents in prostate cancer 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 A71.
Abstract A81: Investigation of possible cell state dependent differential protein homeostasis mechanism(s)
Authors: Fon Gordon-Victor , Keller Chandler R. , Perlman David H. , Legesse-Miller Aster 
Published: October 2015

Abstract
Proteasome inhibition has been shown to be an important strategy for treating many types of cancer. Although proteasome inhibitors are effective at eradicating rapidly proliferating cancer cells, a subset of cancer cells enter quiescence and survive, contributing to tumor recurrence. Using primary human fibroblasts as a model system we have shown that quiescent cells have decreased reactive oxygen species levels and protein aggregates, and undergo apoptosis less frequently than proliferating cells in response to proteasome inhibition. However, the precise mechanism by which quiescent cells become resistant to proteasome inhibition remains largely unknown. Using a GFP-tagged proteasome reporter, we investigated mechanisms protecting quiescent cells from proteasome inhibition-induced apoptosis. We found that, in proliferating cells, proteasome inhibition by MG132 led to high levels of a GFP-tagged proteasome reporter with a visible ubiquitination pattern. In contrast, MG132 treatment of quiescent cells resulted in reduced levels of the ubiquitinated form of this reporter as observed by Western blot analysis. Interestingly, preliminary immunoprecipitation followed by mass-spectrometry analysis revealed none canonical ubiquitin modification on lysine 27 of the reporter in quiescent cells. These findings suggested that quiescent cells may have one or more alternative pathways preventing specific proteasome substrates accumulation in response to proteasome inhibition. Moreover, our data has shown that, upon proteasome inhibition, a GFP-tagged proteasome reporter was secreted into the condition medium. Secretion of cytoplasmic proteins in response to proteasome inhibition is one possible mechanism for reducing protein aggregation and cytotoxicity. Identification of regulatory mechanisms that are activated in quiescent cells in response to proteasome inhibition may help to suggest strategies for improving the effectiveness of proteasome inhibitors in cancer treatment.
Citation Format: Gordon-Victor Fon, Chandler R. Keller, David H. Perlman, Aster Legesse-Miller. Investigation of possible cell state dependent differential protein homeostasis mechanism(s). [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 A81.
Abstract A88: Medicaid expansion and access to care among breast cancer survivors
Authors: Tarazi Wafa W. 
Published: October 2015

Abstract
Background: Breast cancer survival is improving due to early detection of the disease and advances in treatment. In the United States, there are more than 3 million breast cancer survivors and approximately 240 thousand women diagnosed with the disease every year. To receive effective treatment, breast cancer survivors need to follow a treatment plan prescribed by their physicians. However, access to healthcare services remains a barrier to completing needed treatment. Medicaid expansion under the Affordable Care Act improves access to care among vulnerable populations, but almost half of the states opted out of the expansion.
Research Objective: We shed light on the potential effect of Medicaid expansion on access to care among breast cancer survivors by assessing inability to see a doctor due to cost before Medicaid expansion in non-expansion states versus expansion states.
Study Design: We use a logistic model (accounting for the weighted sample) and control for demographics, insurance status, and general health. We calculate the odd ratios of inability of survivors of breast cancer to see a doctor in the past year due to cost.
Population Studied: We use data from the Behavioral Risk Factor Surveillance (BRFSS) for the years 2009, 2010, and 2012, which are the only years containing data on cancer survivorship. The BRFSS is a nationally representative survey that collects information on self-reported preventive health practices and risk behaviors. The sample used for this study consists of women ages 40 to 64, in all 50 states and Washington D.C., and who were diagnosed with breast cancer (n = 3,223).
Results: Preliminary results suggest that breast cancer survivors in non-expansion states had significantly higher odds of being unable to see a doctor due to cost (OR = 1.63, 95% CI =1.10, 2.42).
Conclusions: Living in a state that expands Medicaid will be an advantage for low-income breast cancer survivors because it will improve their access to healthcare services. Existing disparities in access to care are likely to widen between survivors of breast cancer in non-expansion states and expansion states as a result of lack of affordable insurance coverage for low-income cancer survivors in non-expansion states.
Citation Format: Wafa W. Tarazi. Medicaid expansion and access to care among breast cancer survivors. [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 A88.
Abstract A93: Treatment and survival after head and neck cancer diagnosis by race in Louisiana's public hospital system
Authors: Peters Edward S. , Brashear Meghan M. , Ferguson Tekeda F. 
Published: October 2015

Abstract
Incidence and survival rates of head and neck cancer (HNC) vary by demographic characteristics, with significant disparities for men and African Americans. Depending on tumor site and stage, treatments options vary, albeit most often are a combination of surgery, radiotherapy and chemotherapy. The objectives of this study are to examine the effect of race on HNC treatment and survival in Louisiana public hospitals from 2000 to 2010. Cases of HNC were identified using Louisiana Health Care Services Division ICON database, which is composed of diagnostic and billing data for all patients undergoing primary treatment in the facilities. This data was subsequently linked to the Louisiana Tumor Registry (LTR) database. Survival rates by, race, sub-site and stage were calculated. Data were analyzed using SAS Version 9.3. Chi-square statistics were used to calculate difference in proportions while log adjusted mixed models were implemented to evaluate the impact of time to first course treatment between groups. Finally, Cox regression models were performed to estimate hazard ratios. A total of 1,168 HNC cases were diagnosed with from 2000 to 2010. Blacks initiated first course treatment after diagnosis 5.7 days (p=0.002) later than whites, adjusted for site, age and stage. While there was no age difference at the time of diagnosis, blacks were significantly more likely to be diagnosed with a late stage HNC compared to whites (p=0.003). In addition it does not appear that treatment type varied by race. Survival functions by stage and tumor site consistently demonstrated poorer survival among blacks compared to whites. The current study suggests that survival differences between blacks and whites in Louisiana are more likely to be influenced by time to treatment and stage rather than any specific treatment differences.
Citation Format: Edward S. Peters, Meghan M. Brashear, Tekeda F. Ferguson. Treatment and survival after head and neck cancer diagnosis by race in Louisiana's public hospital system. [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 A93.
Abstract B01: PEG3 DNA methylation and cervical intraepithelial neoplasia in African American and European American women
Authors: Vidal Adriana C. , Skaar David , Huang Zhiquing , Valea Fidel , Bentley Rex , Gradison Margaret , Yarnall Kimberly S. H. , Ford Anne , Overcash Francine , Grant Katherine , Murphy Susan K. , Hoyo Cathrine 
Published: October 2015

Abstract
Background: Epigenetic mechanisms are hypothesized to be etiologically involved in progression of cervical intraepithelial neoplasia (CIN) to invasive cervical cancer (ICC), although empirical data are lacking.
Methods: A total of 304 women were enrolled at the time of colposcopic evaluation following an abnormal liquid-based cytology screen. HPV was genotyped by HPV linear array. To ascertain the presence of CIN, the biopsies underwent pathologic review. DNA methylation was measured at differentially methylated regions (DMRs) regulating genomic imprinting of IGF2/H19 PEG1/MEST, KCNQ1OT1, MEG3, HYMAI, PEG10 and PEG3 imprinted domains, using Sequenom EpiTYPER assays. Logistic regression models were used to estimate odd ratios (ORs) and to evaluate the associations between HPV infection and DMR methylation, respectively.
Results: After accounting for age, HPV infection, parity, hormonal contraceptive use, and cigarette smoking, methylation differences at the PEG3 DMR were associated with a modest but significant higher risk of CIN2/3 (OR=1.08, 95%CI 1.02-1.18, p=0.022) in all women. This association remained significant in European American (OR=1.13, 95%CI 1.03-1.27, p=0.011), but not in African American women (OR=1.03, 95%CI 0.90-1.16, p=0.715). HPV infection was associated with altered PEG3 DMR methylation in both groups of women, an association that was also stronger in European Americans (β= -3.42, p=0.041), than in African Americans (β= -2.55, p=0.132). Though altered methylation at IGF2/H19 and PEG10 DMRs was associated with CIN1, no associations were observed with CIN2/3 lesions. No associations were found for PEG1/MEST, KCNQ1OT1, MEG3, and HYMAI DMRs.
Conclusions: Aberrant DNA methylation at the regulatory region of the PEG3 imprinted gene may increase susceptibility to CIN2/3; an association that may be stronger in European American women and which persisted after accounting for HPV infection. If confirmed in larger studies, these findings support the hypothesis that DNA methylation at PEG3 may represent a susceptibility locus that can be exploited to identify, from among a large number of abnormal colposcopy cases, those likely to progress to CIN or worse.
Citation Format: Adriana C. Vidal, David Skaar, Zhiquing Huang, Fidel Valea, Rex Bentley, Margaret Gradison, Kimberly S. H. Yarnall, Anne Ford, Francine Overcash, Katherine Grant, Susan K. Murphy, Cathrine Hoyo. PEG3 DNA methylation and cervical intraepithelial neoplasia in African American and European American women. [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 B01.
Abstract B09: Acculturation, behavioral factors, and family history of breast cancer among Mexican and Mexican-American women
Authors: Nodora Jesse , Cooper Renee , Martinez Maria Elena , Talavera Gregory , Thompson Patricia , Komenaka Ian , Bondy Melissa , Brewster Abenaa , Daneri-Navarro Adrian , Meza-Montenegro Maria Mercedes , Gutierrez-Millan Luis Enrique 
Published: October 2015

Abstract
Introduction: Incidence rates for breast cancer are higher among Mexican-American (MA) women in the US than women living in Mexico. Studies have shown higher prevalence of breast cancer risk factors in higher vs. lower acculturated Hispanic/Latina women in the US. We compared the prevalence for behavioral risk factors and family history of breast cancer by level of acculturation and country of residence in women of Mexican descent.
Methods: Data were collected from 1,201 recently diagnosed breast cancer patients living in Mexico (n=581) and MAs in the US (n=620). MA participants were categorized into three acculturation groups (Spanish dominant, bilingual and English dominant) according to responses to an 8-item language acculturation scale, while women living in Mexico were used as the reference group. Prevalence of behavioral risk factors and family history of breast cancer were compared among the acculturation groups adjusting for age at diagnosis and education level.
Results: In the final adjusted models, bilingual and English-dominant MAs were significantly more likely to have a body mass index &gt; 30 kg/m2, consume more than one alcoholic beverage a week, and report having a family history of breast cancer when compared to women living in Mexico. All three US acculturation groups were significantly more likely to have low total energy expenditure (&lt;533 kcal/day) than women in Mexico. English-dominant women were significantly less likely to smoke cigarettes than the Mexican comparison group.
Conclusions: Our findings on acculturation and distributions of behavioral risk factors and family history of breast cancer add to the growing body of evidence suggesting acculturation has both positive and negative impacts on health behavior in Hispanic/Latino populations living in the US. Interventions and public health policies may benefit from considering these relationships when targeting health programs and campaigns to Mexican-American and Mexican women.
Citation Format: Jesse Nodora, Renee Cooper, Maria Elena Martinez, Gregory Talavera, Patricia Thompson, Ian Komenaka, Melissa Bondy, Abenaa Brewster, Adrian Daneri-Navarro, Maria Mercedes Meza-Montenegro, Luis Enrique Gutierrez-Millan. Acculturation, behavioral factors, and family history of breast cancer among Mexican and Mexican-American women. [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 B09.
Abstract B22: Significance of ethnic-based disparities in prostate cancer risk and outcomes
Authors: Hayes Vanessa M. , Tindall Elizabeth A. , Bornman Riana 
Published: October 2015

Abstract
Ethnic-based disparities have been significantly associated with prostate cancer incidence, age and pathological/biochemical presentation, and mortality. Risk for these parameters are lowest in Asian men relative to men of European ancestry, while the highest in men of African ancestry, in particular African-Americans. Limited studies have, however, addressed clinical presentation and contributing factors within the context of Africa. We established the Southern African Prostate Cancer Study (SAPCS), a unique resource to investigate clinical presentation and risk factors within non-migrant Africans. Enrolling over 1000 men to date we report skewing towards significantly higher prostate specific antigen (PSA) levels in cases (83.0% present with a PSA≥20mg/L; median PSA=98.8mg/L) relative to men with no detectable PCa (18.5% present with a PSA≥20mg/L; median PSA=9.1mg/L). Compared with African-Americans, non-migrant Africans presented with significantly more aggressive disease defined by Gleason score &gt;7 (17% and 36%, respectively) and PSA≥20mg/L (17.2% and 83.2%, respectively), which is further exasperated in men from rural versus urban localities. To determine if the observed clinical presentation is driven by genetics and/or environmental factors, we investigated the power for the most significant genome-wide association study (GWAS) identified PCa risk alleles (n=46) as well as epidemiological measures to predict PCa status and/or disease outcomes within the SAPCS. While we show no evidence that previously defined PCa risk alleles predict disease status within Africa, we show associations with family history of cancer, diabetes, current sexual activity and erectile dysfunction, balding pattern, frequent aspirin usage and high PSA levels. We propose that the SAPCS provides a unique non-PSA tested resource to enhance our understanding that drives significant disparities in PCa associated with ethnic background.
Citation Format: Vanessa M. Hayes, Elizabeth A. Tindall, Riana Bornman. Significance of ethnic-based disparities in prostate cancer risk and outcomes. [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 B22.