bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract C33: Cardiovascular health among black and white breast cancer patients initiating aromatase inhibitor therapy
Authors: Gallicchio Lisa , Calhoun Carla , Helzlsouer Kathy J. 
Published: May 2015

Abstract
Purpose: Breast cancer patients may have poor outcomes due to the toxic effects of breast cancer treatments in the presence of co-morbid conditions. Thus, it is hypothesized that racial disparities in breast cancer outcomes are, in part, related to a higher prevalence of certain co-morbid conditions prior to treatment among black compared to white women. As a first step to addressing this hypothesis, this analysis examined racial differences in cardiovascular health and co-morbid conditions among breast cancer survivors initiating aromatase inhibitor (AI) therapy.
Methods: Baseline data were analyzed from 49 white and 29 black women participating in an ongoing cohort study of the cardiovascular health of breast cancer patients over the first year of AI therapy. Prior to initiating AI therapy, women enrolling in the study completed a questionnaire and had a cardiovascular health evaluation that included a carotid intimal medial thickness (cIMT) ultrasound. Cardiovascular disease risk percentile was assigned using the cIMT data; category assignment was based on published age- and race-specific percentile risk categories from the Atherosclerosis Risk in Communities (ARIC) study.
Results: The white breast cancer patients were slightly older than their black counterparts (mean 62.5 years versus 61.5 years; p=0.6) and less likely to have had chemotherapy (32.6% versus 42.3%; p=0.4). After adjusting for age, the black breast cancer patients were more likely than their white counterparts to report having been diagnosed with hypertension (odds ratio (OR) 6.7; 95% confidence interval (CI) 2.0, 22.9) and diabetes (OR 2.5; 95% CI 0.6, 10.2). However, mean cIMT (mean 0.65 mm versus 0.64; p = 0.6) and the distribution of patients in the cardiovascular disease risk percentile categories did not differ significantly by race (p=0.6).
Conclusions: Black breast cancer survivors have a higher prevalence of cardiovascular co-morbid conditions compared to their white counterparts. The presence of these cardiovascular co-morbidities at diagnosis may affect treatment choices if continued follow-up demonstrates an adverse impact of estrogen deprivation therapy on cardiovascular outcomes. Enrollment into this study is currently ongoing. This research was supported by a Susan G. Komen for the Cure Health Disparities Career Catalyst grant.
Citation Format: Lisa Gallicchio, Carla Calhoun, Kathy J. Helzlsouer. Cardiovascular health among black and white breast cancer patients initiating aromatase inhibitor therapy. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C33. doi:10.1158/1538-7755.DISP13-C33
Abstract C40: Investigating histone deacetylase 3 expression in ovarian cancer cells
Authors: Huya-Kouadio Dembi O. , Khabele Dineo , Saskowski Jeanette L. , Wilson Andrew J. 
Published: May 2015

Abstract
Ovarian cancer is the leading cause of gynecologic death in the United States (1). Newer treatments are being developed to target specific proteins in order to inhibit cancer growth without affecting healthy cells. Histone deacetylase (HDAC) inhibitors have shown promise in this regard. HDAC3 inhibitors cause apoptosis, cell cycle arrest, inhibition of growth and angiogenesis with limited effects on healthy cells (2). Key functions of HDAC3 are the formation of DNA into heterochromatin and the regulation of proapoptotic genes (2). Khabele et al demonstrated that class I HDACs are overexpressed in ovarian cancers. Thus, if HDAC3 is linked to apoptosis, then treating ovarian cancer cell with chemotherapeutic drugs such as cisplatin should increase its translocation to the cytoplasm. We also believe that the overexpression of HDAC3 in ovarian cancer cells modulate the cells response to cisplatin. In order to support our hypothesis, ovarian cancer cells, SKOV3, were transfected with an HDAC3-Myc tagged constructs to allow visualization of HDAC3 in the cells. Before the immunofluorescence was performed, the transfected cells were characterized using Western blot and SRB cell viability assays to assure that their response to cisplatin did not differ from the parental cell line. Our results show that HDAC3 expression is decreased in ovarian cancer cells treated with cisplatin and that in the presence of cisplatin, there is an increase in HDAC3 translocation to the cytoplasm. Fractionation data for this research were omitted because the protocol needed to be optimized. Another limitation of this study is the limited knowledge on HDAC3 translocation mechanism to the cytoplasm. In conclusion, the downregulation and cytoplasmic translocation of HDAC3 are potential novel mechanism of apoptosis in ovarian cancer cell response to cisplatin .
Citation Format: Dembi O. Huya-Kouadio, Dineo Khabele, Jeanette L. Saskowski, Andrew J. Wilson. Investigating histone deacetylase 3 expression in ovarian cancer cells. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C40. doi:10.1158/1538-7755.DISP13-C40
Abstract C48: Racial-specific differences in breast cancer treatment
Authors: Barley Brittany N. , Horton Sara , Dunmore-Griffith Jacqueline , Ricks-Santi Luisel 
Published: May 2015

Abstract
Although the incidence of breast cancer (BCa) among Blacks is lower than Whites, health outcomes are dire, as the cancer is often diagnosed at a higher grade and more advanced stage. Additionally, in Blacks, BCa tends to be more aggressive, as triple negative breast cancer is more prevalent, is more lethal and less treatable than the cognate disease in Whites. In addition to the high prevalence of aggressive disease in Blacks, we hypothesized that recurrence and survival outcomes may also be due to treatment differences between populations. Therefore, the objective of this study was to determine if there were racial-specific treatment differences in BCa cases in Washington, DC (N=5932) between 2000 and 2010. Using chi-square and regression analysis, we demonstrate that after controlling for age, stage, grade, ER, PR, HER2, and BCa molecular subtype, no significant racial-specific differences in surgery or radiation were found. However, overall, Blacks and Hispanics were more likely to receive chemotherapy for BCa when compared to whites (OR for Blacks: 3.57, 95% CI: 1.66-8.33 and OR for Hispanics: 4.76, 95% CI: 1.33-0.16.67). Among those with Stage 3 and 4 BCa, Blacks and Hispanics were still more likely to receive chemotherapy (OR for Blacks: 1.93, 95% CI: 1.16-3.20 and OR for Hispanics: 3.95, 95% CI: 1.03-15.15). Differences in hormonal therapy were also found with Blacks and Hispanics being more likely to receive hormone therapy for ER and/or PR positive disease (OR for Blacks: 3.12, 95% CI: 1.27-7.69 and OR for Hispanics: 8.33, 95% CI: 2.27-33.33). Studies that identify driving factors behind these racial-related treatment differences are warranted.
Citation Format: Brittany N. Barley, Sara Horton, Jacqueline Dunmore-Griffith, Luisel Ricks-Santi. Racial-specific differences in breast cancer treatment. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C48. doi:10.1158/1538-7755.DISP13-C48
Abstract C59: Variable distribution of HIF-1α in human normal and carcinoma tissue, immortal cell lines, and effects of hyperoxia / hypoxia on HIF-1α deficient cells
Authors: Mazzio Elizabeth , Soliman Karam FA 
Published: May 2015

Abstract
Inadequate access to healthcare can lead to greater mortality rates from a delay in cancer diagnosis. It is believe that over time, the hypoxic microenvironment of solid tumors can elicit an elevation of HIF-1α, its translocation to the nucleus and targeted effects on the hypoxic response element (HRE) - initiating invasive metastasis. While this is a universally held supposition, “HIF-1α negative tumors” can also display aggressive pathology and poor clinical outcome. Given inconsistencies in the literature, we analyze public data sets for baseline HIF-1α gene expression amongst 329 human tissues (168 cancer, 161 normal) and NCI60 tumor cell lines. The data show little to no differences between a number of tumor and normal tissue samples, with some exceptions such as the case of bronchial epithelial tissue, exacerbated in respective cancer tissue. The data show extreme variation in HIF-1α across individuals with similar human cancers (below L.O.D. - 60% of GAPDH) with comparable patterns across tissue specific immortal cell lines (1% - 70% of GAPDH). Moreover, the effects of hyperoxia ∼91% O2, hypoxia ∼2.5% O2 versus normoxia ∼21% CO2/ 5% CO2/atm on a HIF-1α deficient malignant neuroblastoma cell line (N2a) were explored using Agilent genomic 4 x 44 k arrays. Hyperoxia evoked a rise in mRNA for 42 mitochondrial OXPHOS genes, DNA/base excision repair, protein synthesis, transcription, cytoskeletal proteins, G-protein signaling and ubiquitin-mediated proteolysis. On the other hand, hypoxia triggered primarily upregulation of chromatin remodeling events such as LDS's, histone-clusters H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST co-repressor. In HIF-1α deficient tumor cells, a decline in O2 initiates epigenetic changes that parallel elevation of VEGF and ubiquitin proteolysis, albeit not related to HIF-1 α. Future research will be required to corroborate similar findings in other HIF-1α deficient models.
Citation Format: Elizabeth Mazzio, Karam FA Soliman. Variable distribution of HIF-1α in human normal and carcinoma tissue, immortal cell lines, and effects of hyperoxia / hypoxia on HIF-1α deficient cells. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C59. doi:10.1158/1538-7755.DISP13-C59
Abstract C70: ABCD3 expression in prostate and breast tumors
Authors: Reams R. Renee , Jones Jacqueline D. , Osborne Daniel , Wang Honghe , Yates Clayton C. 
Published: May 2015

Abstract
Background: In a previous study, we identified the ABCD3 gene as important in aggressive prostate tumors. The ABCD3 gene is a member of the ABC (ATP-Binding Cassette) family. The ABC gene family give instructions for making transporter proteins that carry many types of molecules, such as fats, sugars, protein building blocks (amino acids) and drugs, across cell membranes and is known to play a role in chemoresistance is some cancers.
Purpose: Little is known about role of ABCD3 in prostate cancer, hence in the present study we assessed the expression of ABCD3 in normal and malignant prostate tissue (without regard to racial ethnicity) and determined correlations between ABCD3 expression and clinicopathologic characteristics.
Methods: Clinically annotated duplicate core tissue high-density prostate adenocarcinoma tissue microarray of 92 cases of adenocarcinoma, 2 prostate transitional cell carcinoma, 12 prostate adjacent normal tissue and 8 normal prostate tissue were stained with a monoclonal antibody against ABCD3 and scored for percentage of visible staining.
Results: Increased ABCD3 expression correlated with increasing Gleason score (p=0.0094), age (p=0.0014) and pathology grade (p=0.0007). Interestingly, we also observed that ABCD3 expression was elevated to varying degrees in other types of cancers, breast (stage II a), brain, cervical, head and neck, kidney and pancreatic.
Conclusions: We postulate that ABCD3 may be a putative prognostic biomarker that discriminates between indolent and aggressive cancers, albeit ABCD3 function in cancer progression is still under investigation.
Citation Format: R. Renee Reams, Jacqueline D. Jones, Daniel Osborne, Honghe Wang, Clayton C. Yates, III. ABCD3 expression in prostate and breast tumors. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C70. doi:10.1158/1538-7755.DISP13-C70
Abstract PL01-03: Vitamin D deficiency and prostate cancer in men with African ancestry
Authors: Nonn Larisa 
Published: May 2015

Abstract
African-American men are disproportionally affected by prostate cancer in that African-American men are not only at increased risk of prostate cancer compared to American men of European descent, but also are at the highest risk of aggressive prostate cancer and death from prostate cancer. As well vitamin D3 deficiency is rampant in the African-American population. There is a biological component to this deficiency because sun-induced vitamin D3 synthesis in the skin is significantly reduced in melanin-rich pigmented skin. Consequently, about two thirds of African-American men are vitamin D3 deficient compared to about 20% of men of European descent. It is important to maintain a healthy vitamin D3 status because vitamin D3 deficiency increases the risk of prostate cancer mortality. Our group has examined vitamin D3 concentrations, metabolism and mediators in prostate tissue and cells of a racially diverse group of patients to discern differences in African-American men.
Citation Format: Larisa Nonn. Vitamin D deficiency and prostate cancer in men with African ancestry. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr PL01-03. doi:10.1158/1538-7755.DISP13-PL01-03
Abstract PL02-03: Overcoming cultural and geographic barriers to participation in clinical trials among Native Hawaiians
Authors: Berenberg Jeffrey L. 
Published: May 2015

Abstract
The Native Hawaiian population of Hawaii has disproportionately high cancer incidence and mortality rates. Native Hawaiian women with breast cancer present at an advanced stage and have death rates that are 52 % above the state average. Prostate cancer among Native Hawaiian men is diagnosed at more advanced stage. Native Hawaiian participation in cancer clinical trials was historically low. Reasons for this were varied including access, health literacy, lack of primary and referring physician awareness/time constraints and cultural barriers. Since the establishment of the University of Hawaii Minority Based Clinical Oncology Program (UHMBCCOP) participation in cancer clinical trials has definitely increased. MBCCOP provided clinical trial promotion, increased access and clinical trial support for a group of hospital and office based oncologists across the islands of Oahu and Kauai have all contributed to the increase. Education programs in Hawaii by multiple organizations, in particular, Imi Hale, the Native Hawaiian Cancer Network Program have enhanced knowledge of cancer and clinical trials in the Native Hawaiian community. Imi Hale's emphasis has focused on community based patient training, patient navigation and referring physician cancer clinical trial training. In fact, a recent program was recently initiated in conjunction with Education Network to Advance Clinical Trials (ENNACT) and Queens Medical Center. Review of Native Hawaiian participation in both cancer prevention and treatment trials through the UHMBCCOP over the last 20 years shows a significant gender difference with more women participating in both prevention and treatment trials. The reasons for this are not well understood but are under investigation. In summary, increased focused access and community based education have improved Native Hawaiian participation in cancer clinical trials but challenges persist including gender disparities in enrollment onto clinical trials and lack of access outside of Oahu and Kauai islands.
Citation Format: Jeffrey L. Berenberg. Overcoming cultural and geographic barriers to participation in clinical trials among Native Hawaiians. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr PL02-03. doi:10.1158/1538-7755.DISP13-PL02-03
Abstract SS02-02: A long walk from FGFR2 alternative splicing to cancer progression
Authors: Somarelli Jason A. , Somarelli Jason A. , Schaeffer Daneen , Schaeffer Daneen , Marengo Mathew S. , Marengo Mathew S. , Bepler Tristan , Bepler Tristan , Rouse Douglas , Buckley Anne F. , Epstein Jonathan I. , Armstrong Andrew J. , Garcia-Blanco Mariano A. , Garcia-Blanco Mariano A. 
Published: May 2015

Abstract
Previously, our group developed fluorescence-based alternative splicing reporters of epithelial plasticity to visualize phenotypic transitions in real time in vivo (Oltean et al., 2008; Oltean et al., 2006; Somarelli et al., 2013). We reasoned that our mesenchymal-epithelial transition (MET) reporters could be extremely useful to test the hypothesis that MET is a modulator of metastatic colonization in undifferentiated, sarcomatoid-like cancers. Along these lines, we generated a lineage-tracing reporter based on combined transcription and alternative splicing regulatory elements to measure the frequency of MET-like events during tumor growth and metastasis in the post-EMT Dunning rat AT3 model of prostate cancer. In a parallel set of experiments, we also used the combinatorial control strategy to drive a suicide reporter that kills cells undergoing MET to test the hypothesis that MET is required for metastatic colonization in undifferentiated, mesenchymal-like cancers. The combinatorial use of both transcription and alternative splicing regulation provided exquisite cell-type discrimination in the expression of enzymes, such as the Cre recombinase and Diphtheria A (DipA) toxin. Using the lineage tracing reporter system, we were able to quantify, for the first time, overall frequencies of MET during primary tumor and metastatic growth. Remarkably, we observed that the frequency of MET within primary tumors and metastatic nodules was not significantly different, with very low rates of MET taking place during the growth of tumors and metastases. Moreover, targeted killing of cells undergoing MET did not reduce the number of macrometastatic colonies in the lungs. This work demonstrates the ability of tumors to metastasize efficiently without the need for MET, and we suggest that this may be similar to the behavior of highly aggressive prostate carcinosarcomas or undifferentiated carcinomas. Using this system we will describe new experiments that will address differential behavior in different types of prostate cancer.
Citation Format: Jason A. Somarelli, Jason A. Somarelli, Daneen Schaeffer, Daneen Schaeffer, Mathew S. Marengo, Mathew S. Marengo, Tristan Bepler, Tristan Bepler, Douglas Rouse, Anne F. Buckley, Jonathan I. Epstein, Andrew J. Armstrong, Mariano A. Garcia-Blanco, Mariano A. Garcia-Blanco. A long walk from FGFR2 alternative splicing to cancer progression. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr SS02-02. doi:10.1158/1538-7755.DISP13-SS02-02
Adenovirus Improves the Efficacy of Adoptive T-cell Therapy by Recruiting Immune Cells to and Promoting Their Activity at the Tumor
Authors: Tähtinen Siri , Grönberg-Vähä-Koskela Susanna , Lumen Dave , Merisalo-Soikkeli Maiju , Siurala Mikko , Airaksinen Anu J. , Vähä-Koskela Markus , Hemminki Akseli 
Published: May 2015

Abstract
Despite the rapid progress in the development of novel adoptive T-cell therapies, the clinical benefits in treatment of established tumors have remained modest. Several immune evasion mechanisms hinder T-cell entry into tumors and their activity within the tumor. Of note, oncolytic adenoviruses are intrinsically immunogenic due to inherent pathogen-associated molecular patterns. Here, we studied the capacity of adenovirus to overcome resistance of chicken ovalbumin-expressing B16.OVA murine melanoma tumors to adoptive ovalbumin-specific CD8+ T-cell (OT-I) therapy. Following intraperitoneal transfer of polyclonally activated OT-I lymphocytes, control of tumor growth was superior in mice given intratumoral adenovirus compared with control mice, even in the absence of oncolytic virus replication. Preexisting antiviral immunity against serotype 5 did not hinder the therapeutic efficacy of the combination treatment. Intratumoral adenovirus injection was associated with an increase in proinflammatory cytokines, CD45+ leukocytes, CD8+ lymphocytes, and F4/80+ macrophages, suggesting enhanced tumor immunogenicity. The proinflammatory effects of adenovirus on the tumor microenvironment led to expression of costimulatory signals on CD11c+ antigen-presenting cells and subsequent activation of T cells, thus breaking the tumor-induced peripheral tolerance. An increased number of CD8+ T cells specific for endogenous tumor antigens TRP-2 and gp100 was detected in combination-treated mice, indicating epitope spreading. Moreover, the majority of virus/T-cell–treated mice rejected the challenge of parental B16.F10 tumors, suggesting that systemic antitumor immunity was induced. In summary, we provide proof-of-mechanism data on combining adoptive T-cell therapy and adenovirotherapy for the treatment of cancer. Cancer Immunol Res; 3(8); 915–25. ©2015 AACR.
Incidence, Cause, and Comparative Frequency of Sudden Cardiac Death in National Collegiate Athletic Association Athletes
Authors: Harmon Kimberly G. , Asif Irfan M. , Maleszewski Joseph J. , Owens David S. , Prutkin Jordan M. , Salerno Jack C. , Zigman Monica L. , Ellenbogen Rachel , Rao Ashwin L. , Ackerman Michael J. , Drezner Jonathan A. 
Published: May 2015

Background—
The incidence and cause of sudden cardiac death (SCD) in athletes is debated with hypertrophic cardiomyopathy often reported as the most common cause.

Methods and Results—

A database of all National Collegiate Athletic Association deaths (2003–2013) was developed. Additional information and autopsy reports were obtained when possible. Cause of death was adjudicated by an expert panel. There were 4 242 519 athlete-years (AY) and 514 total student athlete deaths. Accidents were the most common cause of death (257, 50%, 1:16 508 AY) followed by medical causes (147, 29%, 1:28 861 AY). The most common medical cause of death was SCD (79, 15%, 1:53 703 AY). Males were at higher risk than females 1:37 790 AY versus 1:121 593 AY (incidence rate ratio, 3.2; 95% confidence interval, 1.9–5.5;
P
<0.00001), and black athletes were at higher risk than white athletes 1:21491 AY versus 1:68 354 AY (incidence rate ratio, 3.2; 95% confidence interval, 1.9–5.2;
P
<0.00001). The incidence of SCD in Division 1 male basketball athletes was 1:5200 AY. The most common findings at autopsy were autopsy-negative sudden unexplained death in 16 (25%), and definitive evidence for hypertrophic cardiomyopathy was seen in 5 (8%). Media reports identified more deaths in higher divisions (87%, 61%, and 44%), whereas the percentages from the internal database did not vary (87%, 83%, and 89%). Insurance claims identified only 11% of SCDs.

Conclusions—
The rate of SCD in National Collegiate Athletic Association athletes is high, with males, black athletes, and basketball players at substantially higher risk. The most common finding at autopsy is autopsy-negative sudden unexplained death. Media reports are more likely to capture high-profile deaths, and insurance claims are not a reliable method for case identification.