bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A91: [Advocate Abstract:] Evidence-based, human-powered, patient-centric
Authors: Fuller Juliana 
Published: February 2019

Abstract
The Lymphoma Research Foundation (LRF) is the nation's largest nonprofit organization devoted exclusively to funding innovative lymphoma research and providing people with lymphoma and health care professionals with up-to-date information about this type of cancer. We are dedicated to funding biomedical research focused on the origins, treatment, and identification of a cure for lymphoma; to raising public awareness of the disease; and to providing support and services to people with lymphoma, their families, and caregivers. The Lymphoma Research Foundation has awarded more than $60 million in research grants to date. Guided by its world-leading Scientific Advisory Board (SAB), LRF has awarded over 340 evidence-based research grants since its inception, and with its unique commitment to young investigators, LRF continues to fund more than 40,000 research hours for early-career lymphoma scientists each year. LRF assists members of the lymphoma community by providing comprehensive, disease-specific programs and services, including Clinical Trials Information Services, Disease-Specific Publications and Websites, Focus on Lymphoma Mobile Apps, and In-person Workshops and Educational Forums.
Citation Format: Juliana Fuller. [Advocate Abstract:] Evidence-based, human-powered, patient-centric [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr A91.
Abstract B14: Promising effects of a culturally tailored pilot intervention to increase HPV vaccination uptake among female and male adolescents
Authors: Ma Grace X. , Tan Yin , Zhai Shumenghui , Siu Philip , Lai Sarah , Zhu Lin , Ilboudo Adeodat , Wang Min Qi 
Published: February 2019

Abstract
Background: HPV vaccination is recommended for female and male adolescents in the U.S. to prevent HPV-related cancer, yet the uptake remains suboptimal nationwide. Asian American female adolescents have the lowest HPV vaccine rates. Successful HPV vaccine depends heavily on parents' attitudes, perceptions, and willingness to have their adolescents vaccinated.
Objective: This study was designed to test the feasibility and outcomes of a provider-based culturally tailored intervention among Asian American parents and their eligible adolescents.
Methods: Asian American parents (n=120) who had adolescent girls and boys aged 11 to 18 (n=170) were recruited from a primary-care community health center. The primary outcome was first and second shots of HPV vaccination uptake 6 months following the intervention. Secondary outcomes included third shot of HPV vaccine at 6 months after the intervention for adolescents over the age of 12, increase in knowledge and belief in HPV vaccine, and engagement of adolescents in decision-making at post intervention.
Results: Among 170 adolescents, 68% of them received first and second shots of HPV vaccine (73% for girls vs 63% for boys). Among 81 adolescents over the age of 12, 63% of them received third shot (63% for girls vs 76% for boys). Parents' (n=120) knowledge and belief in HPV vaccine and engagement of adolescents in decision-making have significantly increased from baseline to post intervention (p&lt;0.001).
Conclusion: A culturally tailored pilot intervention in a clinical setting demonstrated promising effects, which can potentially yield significant increase in HPV vaccine uptake among Asian American and other underserved ethnic minority female and male adolescents to prevent cancer.
Citation Format: Grace X. Ma, Yin Tan, Shumenghui Zhai, Philip Siu, Sarah Lai, Lin Zhu, Adeodat Ilboudo, Min Qi Wang. Promising effects of a culturally tailored pilot intervention to increase HPV vaccination uptake among female and male adolescents [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr B14.
Abstract B36: Overexpression of PVT1 exons 4A, 4B, and 9 is characteristic of aggressive prostate cancer in males of African ancestry
Authors: Ilboudo Adeodat , Orunmuyi Akintunde , Bach Cuong , Ogunwobi Olorunseun 
Published: February 2019

Abstract
African ancestry is an established nonmodifiable risk factor for aggressive prostate cancer (PCa). The underlying biologic mechanisms are still unclear. We previously demonstrated that exon 9 of PVT1, a long nonprotein coding gene, may be involved in racial disparity in PCa. Using the most recent full-genome variability panel from the 1000 Genomes project, we recently identified a string of 75 SNPs in a 26-kb region spanning PVT1 exons 4A and 4B as consistently showing the highest level of genetic differentiation between African and non-African populations. However, the expression of PVT1 exons 4A, 4B, and 9 in prostate tissues of males of African ancestry (MoAA) has never been investigated. We aimed to determine the expression of PVT1 exons 4A, 4B, and 9 in histologically confirmed normal prostate (n=22), benign tumor prostate (n=35), and malignant tumor prostate tissue (n=28) samples obtained from males who had undergone prostatectomy or transrectal ultrasound-guided biopsy in Nigeria, a sub-Saharan Black African population. Tissues were collected in compliance with Institutional Review Board-approved protocols and histopathologic analysis was performed. RNA extraction, cDNA synthesis, and quantitative-PCR were performed to analyze mRNA expression of PVT1 exon 4A, PVT1 exon 4B, and PVT1 exon 9. There was a statistically significant difference in the expression of PVT1 exon 4A (F(2,61)=9.031, p=0.000); PVT1 exon 4B (F(2,61)=5.294, p=0.004); and PVT1 exon 9 (F(2,61)=3.700, p=0.029) between groups as determined by one-way ANOVA. Tukey post-hoc test revealed mean expression of PVT1 exon 4A = 3.15±0.49 (95% CI [2.13, 4.17]), PVT1 4B = 2.24±0.360 (CI [1.47, 2.95]), and PVT1 exon 9 = 1.644±0.95 (95% CI [1.265, 2.023]) in prostate tumor tissues. The results show an overexpression of PVT1 exon 4A, PVT1 exon 4B, and PVT1 exon 9 in malignant prostate tissue compared with nonmalignant tissue in MoAA. Also, using RNA ISH, PVT1 exon 9 was detected overexpressed primarily in the epithelium of prostate tumor tissue. In conclusion, the results also suggest that (1) the overexpression of PVT1 exon 4A, PVT1 exon 4B, and PVT1 exon 9 is characteristic of PCa in MoAA and (2) overexpression of PVT1 exon 4B and PVT1 exon 9 is specific for PCa, and that PVT1 exon 4B may distinguish between indolent and aggressive PCa in MoAA.
Citation Format: Adeodat Ilboudo, Akintunde Orunmuyi, Cuong Bach, Olorunseun Ogunwobi. Overexpression of PVT1 exons 4A, 4B, and 9 is characteristic of aggressive prostate cancer in males of African ancestry [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr B36.
Abstract B41: Transcriptome-wide profiling identifies novel differential genes associated with health disparity of prostate cancer
Authors: Ali Hamdy , Lung Pei-Yau , Gad Shaimaa , Sholl Andrew , Ali Hamed I. , Zhang Jinfeng , Elmageed Zakaria Y. Abd 
Published: February 2019

Abstract
Background: The incidence and mortality rates of prostate cancer (PCa) are twice as high in African American (AA) than in Caucasian American (CA) men. The molecular alterations associated with this racial disparity have not been fully elucidated. We aim to compare the expression profile of AA and CA men using microarray available data and paraffin-embedded tissues to identify the underlying molecular mechanisms contributing to the disproportionate of PCa among AA men.
Methods: Microarray data of 619 PCa patients, 412 AA and 207 CA, were retrieved from 11 data sets deposited in Gene Expression Omnibus (GEO) database. False discovery rates (FDR) were used for reporting differentially expressed genes and the differentially regulated pathways of these genes were predicted. To validate the microarray data, qPCR analyses were performed in forty paraffin-embedded samples collected from AA and CA men.
Results: Of 362 differential transcripts of array data, TIMP4, LTC4S, SHH, ADIPOQ, and ALOX12 were downregulated (p&lt;0.001) while KLK2, COX5A, AZGP1, AMD1, and ALDH1A3 were upregulated (p&lt;0.001) in PCa AA compared to CA men. qPCR analyses demonstrated that OAT, NKX3, LTC4S, APPL2, TPD52, ALDH, and AMD1 were significantly upregulated (p&lt;0.05) in AA regarding CA men with PCa. Overexpression of OAT, LTC4S, and TPD52 in AA cell lines was confirmed by Western blot analysis. These genes were involved in regulation of cell apoptosis, lipid metabolism, migration, angiogenesis, and response to reactive oxygen species. These transcripts are involved in focal adhesion, PI3K/Akt, EGFR, beta-catenin, and MAPK signaling pathways.
Conclusions: Gene expression data from PCa specimens and microarray suggest that dysregulation of transcripts in PCa of AA compared to CA men may underlie health disparity of PCa. These data might provide new insights into development of reliable diagnostic and prognostic markers of aggressive PCa.
Citation Format: Hamdy Ali, Pei-Yau Lung, Shaimaa Gad, Andrew Sholl, Hamed I. Ali, Jinfeng Zhang, Zakaria Y. Abd Elmageed. Transcriptome-wide profiling identifies novel differential genes associated with health disparity of prostate cancer [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr B41.
Abstract B44: Exosomes-associated miR-3128 and miR-3613 are dysregulated in African American men with prostate cancer and correlated with poor prognosis
Authors: Ali Hamdy , Sholl Andrew B. , Lung Pei-Yau , Bustamante Juan , Zhang Jinfeng , Coffield King S. , Elmageed Zakaria Y. Abd 
Published: February 2019

Abstract
Background: The mortality rate of prostate cancer (PCa) is two times higher in African American (AA) than in Caucasian American (CA) men. The molecular mechanisms underlying these discrepancies among AA men have yet to be fully elucidated. We aimed to evaluate the role of exosomes (Exo)-associated microRNAs (miR-3613 and miR-3128) as epigenetic determinant for the racial disparity of PCa patients.
Methods: Exosomes were isolated from the conditioned medium of MDA-PCa-2b and E006-A (AA-origin), and PC-3 and Du-145 (CA origin) cell lines. Exo-miRs profiling was performed to study the differential expression of AA vs CA in cells. The potential candidates were validated in Exo procured from plasma of forty AA and CA PCa patients and their aged-matched healthy subjects (n=20) using real-time PCR analysis. Circulating miRs were also determined in the plasma. The sensitivity and specificity of Exo-miRs were assessed using receiver operating characteristic (ROC) curve analysis.
Results: Exosomes-associated miR-3613 and miR-3128 were downregulated (P&lt;0.001) in PCa regarding normal subjects. These Exo-miRs were also downregulated (p&lt;0.01) in AA versus CA PCa. Exo-miR-3128 was able to discriminate PCa patients from normal subjects (AUC=0.70) and when age and Gleason score were combined to miR-3128, the discriminatory power was increased (AUC=1.00). Exo-miR-3128 was able to segregate AA from CA PCa (AUC=0.63) and when Exo-miR-3128 combined with -miR-3613, the power was increased (AUC=0.84, P&lt;0.01).
Conclusion: Our findings underline the role of exosomes-associated miRs in health disparity of PC. The differential expression of miRs in AA men demonstrates their potential role as prognostic markers in the context of racial disparity.
Citation Format: Hamdy Ali, Andrew B. Sholl, Pei-Yau Lung, Juan Bustamante, Jinfeng Zhang, King S. Coffield, Zakaria Y. Abd Elmageed. Exosomes-associated miR-3128 and miR-3613 are dysregulated in African American men with prostate cancer and correlated with poor prognosis [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr B44.
Abstract B50: The role of CXCL13-CXCR5 signaling in triple-negative breast cancer progression
Authors: Dill Courtney D. , Okoro Adaugo , Chen Dongquan , Lillard James W. 
Published: February 2019

Abstract
Triple-negative breast cancer (TNBC) is an aggressive cancer with poor prognosis and is difficult to treat. There is a major health disparity associated with TNBC; the number of fatalities associated with this disease is significantly higher in African American women compared to their Caucasian counterparts. The mechanisms behind these differences have not been entirely elucidated. There are no targeted therapies for TNBC; instead, standard therapy for this disease includes a combination of chemotherapeutic drugs: doxorubicin (DOX), paclitaxel (TAX), and/or cyclophosphamide (CTX). Even more troubling, the efficacy of standard TNBC therapies is marginal and patients eventually become resistant to this intervention. TNBC patients suffer from chemoresistance and metastasis and ultimately succumb to this disease. Understanding TNBC and its health disparity requires a better understanding of the race-specific differences in breast tumor biology, molecules leading to breast inflammation, and the mechanisms associated with TNBC chemoresistance. Chemokines and their receptors play a significant role in TNBC. Our laboratory was the first to show that CXCL13-CXCR5 signaling mediates prostate cancer cell growth, migration, invasion, and survival (1-3). We also demonstrated that CXCL13-CXCR5 signaling induces cancer progression signaling pathways PI3K, AKT, ERK, and Jun (1;4). These preliminary and published findings provide the rationale or scientific premise in support of our hypothesis that CXCL13-CXCR5 signaling promotes TNBC progression migration, invasion, proliferation, and chemoresistance. To determine whether CXCL13-CXCR5 signaling induces TNBC, the expression profile of CXCL13 and CXCR5 RNA, associated miRNAs, and cancer progression genes (epithelial mesenchymal transition [EMT] markers) will be correlated with disease-free and overall survival of TNBC patients in silico using RNA-seq datasets from the Sequence Read Archive (SRA). Fastq data set files were downloaded from SRA, checked for quality control, aligned, and normalized using open-source platforms. Hierarchical clustering, gene set enrichment analysis, disease progression analysis, and statistics were conducted using Partek Genomic Suite. Pathway enrichment analysis was conducted using Ingenuity Pathway Studios. Overall, CXCL13-CXCR5 signaling is implicated in TNBC progression, migration, and invasion.
Citation Format: Courtney D. Dill, Adaugo Okoro, Dongquan Chen, James W. Lillard, Jr.. The role of CXCL13-CXCR5 signaling in triple-negative breast cancer progression [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr B50.
Abstract B56: Regulation of CXCR5-CXCL13 signaling in prostate cancer etiologic disparities
Authors: Ohandjo Adaugo Queen , Dill Courtney , Dongquan Chen , Lillard James W. 
Published: February 2019

Abstract
The prevalence of prostate cancer (PCa) has been a worldwide burden. Cancer of the prostate is the most prevalent form of cancer in men and the second leading cause of death due to cancer in men in the United States and Europe. There is a major health disparity associated with PCa; the number of fatalities associated with this disease is more significant in African-American (AA) men than in European American (EA) men. Disease progression occurs despite hormone ablation therapy, which leads to a condition called castration-resistant prostate cancer (CRPC). Further complicating the matter, CRPC is a disease that affects a variety of patients differently, which can be problematic for physicians to provide standardized treatments with similar outcomes. AAs with CRPC can experience significantly lower rates of overall survival, faster rates of tumor progression, and poor responses to chemotherapy compared to EAs with this disease.
We previously showed that CXCL13:CXCR5 axis plays a role in PCa pathobiology and is also associated with PCa aggressiveness; CXCR5 signaling mediates PCa cell growth, migration, invasion, and docetaxel resistance. To further understand the implication of CXCR5-CXCL13 in CRPC, we characterize the reason behind the health disparities seen across groups of PCa patients by evaluating the difference in regulatory molecules (miRNAs) on CXCL13-CXCR5 signaling.
We found the expression profile of CXCL13 and CXCR5 RNA to be associated with miRNAs (miR-140-3p.1, miR-24-3p, miR-200c, miR-221-3p/22-3p, miR-192-5p/215-5p, miR-214-5p). Using RNA-seq datasets from the Gene Expression Omnibus (GEO) and the Sequence Read Archive (SRA), CXCL13 and CXCR5 RNA as well as associated miRNAs (miR-140-3p.1, miR-24-3p, miR-221-3p/22-3p, miR-192-5p/215-5p, and miR-214-5p) were defined by etiologic disparities among PCa patients; this correlation is different among AA men compared to EA men.
Understanding PCa and specifically CRPC disparities requires a better understanding of the race-specific differences in prostate tumor biology, molecules leading to prostate inflammation, and the mechanisms associated with CRPC therapeutic resistance and its aggressive phenotype.
Citation Format: Adaugo Queen Ohandjo, Courtney Dill, Chen Dongquan, James W. Lillard, Jr.. Regulation of CXCR5-CXCL13 signaling in prostate cancer etiologic disparities [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr B56.
Abstract B60: Nanoparticles directed to IL13RA2 for targeted therapy of basal-like breast cancer
Authors: Wong Chen Khuan , Zhang Sandy , Reinhard Bjorn , Thiagalingam Sam 
Published: February 2019

Abstract
Basal-like breast cancer (BLBC) is among the most aggressive forms of breast cancer and is highly prevalent in young African-American women. It is nonresponsive to targeted hormonal therapy due to the lack of estrogen receptor, progesterone receptor, and HER2 expression. To identify effective targetable biomarkers for BLBC, we performed gene expression profiling of a breast cancer progression model system representing the different stages of the cancer. We discovered in metastatic BLBC cells high expression of IL13RA2, a cell surface receptor, which corresponded to poor survival in patients with high-grade tumors based on in silico meta-analysis of publicly available microarray datasets. To assess its functional roles in breast cancer progression, we knocked down IL13RA2 in BLBC cells and found that it is essential for lung colonization and tumorigenesis in vivo. Next, to establish the clinical utility of this candidate biomarker to inform prognosis, we performed immunohistochemical analysis of breast cancer tissue microarrays and found that IL13RA2 is overexpressed in a subset of lymph node metastases, hence supporting its role as a metastasis promoter. Based on these observations, we hypothesize that IL13RA2 may serve as a biomarker for disease stage and an active target for nanoparticle-mediated delivery of therapeutic agents to eradicate metastatic BLBC cells. We are in the process of conjugating gold nanoparticles with monoclonal antibodies to assess their binding specificity to IL13RA2-overexpressing cells in vitro and in vivo. Ultimately, these nanoparticles could be used to monitor disease spread as well as to actively target metastatic BLBC cells overexpressing IL13RA2 to block metastasis.
Citation Format: Chen Khuan Wong, Sandy Zhang, Bjorn Reinhard, Sam Thiagalingam. Nanoparticles directed to IL13RA2 for targeted therapy of basal-like breast cancer [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr B60.
Abstract B64: Race and prostate cancer: miRNA isoforms and tRNA fragments could hold some of the answers
Authors: Magee Rogan G. , Telonis Aristeidis G. , Loher Phillipe , Londin Eric , Rigoutsos Isidore 
Published: February 2019

Abstract
Prostate cancer is the most frequently occurring cancer in men. Compared to White (Wh) men, Black/African American (B/Aa) men exhibit higher mortality and higher incidence rates of prostate cancer. This difference remains even after modifiable factors are taken into account, which suggests an underlying cause. Recent studies greatly improved our understanding of the biochemistry of prostate cancer. Nonetheless, many open questions remain, especially with regard to the molecular underpinnings of the observed race disparities.
In this study, we analyzed 526 transcriptomic datasets from prostate adenocarcinoma (PRAD) patients. We obtained the data from The Cancer Genome Atlas (TCGA) repository. We focused on two categories of noncoding RNAs that regulate messenger RNA (mRNA) and protein abundance: (1) microRNAs (miRNAs) and their isoforms (isomiRs) and (2) tRNA-derived fragments (tRFs). Both tRFs and isomiRs regulate mRNAs and their proteins through the RNA induced silencing complex (RISC). Furthermore, tRFs have a number of other regulatory roles in healthy and diseased cells, including direct physical interactions with ribosomal proteins and initiation factors. Notably, we have demonstrated and reported previously that isomiRs and tRFs are constitutive and transcribed in a manner that depends strongly on a person's gender, race, and population origin, as well as on tissue type, tissue state, and disease type/subtype.
Our analyses of the TCGA PRAD datasets revealed that both isomiRs and tRFs are disrupted in PRAD. By extension, the regulatory networks that link isomiRs and tRFs to mRNAs are also disrupted. We also uncovered transcriptomic differences and differential regulatory relationships that are aligned with patient race. Moreover, we found that the molecular differences between B/Aa and Wh PRAD patients extend to normal prostate tissue as well. These findings mirror earlier results that we obtained from both healthy individuals and cancer patients.
The race-dependent regulatory profiles highlight differences in the underlying biology in B/Aa and Wh individuals that have yet to be explored. For example, the corresponding molecules could potentially be leveraged as novel biomarkers or alternative therapeutic targets. This study represents the first characterization of isomiRs and tRFs in a large cohort of PRAD patients.
Citation Format: Rogan G. Magee, Aristeidis G. Telonis, Phillipe Loher, Eric Londin, Isidore Rigoutsos. Race and prostate cancer: miRNA isoforms and tRNA fragments could hold some of the answers [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr B64.