bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract C24: An integrative review of psychosocial concerns among young African American breast cancer survivors
Authors: Nolan Timiya S. , Frank Jennifer , Gisiger-Camata Silvia , Meneses Karen 
Published: May 2016

Abstract
Background: African American women are more likely to be diagnosed with breast cancer at an early age, more likely to experience morbidity after treatment, and disparities in survivorship. While psychosocial well-being is well known among breast cancer survivors, data are few regarding minorities such as African Americans, particularly those who are young.
Objective: This integrative review examines psychosocial concerns in survivorship among young African American breast cancer survivors (YAABCS) using a holistic quality of life framework.
Methods: Pubmed, CINHAL, and Scopus were searched for articles exploring psychological or social well-being in YAABCS.
Results: The search yielded 264 articles. Thirty-six articles were retrieved and reviewed for relevance. Of these, 14 articles were selected based on inclusion/exclusion criteria. Themes of YAABCS psychosocial concerns were sexuality, mood, social support, and spirituality.
Conclusions: The review demonstrated need for further research in YAABCS quality of life to adapt a more fitting quality of life model and to develop culturally-appropriate survivorship interventions.
Implications for Practice: Clinicians, researchers, and YAABCS must partner to increase knowledge of the multidimensional survivorship of YAABCS. With knowledge, we may be able to decrease health disparities among YAABCS.
The project was funded by an American Cancer Society Doctoral Degree in Nursing Scholarship, Jonas Nurse Leadership Scholarship, and Gladys F. Colvin Doctoral fellowship. Additional support received from a Komen Graduate Training in Disparities Research Award.
Citation Format: Timiya S. Nolan, Jennifer Frank, Silvia Gisiger-Camata, Karen Meneses. An integrative review of psychosocial concerns among young African American breast cancer survivors. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C24.
Abstract C29: Racial disparities in endometrial cancer epidemiology and mortality-to-incidence ratios in South Carolina
Authors: Babatunde Oluwole Adeyemi , Adams Swann Arp , Eberth Jan M. , Wirth Michael D. , Choi Seul Ki , Hebert James R. 
Published: May 2016

Abstract
Background: Endometrial cancer (EC) exhibit striking racial disparities with higher mortality in African Americans (AA) compared to European Americans (EA). The mortality-to-incidence rate ratio (MIR) gives a population based measure for survival which accounts for incidence. The objective of this study was to map EC MIRs by race for eight health regions within South Carolina (SC) and chart EC incidence by race and grade across the four cancer stages.
Methods: Data on EC incidence and deaths were obtained from the South Carolina Central Cancer Registry, and Vital Registry respectively to construct MIRs. ArcGIS 10.1 software was used to map EC MIRs by race for eight health regions within South Carolina. Four classes of MIR were derived using the national MIR for EC among EAs as the reference.
Results: When stratified by tumor stage, AAs had higher levels of poorly differentiated tumors across all stages. The incidence and mortality were consistently higher among AAs. Striking racial differences were observed with incidence and mortality consistently higher among AAs. In all eight health regions, AAs were in the highest MIR category. By contrast, EA MIRs were more evenly represented over the 4 classes.
Conclusions: The MIR proved useful for identifying disparities in EC incidence, mortality and virulence among AA and EA women in SC. Cancer surveillance programs may use the MIR to monitor disparities across racial/ethnic groups and geographic regions going forward. MIRs have the potential to serve as an indicator of the long-term success of cancer surveillance programs.
Citation Format: Oluwole Adeyemi Babatunde, Swann Arp Adams, Jan M. Eberth, Michael D. Wirth, Seul Ki Choi, James R. Hebert. Racial disparities in endometrial cancer epidemiology and mortality-to-incidence ratios in South Carolina. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C29.
Abstract C32: Native American genetic ancestry is protective against prostate cancer in African Americans and European Americans
Authors: Murphy Adam , Batai Ken , Shah Ebony , Kittles Rick A. 
Published: May 2016

Abstract
Prostate cancer (PCa) incidence and mortality varies by racial/ethnic groups in the U.S. African American (AA) men have a 60% higher incidence and twice the mortality rate of European America (EA) men, while Hispanic Americans and Native Americans have lower incidence rates than EA men. Several genetic admixture studies have examined the role of west African ancestry on prostate cancer risk in AA men, however the influence of Native American ancestry on PCa risk has not been explored. Here we evaluated the relationship between individual genetic ancestry proportions and the likelihood of PCa diagnosis and aggressiveness.
Methods: We recruited 40-79 year old men who were undergoing prostate biopsy or routine PSA screening at outpatient urology clinics in Chicago, IL. Blood was drawn at the time of enrollment for genotyping of 105 ancestry informative markers. West African, European, and Native American genetic ancestry was estimated using the Bayesian Markov Chain-Monte Carlo method implemented in the program STRUCTURE. Unconditional binary logistic regression models were used to estimate odds ratios for the likelihood of PCa diagnosis and for the likelihood of having high-risk PCa relative to controls, adjusting for age and family history of PCa.
Results: In AAs, NAA ranged from 0.4% to 28.8%. Mean NAA was 4.6% in AA cases, while controls had mean NAA of 6.6%. NAA ranged from 0.5% to 17.4% in EAs. Mean NAA was 5.1% in cases and 6.8% in controls. NAA was negatively associated with PCa diagnosis. AA men in the highest quartile of NAA had significantly reduced odds of PCa diagnosis compared to men in the lowest quartile of NAA (OR 0.47, 95% C.I.: 0.29-0.77). Similarly, EA men in the highest quartile of NAA had significantly reduced odds of PCa diagnosis compared men in the lowest NAA quartile (OR 0.36, 95% C.I.: 0.21-0.61). Additional adjustment of body mass index, education, smoking, alcohol use, and marital status did not change the results. NAA was also negatively associated with diagnosis of high risk PCa in EAs (P=0.04) and also trending in the same direction in AAs however not significant.
Conclusions: Our study reveals that NAA is protective against PCa diagnosis and high-risk PCa. Hispanic Americans and Native Americans have lower PCa incidence rates than AAs and EAs, and the identification of inherited genetic or environmental factors that are associated with high NAA may improve PCa risk prediction and/or help to develop prevention strategies.
Citation Format: Adam Murphy, Ken Batai, Ebony Shah, Rick A. Kittles. Native American genetic ancestry is protective against prostate cancer in African Americans and European Americans. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C32.
Abstract IA13: Understanding and preventing breast cancer disparities in Latinas
Authors: Thompson Beti , Beresford Shirley AA , Coronado Gloria D. , Neuhouser Marian , Li Christopher I. , Cook Linda S. , Porter Peggy 
Published: May 2016

Abstract
Background: Although Latinas have lower breast cancer rates compared to non-Hispanic Whites (NHW), breast cancer is the top cancer killer of Latinas. There are many reasons for this, some involve biology, types of breast cancer found in Latinas, metabolic increases thought to be due to adoption of western diets, and lack of screening for early detection. In a large breast cancer program examining such cancers in Latinas, we overcame a number of challenges in each of four studies examining the fore-named factors.
Methods: Four projects and four cores made up our Center for Population Health and Health Disparities (CPHHD). Using a community-based participatory research (CBPR) model, we recruited Latinas to participate in studies investigating the various factors related to breast cancer. Projects used robust methodologies to assess the relationship between elevated risks of triple negative breast cancers; the effects of a typical US diet compared to a traditional Mexican diet; the role of genetic ancestry on breast cancer in Latinas; and the effectiveness of a lay health worker intervention to increase breast cancer screening. As part of the program, we asked investigators to identify challenges encountered and how they were resolved.
Results: All four projects were completed on time. Overall results of each project will be presented. Challenges in each project will be described as well as how the challenges were overcome. The role of the Community Advisory Board will be described and how its suggestions for sending results back to participants were adopted and incorporated in the program.
Discussion: Embarking on a large transdisciplinary program to understand Latinas' breast cancer risks and to translate those risks to the population of interest has been stimulating and thought-provoking. Addressing challenges as they emerged and finding solutions required a team effort. By obtaining perspectives from a variety of disciplines, we were able to solve the challenges. This team approach is recommended for similar studies.
Citation Format: Beti Thompson, Shirley AA Beresford, Gloria D. Coronado, Marian Neuhouser, Christopher I. Li, Linda S. Cook, Peggy Porter. Understanding and preventing breast cancer disparities in Latinas. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr IA13.
Abstract A55: Exosome-associated microRNAs as plasma biomarkers for breast cancer
Authors: Hannafon Bethany N. , Trigoso Yvonne D. , Lum David H. , Welm Alana L. , Dooley William C. , Ding Wei-Qun 
Published: May 2016

Abstract
Introduction: microRNAs are promising candidate biomarkers due to their cancer-specific expression profiles. However, efforts to develop circulating breast cancer biomarkers are challenged by the heterogeneity of microRNAs in the blood. To overcome this challenge, we aimed to develop a molecular profile of microRNAs specifically secreted from breast cancer cells. The key to identifying breast cancer-derived microRNAs relies on capturing and analyzing the contents of exosomes, which are small secretory vesicles that selectively encapsulate microRNAs indicative of their cell of origin.
Methods: Exosomes were collected from the conditioned media of breast cancer cell lines, breast ductal fluids, mouse plasma from patient-derived breast tumor orthotopic xenograft models (PDX), and from human plasma samples. Exosomes were verified by electron microscopy and western blot analysis. Cellular and exosome microRNAs from breast cancer cell lines were profiled by next-generation small RNA sequencing. Plasma exosome populations were selected by immunoaffinity isolation utilizing antibodies against CD63 and MUC1. Exosome microRNA expression was measured by qRT-PCR.
Results: Small RNA sequencing and qRT-PCR analysis showed that several microRNAs are selectively expressed in breast cancer exosomes. Importantly, human breast cancer specific microRNAs were detectable in PDX mouse plasma. The microRNA expression patterns in the MUC1-precipitated plasma exosomes differed between breast cancer patients and control subjects. These results provide a potential new strategy to selectively analyze plasma breast cancer microRNAs that may be indicative of the presence of breast cancer.
Conclusions: Several microRNAs are selectively enriched in breast cancer exosomes, which can be detected in the plasma of PDX mice and breast cancer patients. MUC1 is a viable membrane protein candidate for selective capture of circulating breast cancer specific exosomes from the plasma. These results suggest that selective capture and molecular analysis of breast cancer specific circulating exosomes is a promising strategy for breast cancer biomarker development.
Citation Format: Bethany N. Hannafon, Yvonne D. Trigoso, David H. Lum, Alana L. Welm, William C. Dooley, Wei-Qun Ding. Exosome-associated microRNAs as plasma biomarkers for breast cancer. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Breast Cancer Research; Oct 17-20, 2015; Bellevue, WA. Philadelphia (PA): AACR; Mol Cancer Res 2016;14(2_Suppl):Abstract nr A55.
Abstract A37: Yes-associated protein 1 (YAP) in the growth and tumorigenesis of ovarian granulosa cells.
Authors: Lv Xiangmin , He Chunbo , Hua Guohua , Dong Jixin , Davis John S. , Wang Cheng 
Published: May 2016

Abstract
Ovarian granulosa cells are essential for successful follicle development. Dysregulation of granulosa cell proliferation and differentiation may lead to impairment of female fertility or development of ovarian tumors. Although studies indicate that the Hippo signaling pathway plays critical roles in both development and tumorigenesis of several organs, its role in ovarian physiology and pathology remains largely unknown. The present study aims to investigate the role of YAP in ovarian granulosa cell proliferation, differentiation and transformation. Immunohistochemical analyses showed that the active form of YAP (nuclear YAP) was highly expressed in proliferative granulosa cells, whereas the inactive form of YAP (cytoplasmic YAP) was detected mainly in terminally-differentiated luteal cells, indicating that YAP may be involved in proliferation and differentiation of ovarian granulosa cells. Knockdown of YAP or pharmacological inhibition of YAP activity in human granulosa cells suppressed cell growth and reduced cell survival in both traditional 2D cell culture system and a novel 3D hanging-drop culture system, suggesting that YAP is essential for the growth and survival of human granulosa cells. In addition, ectopic expression of wild-type or constitutively active YAP impaired gonadotropin-induced differentiation of granulosa cells and stimulated the rapid growth and transformation of granulosa cells, findings which were reflected by increased colony formation in soft agar assay and growth of tumors in a xenograft mouse model. Injection of verteporfin (a selective antagonist of YAP) into female CD1 mice inhibited granulosa cell growth, induced GC apoptosis, and disrupted mouse ovarian follicle development, leading to severe subfertility. Consistently, mice with ovarian granulosa cell-specific expression of constitutively active YAP demonstrated disruption of granulosa cell differentiation and failure of ovarian follicle development. In conclusion, our studies demonstrate that homeostatic YAP expression and activation are essential for ovarian granulosa cell proliferation, differentiation and survival. YAP is a novel therapeutic target for treatment of ovarian diseases associated with granulosa cell dysregulation.
Citation Format: Xiangmin Lv, Chunbo He, Guohua Hua, Jixin Dong, John S. Davis, Cheng Wang. Yes-associated protein 1 (YAP) in the growth and tumorigenesis of ovarian granulosa cells. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr A37.
Abstract A58: Bispecific anti-CD3-folate for the treatment of ovarian cancer.
Authors: Xia Jinming , deDios Kristine , Rodrigo Evelyn , Humphreys Robin , Wahl Alan , Gymnopoulos Marco 
Published: May 2016

Abstract
Folic acid receptor 1 (FOLR1, FRα) is highly expressed in 80% of ovarian tumors and has a low nanomolar affinity for folic acid. Although ovarian tumors are intrinsically immunogenic, immune reactions to them are inhibited by a suppressive environment. We are developing a bispecific anti-CD3-folate to redirect T cells to engage with and kill tumor cells. Folic acid was site-specifically conjugated to a FAb fragment of an anti-CD3 antibody through an engineered linkable non-natural amino acid. Anti-CD3-folate bispecific FAb is able to engage T cells and exert cytotoxicity in a variety of tumor cell lines including ovarian; OV-90, OVCAR3, and breast cancer; SKOV-3. Cytotoxicity assays generated EC50 in the femtomolar range. This cytotoxicity could be modulated by varying folic acid concentrations in the assay medium. T-cell activation was confirmed by appearance of activation markers on the cell surface and secretion of pro-inflammatory cytokines after treatment of tumor cells in combination with human PBMC's. T cell activation and subsequent cytokine release is dependent on simultaneous binding of tumor and T cell to anti-CD3-Folate. In a xenograft mouse model of ovarian cancer, anti-CD3-folate significantly inhibited tumor growth, and increased life span (ILS)of 30% and 50% for SKOV-3 and OV-90, respectively when compared to control treated animals. These data suggest that anti-CD3-folate bispecifc FAb- mediated T cell engagement could be a powerful tool for immune-ablation of ovarian cancer.
Citation Format: Jinming Xia, Kristine deDios, Evelyn Rodrigo, Robin Humphreys, Alan Wahl, Marco Gymnopoulos. Bispecific anti-CD3-folate for the treatment of ovarian cancer. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr A58.
Abstract A65: Nodal contributes to cisplatin resistance in ovarian cancer cells.
Authors: Bilyk Olena , Postovit Lynne-Marie 
Published: May 2016

Abstract
The capacity of ovarian tumors to grow and propagate is dependent on a small subset of tumor cells, termed cancer stem-like cells, which contribute to drug resistance, and metastasis. Nodal, an embryonic morphogen has been found to sustain stem cell pluripotency and cellular plasticity, but in cancer cells its expression promotes cancer stem cell renewal, tumor growth, invasion, angiogenesis and metastasis. The role of Nodal in the development of recurrent chemoresistant ovarian cancer (OC) has not been previously investigated. The aim of this study was to investigate whether Nodal can modulate resistance of OC cell line A2780s to cisplatin.
Methods. Human OC cell line A2780s was cultured in DMEM/F12 medium supplemented with 10% FBS and treated with cisplatin. Cytotoxity of cisplatin was determined by MTT assay (Roche) and clonogenic assay. Nodal expression after cisplatin treatment was determined by digital PCR and immunofluorescence staining. To increase Nodal signaling, we used a Nodal expression vector (versus an empty pcDNA3.3 vector; pcDNATM3.3-TOPO cloning kit; Invitrogen). We also employed recombinant human Nodal (rhNodal; R&D). Transfection was performed with Lipofectamine (Invitrogen) as per manufacture instructions. Cell cycle analysis after cisplatin treatment and expression of cancer stem cell marker CD133 were determined using flow cytometry analysis (FACS). In vitro sphere limiting diluting assay was applied to measure ovarian cancer stem cell (OCSC) self-renewal.
Results. The expression of Nodal increased significantly in A2780s cells after 24h cisplatin treatment (20,000 copies/1ug RNA versus 800 copies/1ug RNA in untreated cells) and retained for 96h after cisplatin withdrawal (120,000 copies/1ug RNA). Overexpression of Nodal rendered A2780s cells more resistant to cisplatin (IC50 2.9ug/ml) compared to control cells (IC50 1.3ug/ml). Treatment of A2780s cells with rhNodal (100ng for 24h) during cisplatin treatment increased the ability of ovarian cancer cells to form spheres. FACS analysis revealed that cisplatin along with rhNodal treatment increased the population of CD133 positive cancer stem cells in A2780s cell line (5.85% versus 0,65% in untreated cells and 1.75% after cisplatin treatment alone). Treatment of A2780s cells with rhNodal prevented cell arrest in S phase after cisplatin treatment (19.4% of cells in S phase after rhNodal+cisplatin versus 63.6% - after cisplatin alone).
Conclusison. Our findings demonstrate that Nodal may contribute to cisplatin resistance in OC cells and tumor initiation capacity after drug therapy, and may hold promise as a therapeutic target to prevent chemoresistant recurrence.
Citation Format: Olena Bilyk, Lynne-Marie Postovit. Nodal contributes to cisplatin resistance in ovarian cancer cells. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr A65.
Abstract B13: Discovery of novel subtype-specific ovarian cancer biomarkers via integrated tissue proteomics.
Authors: Leung Felix , Bernardini Marcus Q. , Clarke Blaise , Rouzbahman Marjan , Diamandis Eleftherios P. , Kulasingam Vathany 
Published: May 2016

Abstract
Introduction and Objectives: It is evident that ovarian cancer (OvCa) is not a single disease but is made up of several distinct subtypes, including serous, endometrioid, clear cell and mucinous. The gold-standard biomarker CA125 performs well in serous but not in the other histotypes. We hypothesize that a more focused discovery effort (on non-serous OvCa biomarkers and/or markers that can complement serum CA125) may bring about a sensitivity that is acceptable for all histotypes and be suitable for early diagnosis of OvCa.
Methods: Tissues from patients diagnosed with endometrioid (EC), clear cell (CC), and mucinous ovarian carcinoma (MC), as well as from their appropriate controls (endometriosis and healthy endometrium for EC and CC; mucinous cystadenoma for MC) were subjected to proteomic analysis using a label-free, offline 2-dimensional liquid chromatography tandem mass spectrometry-based approach. Discovery candidates were then filtered using an in-house developed algorithm combining publicly-available resources with our own warehouse of transcriptomic and proteomic sets.
Results and Discussion: Over 8000 unique proteins were identified in this proteomic exercise; specifically, approximately 1500 protein unique to MC, 1100 unique to CC, and 3000 unique to EC were identified when comparing the appropriate cases and controls. A curated list of 60 high-potential candidates was generated after using a range of bioinformatics tools to ensure criteria based on factors including (but not limited to) tissue specificity, cellular localization and transcriptional upregulation were met. These 60 candidates represent putative subtype-specific markers which will be further analyzed and validated in serum cohorts.
Conclusions: The identification and validation of markers specific to the non-serous subtypes of OvCa remains an unmet clinical need. With our list of putative subtype-specific markers, we aim to develop a novel biomarker panel able to detect all OvCa histotypes with greater sensitivity and specificity than any existing clinical tools.
Citation Format: Felix Leung, Marcus Q. Bernardini, Blaise Clarke, Marjan Rouzbahman, Eleftherios P. Diamandis, Vathany Kulasingam. Discovery of novel subtype-specific ovarian cancer biomarkers via integrated tissue proteomics. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr B13.