bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A20: Innovative drug discovery for bladder cancer by miR-130 family seed-targeting locked nucleic acid
Authors: Egawa Hiroshi , Jingushi Kentaro , Ueda Yuko , Kitae Kaori , Nakata Wataru , Fujita Kazutoshi , Uemura Motohide , Nonomura Norio , Tsujikawa Kazutake 
Published: May 2016

Abstract
Bladder cancer causes an estimated 150,000 deaths per year worldwide. Although 15% of the recurrent bladder cancer becomes an invasive type, targeted therapy for malignant bladder cancer does not make much progress. To investigate a novel therapeutic target, we focused on miRNA expression signatures obtained from bladder cancer clinical specimens, and found that the miR-130 family (miR-130b, miR-301a and miR-301b) was significantly up-regulated in bladder cancer specimens compared to adjacent normal urothelial specimens. Functional analyses revealed that the miR-130 family promoted bladder cancer cell migration and invasion by regulating both focal adhesion kinase (FAK) and Akt phosphorylation. Moreover, miR-130b directly targeted Phosphatase and Tensin Homolog Deleted from Chromosome 10 (PTEN), which suppresses FAK and Akt activation. Furthermore, Argonaute2-immunoprecipitation and the subsequent gene array analysis identified tyrosine-protein phosphatase non-receptor type 11 (PTPN11) as another target gene of both miR-130b and miR-301b. Thus, the miR-130 family promotes bladder cancer cell motility by regulating these target genes. We next designed miR-130 family-targeted LNA (Locked Nucleic Acid) that can inhibit entire miR-130 family through a common seed sequence. miR-130 family-targeted LNA suppressed bladder cancer cell proliferation, migration and invasion powerfully by targeting both PTEN and PTPN11. Furthermore, miR-130 family-targeted LNA significantly inhibits bladder tumor growth in a murine xenograft model. Taken together, the miR-130 family has a crucial role for malignant progression of bladder cancer and thus miR-130 family-targeted LNA could be a promising molecular-targeted drug for bladder cancer.
Citation Format: Hiroshi Egawa, Kentaro Jingushi, Yuko Ueda, Kaori Kitae, Wataru Nakata, Kazutoshi Fujita, Motohide Uemura, Norio Nonomura, Kazutake Tsujikawa. Innovative drug discovery for bladder cancer by miR-130 family seed-targeting locked nucleic acid. [abstract]. In: Proceedings of the AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines ; 2015 Dec 4-7; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2016;76(6 Suppl):Abstract nr A20.
Abstract A35: Characterization of the genomic landscape of osteosarcoma metastasis
Authors: Koehne Amanda L. , Sayles Leanne C. , Breese Marcus R. , Vaka Dedeepya , Sweet-Cordero Alejandro 
Published: May 2016

Abstract
Early metastasis to the lungs is a cardinal feature of osteosarcoma (OS), and complications from metastatic disease remain the most common cause of cancer-related death. Despite the prevalence of metastasis in OS, the pathogenesis is poorly understood. We have established a collection of 16 patient-derived xenografts (PDX) from human OS tumors, both from the primary site as well as metastasis. Our collection includes 9 diagnostic biopsies from primary site tumors, 2 primary tumor resections, 3 lung metastases, and 1 ascites fluid metastasis. Gene expression analysis of an initial set of 5 PDX models (3 metastases, 2 primaries) has been completed. A more extensive analysis of all 16 models by RNAseq and WGS is currently underway. Preliminary gene expression analysis identified a significant number of genes differentially expressed between metastatic samples and non-metastatic samples. This list included genes associated with cell adhesion and motility such as MEGF10, genes associated with endochondral ossification and bone remodeling such as RANKL, and genes associated with deposition of extracellular matrix (ECM) such as COL21A. Another candidate gene, ENPP1, is responsible for mineralization of the ECM and has been implicated in breast cancer metastasis to bone. We have validated differential expression of a number of these genes in independent samples of metastatic OS. We are currently using small hairpin RNA (shRNA), CRISPR, and overexpression vectors to knockdown, silence, and overexpress ENPP1 and other candidate genes in OS cell lines. Using in vitro migration and invasion assays as well as intravenous injection and orthotopic mouse models, we are characterizing the contribution of candidate genes to the metastatic propensity of OS.
Citation Format: Amanda L. Koehne, Leanne C. Sayles, Marcus R. Breese, Dedeepya Vaka, Alejandro Sweet-Cordero. Characterization of the genomic landscape of osteosarcoma metastasis. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; 2015 Nov 9-12; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(5 Suppl):Abstract nr A35.
Abstract P1-12-08: Factors associated with delays in chemotherapy initiation among patients with breast cancer
Authors: Losk K , Vaz Duarte Luis I , Camuso K , Lloyd M , Kadish S , Hirshfield-Bartek J , Cutone L , Golshan M , Lin N , Bunnell C 
Published: May 2016

Abstract
Background: National guidelines endorse time-dependent quality metrics for breast cancer care. We examined factors associated with delays in chemotherapy initiation at an NCI designated comprehensive cancer center.
Methods: We identified 523 patients who received post-operative adjuvant chemotherapy between January 2011 and December 2013 at our center. We defined 28 days from last definitive surgery (LDS) to chemotherapy as the target timeframe, and unacceptable delay in chemotherapy initiation (UCD) as more than 42 days from LDS. Multivariate regression models were used to identify factors associated with UCD and the impact of Oncotype testing in HR+ patients.
Results: Median days between LDS and chemotherapy initiation was 34 (IQR 15), with 30% of patients starting within 28 days of LDS and 23% having UCD (Table 1). Tumor characteristics such as subtype and stage affected UCD; patients with HR+ or HER2+ tumors were more likely to be delayed compared to those with TNBC. Patients with stage I disease were more likely to be delayed as well as patients undergoing mastectomy or mastectomy with reconstruction. Patients whose pathology sign-out was more than 10 days post-operatively were more likely to be delayed. A higher proportion of UCD was found in HR+ patients (31%) who received an Oncotype recurrence score compared to those who did not (20%).
Table 1: Factors associated with delays in chemotherapy initiation N% DelayOdds Ratio95% CITotal52323 Age&lt;4068191.00.5-2.340 to 49165161.0--50 to 59150252.01.1-3.660 to 69113282.51.3-5.070+27374.11.4-12.3RaceWhite424221.0--Non-White79271.50.8-2.7Missing20251.10.4-3.3InsurancePrivate419211.0--Public104321.60.8-2.9StageI208211.0--II243281.30.8-2.1III72110.30.1-0.7Tumor SubtypeHER2-/HR-105151.0--HR+HER2-264242.11.1-4.2HER2+154272.01.0-3.9Surgery TypeLumpectomy265161.0--Mastectomy89292.51.3-4.5Mastectomy with Immediate Reconstruction169313.31.9-5.6Pathology Sign-Out (&gt;10 days)No331191.0--Yes192322.01.3-3.2Post-Op ComplicationsNo506221.0--Yes17412.20.7-6.6Clinical trial considerationNo435231.0--Yes88240.90.5-17
Conclusions: This study provides insight into populations that may be at risk to experience delays in chemotherapy initiation, directing interventions to improve the timeliness of care.
Citation Format: Losk K, Vaz Duarte Luis I, Camuso K, Lloyd M, Kadish S, Hirshfield-Bartek J, Cutone L, Golshan M, Lin N, Bunnell C. Factors associated with delays in chemotherapy initiation among patients with breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-12-08.
Abstract P2-05-03: Whole genome transcriptome analysis of sequential breast to brain metastasis uncovers new signalling pathways and druggable targets
Authors: Varešlija D , Fagan A , Buckley P , Farrell M , Hill A , Young L 
Published: May 2016

Abstract
The occurrence of brain metastasis (BM) in breast cancer (BC) is currently on the rise across all molecular subtypes with 10-30% reported incidence. The need to uncover the mechanisms underlying this clinically devastating complication is apparent, and in the current study we sought to identify BC cell mediators of BM.
In our cohort of metastatic patients (n=196) we found that BM developed in 13% of the cases. Despite the previous reports of negative ER status being a risk factor for BM, the ER+ve patients accounted for 42% of all diagnosed BM. To elucidate the gene alterations required for successful colonisation of the brain we undertook RNA sequencing (RNA-seq) of sequential breast to brain metastasis of known receptor status (n=7).This study presents the first whole transcriptome next-generation RNA-seq analysis of resected BM and their matching primary breast tumours.
We identified 500 differentially expressed genes (DEGs) (&lt; 0.05, fcThreshold &gt;±1.5), accounting for those that were both upregulated and downregulated in BM compared to the primary. Analysis of protein-coding genes identified collective ER-specific metastatic pathways. Additionally, common functional pathways altered included ECM, cell adhesion and neuronal differentiation. Our analysis of the BM transcriptomic landscape and verification in cell line models that preferentially metastasise to the brain has unravelled a complex network of driver genes, cooperating with stromal derived factors, responsible for the organ-specific behaviour of the metastatic cells. Genes such as ANTRX1, THBS2, FAP, VCAN and TIMP2 were found to be part of the invasion and migration network that drives the extravasation of the BM cells. Furthermore, an EMT stemness signalling network driven by ANTRX1and WNT pathway driven RUNX was prominent in the cells acquiring the ability to migrate to the brain. Additional work is being carried out on uncovering the adaptations that re-activate the dormant brain metastatic cells and the contribution of the neuronal niche in the facilitating the colonisation by the MBC.
This study highlights the requirement of unique gene sets for the invasion, migration and colonisation to the brain and that functional characterisation of the DEGs will enable the identification of novel molecular targets for prevention and treatment of breast cancer BM.
Citation Format: Varešlija D, Fagan A, Buckley P, Farrell M, Hill A, Young L. Whole genome transcriptome analysis of sequential breast to brain metastasis uncovers new signalling pathways and druggable targets. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P2-05-03.
Abstract A07: Exploring the distribution of environmental cancer risk by air toxics using geographic information systems
Authors: Rice LaShanta J. , Emrich Christopher T. , Brandt Heather M. , Ingram Lucy Annang , Hardin James W. , Wilson Sacoby M. , Halbert Chanita Hughes 
Published: May 2016

Abstract
We examined environmental cancer risk disparities in Metropolitan Charleston by determining the variability in cancer risk and outcomes geographically by racial and socioeconomic characteristics.
We mapped total cancer risk from the 2005 National-Scale Air Toxics Assessment (NATA) and five-year (2006-2010) cancer outcomes (incidence and mortality) from the South Carolina Central Cancer Registry. Data were georeferenced to the 2000 Decennial United States Census tract boundaries in Metropolitan Charleston (i.e. Berkeley, Charleston, and Dorchester County). A Spearman's rank-order correlation was run to determine the relationship between cancer risk or cancer outcomes and characteristics of environmental justice (percent (%) Black, poverty, and low-income). Correlations were performed in SPSS 22.0. Bivariate choropleth maps were created in ArcGIS 10.2 to represent the geographic associations between cancer data and environmental justice variables.
Our findings demonstrate an inverse relationship between cancer risk and five-year cancer incidence (rs = -1.90, p = .040). Cancer risk was positively correlated with % Black (rs = .324) and % poverty (rs = .474), yet negatively related to % income (rs = -.542). Bivariate maps showed that 80% of the tracts with high cancer incidence/high percent Black population were simultaneously high cancer mortality/high Black population tracts. None of the high incidence or high mortality tracts had simultaneously high cancer risk.
Findings from this study have implications for reducing place-based environmental cancer disparities. With a better understanding of patterns of risk, public health professionals can tailor interventions and develop community-based environmental health programs that will inform policies to reduce cancer inequities.
Citation Format: LaShanta J. Rice, Christopher T. Emrich, Heather M. Brandt, Lucy Annang Ingram, James W. Hardin, Sacoby M. Wilson, Chanita Hughes Halbert. Exploring the distribution of environmental cancer risk by air toxics using geographic information systems. [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 A07.
Abstract A45: Racial differences in psychosocial barriers to initiate prostate cancer treatment information seeking
Authors: Guerreso Heather , Johnson Jarrett , Ross Levi 
Published: May 2016

Abstract
Purpose: All men diagnosed with prostate cancer must undergo the complex process of treatment decision-making. Research indicates that most men are not prepared to fully interact with the information environment when they are initially diagnosed. The reasons behind this lack of preparedness are not fully understood. More information is needed about psychosocial facilitators and barriers to information gathering before appropriate interventions can be developed. The purpose of this research was to explore the different types of psychosocial assistance that men might need to help them begin gathering treatment information. Methods: A purposive sample of 63 African-American and Caucasian men treated for or actively monitoring localized prostate cancer (Stage T1 or T2) was recruited to participate. All recruitment was completed via cancer registries, newspaper ads, and word-of-mouth. All participants completed a 30-45 minute self-administered survey on a laptop or touchscreen computer. Data collected included: (1) demographic information and (2) information about their self-reported levels of (a) confidence, (b) confusion, (c) worry, (d) comfort, (e) ease, and (f) organization during their initial searches for treatment information. All men received a $25.00 honorarium for participating. Results: The mean age of participants was 64.17 years. Participants were between six months to 10 years post prostate cancer diagnosis (mean = 5.21 years, SD= 3.23). At the initial search for treatment information, the majority of men (82.5%) were not confident they knew all of the right information to look for and were not confident they could find answers for all of their questions (79.3%). When psychosocial barriers were compared by race, one significant relationship was found. A greater proportion of African Americans (19.2%) found the initial information gathering process more difficult than their Caucasian counterparts (13.5%) (p &lt; .05). Conclusions: Knowing what to look for and where to find answers is a common problem for both African American and Caucasian prostate cancer patients. Interventions need to be developed that make initial searches for information easier for African-American men.
Citation Format: Heather Guerreso, Jarrett Johnson, Levi Ross. Racial differences in psychosocial barriers to initiate prostate cancer treatment information seeking. [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 A45.
Abstract A53: Revisiting the importance of a culturally integrated liver cancer education program among Asian Americans
Authors: Juon Hee-Soon , Kim Frederic , Lam Patrick 
Published: May 2016

Abstract
Background: Asian Americans are at high risk of contracting the hepatitis B virus (HBV). Culturally integrated liver cancer educational program has increased HBV knowledge which leads to HBV screening, vaccinations, and treatment, which reduce cancer health disparities from HBV infection. The purpose of this study is to evaluate the effect of culturally integrated education program on HBV knowledge as opposed to a stand-alone video education program.
Methods: Asian American adults were recruited from community-based organizations (Study 1) and from Pan Asian Volunteer Health Clinic (Study 2) in the Baltimore-Washington Metropolitan area. 441 participants in Study 1 received the 30-minute intervention program including power point presentation with Q & A, role play video, and distribution of photonovel. In Study 2, 276 participants watched the 10-minute video presentation without any interaction with the staff. Both intervention programs focus on general knowledge of the HBV, the importance of vaccinations, and follow-up for those infected. All participants completed baseline survey after signing the informed consent. Then they received two different education programs either a culturally integrated program or a video presentation. After the education program, they completed a post-education survey. The outcome measures were correct answers to knowledge questions related to HBV infection, including the modes of HBV transmission (10 questions) and sequelae of chronic HBV (7 questions). Paired sample t-test was used.
Results: The culturally integrated education program was more effective than the video education. It increased their knowledge of HBV infection appreciably (4.18 vs 1.31 for mode of transmission, p&lt;.001; 2.06 vs. 0.69 for sequelae, p&lt;.001). In the pretest, less than one fourth of the participants had the correct answer to two questions: (1) eating food that had been pre-chewed by an infected person; and (2) breast feeding from an infected mother. Only one third knew that HBV is significantly more contagious than HIV/AIDS.
Conclusion: This study suggests that it is very critical to implement the culturally integrated education program to reduce liver cancer health disparities among Asian Americans.
Citation Format: Hee-Soon Juon, Frederic Kim, Patrick Lam. Revisiting the importance of a culturally integrated liver cancer education program among Asian 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 A53.
Abstract B16: IL-10 promoter polymorphisms are associated with prostate cancer risk in African Americans
Authors: Abbas Muneer M. , Mason Tshela , Ricks-Santi Luisel , Apprey Victor , Kittles Rick , Ahaghotu Chiledum , Dunston Georgia 
Published: May 2016

Abstract
Background: African American men have the highest rates of prostate cancer (PCa) worldwide and immunogenetic studies suggest emerging evidence that prostate inflammation may contribute to prostatic carcinogenesis. Since genetic susceptibility is an etiological factor in PCa, we hypothesize that sequence variants in the promoter region of the IL-10 gene that regulate pro inflammatory cytokines, may modify individual susceptibility to this disease.
Methods: four SNPs in the promoter regions with allele frequency differences between Europeans and West Africans were genotyped using pyrosequencing in 538 unrelated men enrolled in a PCa genetic association study at the Howard University Hospital between 2000-2004.
Results: SNP rs12122923 was found to have the strongest association using the dominant (p=0.048) and the log additive (p=0.029) genetic models. rs1800871 was found to be associated with PCa using the log additive model(p=0.057). However, after adjusting for age, both SNPs became insignificantly associated with PCa.
Conclusions: This study showed an association between IL-10 promoter SNP variation and PCa. This supports the hypothesis that genetic variation in the inflammatory process can contribute to prostate cancer susceptibility. Research supported in part by NIH/NIGMS/MBRS/SCORE grant # S06GM008016.
Citation Format: Muneer M. Abbas, Tshela Mason, Luisel Ricks-Santi, Victor Apprey, Rick Kittles, Chiledum Ahaghotu, Georgia Dunston. IL-10 promoter polymorphisms are associated with prostate cancer risk in African 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 B16.