bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1172: Disparities in pancreatic ductal adenocarcinoma - the significance of Hispanic ethnicity, by subgroup analysis, and treatment facility on clinical outcomes
Authors: Riner Andrea N. , Underwood Patrick W. , Yang Kai , Herremans Kelly M. , Cameron Miles E. , Chamala Srikar , Qiu Peihua , George Thomas , Permuth Jennifer , Merchant Nipun B. , Trevino Jose G. 
Published: September 2020

Abstract
Background: Disparities exist among patients with pancreatic ductal adenocarcinoma (PDAC). Non-White race is regarded as a negative predictor of expected treatment and overall survival. Data suggest Academic Research Programs (ARP) provide better outcomes for minorities, but ethnic/minority outcomes are underreported. We sought to evaluate outcomes among diverse patients with PDAC, with a focus on Hispanic subgroups. We hypothesize that outcomes among racially/ethnically diverse PDAC patients may be influenced by treatment facility.
Methods: The National Cancer Database was used to identify 170,327 patients diagnosed with PDAC between 2004 and 2015. Cox proportional-hazard regression was used to compare survival between race/ethnic groups across facilities.
Results: In unadjusted models, compared to Non-Hispanic Whites (NHW), Non-Hispanic Blacks (NHB) had the worst overall survival (HR=1.05, 95%CI:1.03-1.06, p&lt;0.001) and Hispanics had the best overall survival (HR=0.92, 95%CI:0.90-0.94, p&lt;0.001). After controlling for socioeconomic and clinical covariates, NHB (HR=0.95, 95%CI:0.93-0.96, p&lt;0.001) had better overall survival compared to NHW, and Hispanics continued to have the best comparative outcomes (HR=0.84, 95%CI:0.82-0.86, p&lt;0.001). Amongst Hispanics, Dominicans and South/Central Americans lived the longest, at 10.25 and 9.82 months, respectively. The improved survival in Hispanics was most pronounced at ARP (HR=0.80, 95%CI:0.77-0.84, p&lt;0.001) and Integrated Network Cancer Programs (HR=0.78, 95%CI:0.73-0.84, p&lt;0.001). NHB had improved survival over NHW at Comprehensive Community Care Programs (HR=0.96, 95%CI:0.93-0.98, p=0.002) and ARP (HR=0.96, 95%CI:0.94-0.98, p=0.001), which was influenced by income, education, and surgical resection.
Conclusion: Hispanics with PDAC have better overall survival compared to Non-Hispanics at all facilities, but most profoundly at ARP and INCP. Dominicans and South/Central Americans in particular have significantly improved survival at ARP. Survival was improved at ARP for all populations. NHB had improved overall survival at higher volume centers, but this was dependent upon income, education, and surgical resection.
Citation Format: Andrea N. Riner, Patrick W. Underwood, Kai Yang, Kelly M. Herremans, Miles E. Cameron, Srikar Chamala, Peihua Qiu, Thomas George, Jennifer Permuth, Nipun B. Merchant, Jose G. Trevino. Disparities in pancreatic ductal adenocarcinoma - the significance of Hispanic ethnicity, by subgroup analysis, and treatment facility on clinical outcomes [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1172.
Abstract 1185: Impact of distance traveled to radiosurgery center on time to initiation of gamma knife treatment for brain metastases in a rural patient population
Authors: Rehman Azeem A. , Singh Sarah , Arsanious David , Renz Paul , Cifarelli Christopher P. 
Published: September 2020

Abstract
The West Virginia University Gamma Knife center provides care for largely rural areas with patients that often travel 1-3 hours for treatment. Studies investigating whether distance to a tertiary cancer center results in meaningful delays in care are limited. This study examines patients treated with gamma knife for brain metastases to identify predictors of delay in care based on distance from the treatment center. Retrospective data for patients treated at the West Virginia University Gamma Knife center (2010-2017) for brain metastases with a primary diagnosis of lung or breast cancer was analyzed. Study variables included age, gender, primary histology, ECOG, KPS, RPA, interval time to initiation (TTI) of gamma knife treatment from diagnosis, and distance from home to the center. Statistical significance was determined by p&lt;0.05. A total of 182 patients with a median age of 60 years (IQR: 53.5-69 years), median ECOG of 1 (Range: 0-3), median KPS of 80 (IQR: 70-100), and RPA of 2 were included. Median TTI of GK treatment was 21 days (IQR: 14-29 days) while median distance traveled to the facility was 45.8 miles (IQR: 24.5-86.7 miles). For patients residing within 45.8 miles, median TTI was 22 days (IQR: 15-33 days) compared with a median TTI of 20.5 days (IQR: 13.75-27 days) for patients living beyond 45.8 miles. There was no statistical difference between groups based on age, diagnosis, or distance to center with respect to TTI (p=0.28). Despite geographical disadvantages in a rural population, including distance traveled for treatment, no significant delay in TTI was identified in patients treated with gamma knife for brain metastases.
Citation Format: Azeem A. Rehman, Sarah Singh, David Arsanious, Paul Renz, Christopher P. Cifarelli. Impact of distance traveled to radiosurgery center on time to initiation of gamma knife treatment for brain metastases in a rural patient population [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1185.
Abstract 1188: The effect of insurance status on diagnosis stage and overall survival among children and adolescents with cancer: A propensity score weighting analysis
Authors: Wang Xiaoyan , Johnson Kimberly 
Published: September 2020

Abstract
Background. Differences in access, delivery or utilization of health care may impact childhood and adolescent cancer survival. In this study, we evaluated the impact of insurance coverage on diagnosis stage, treatment received, and overall survival among children and adolescents diagnosed with cancer based on a counterfactual framework.
Methods. We identified 58,421 individuals diagnosed with any cancer type at ≤ 19 years old from 2004-2010 from the National Cancer Database. We applied the inverse probability of treatment weighting (IPTW) estimator to correct for observed selection biases generated by insurance enrollment at diagnosis or initial treatment and examined associations between insurance status and diagnosis stage, treatment received (any vs. none), and all-cause mortality using weighted logistic and weighted Cox proportional hazard regressions.
Results. Compared to privately insured individuals, there was a higher percentage of younger individuals in the Medicaid category for all cancers, whereas the uninsured category had a higher percentage of older individuals. Children and adolescents with Medicaid and no insurance were more likely to be non-White and from lower income counties. Applying the IPTW estimator, all the imbalances on the above covariates were removed. Results from weighted analysis showed a 15% (95 confidence interval (CI): 0.78-0.93) lower odds of being diagnosed at metastatic stage had children and adolescents with Medicaid been enrolled on private insurance but comparable odds for uninsured individuals (odds ratio: 0.98, 95%CI: 0.79-1.22), vs. those with private insurance. The odds of receiving any treatment were 17% (95%CI: 1.08-1.28) and 68% (95%CI: 1.39-2.04) higher had those with Medicaid and no insurance been enrolled on private insurance at diagnosis or initial treatment. Medicaid and uninsured individuals would have a 24% (95%CI: 0.72-0.80) and 24% (95%CI: 0.66-0.87) lower hazard of death during 5 years of follow-up if they were enrolled on private insurance at diagnosis or initial treatment.
Conclusion. Children and adolescents without private insurance would have a lower risk of being diagnosed at metastatic stage, higher odds of receiving any treatment, and lower hazard of death within five years following cancer diagnosis had they been enrolled on private insurance at diagnosis or initial treatment. Additional research is needed to further understand underlying mechanisms.
Citation Format: Xiaoyan Wang, Kimberly Johnson. The effect of insurance status on diagnosis stage and overall survival among children and adolescents with cancer: A propensity score weighting analysis [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1188.
Abstract 1211: Recurrent germline mutations in RAD51D and PALB2 are present in Colombian hereditary breast and ovarian cancer families
Authors: Sanabria-Salas Maria Carolina , Rivera-Herrera Ana Lucía , Gómez-Camargo Ana Milena , Carvajal-Carmona Luis G. , Serrano-López Martha Lucía 
Published: September 2020

Abstract
Hereditary breast cancer (BC) syndromes corresponds to 10% - 15% of all cases diagnosed worldwide. Most of these cases are due to deleterious germline genetic variants in BRCA1/2 genes; nevertheless, multipanel testing have contribute to the identification of other risk genes, including other homologous recombination (HR) repair genes, such as PALB2, ATM, CHEK2 and RAD51D. Here we explore the mutation spectrum of Hereditary Breast and Ovarian Cancer (HBOC) Colombian cases as part of the Hereditary Cancer Program from the National Cancer Institute from Colombia, the largest reference cancer center in the country, that seeks to identified high risk families to offer preventive measures and screening recommendations. A total of 358 patients fulfilling criteria for HBOC have been so far analyzed with Next Generation Sequencing using a multigene panel. Overall, 47% have negative results and in the 33% we identified VUSs. In general, 20% have a pathogenic or potentially pathogenic genetic variant; from those, BRCA1 (n = 17) and BRCA2 (n = 17) were the most frequently mutated genes (47.2% among all positive results). Deleterious mutations in RAD51D and PALB2 (also important HR repair genes) were found in 7% and 5.6% of the cases tested. Interestingly, genotype:phenotype correlations were found for these genes, as breast cancer molecular subtypes were distributed differently depending on the gene affected. In concordance with other reports, triple negative breast cancers (TNBC) were more frequent in BRCA1 (9/17, 53%) and PALB2 (4/4, 100%) carriers, and luminal subtypes were more frequent in BRCA2 carriers (10/17, 59%). Mutations in RAD51D: c.94_95del (p.Val32Phefs*67) and PALB2: c.2288_2291del (p.Leu763Ter), were both recurrent mutations in our Colombian cases. Further haplotype analysis will help us to determine if mutation carriers shared a common ancestry.
Citation Format: Maria Carolina Sanabria-Salas, Ana Lucía Rivera-Herrera, Ana Milena Gómez-Camargo, Luis G. Carvajal-Carmona, Martha Lucía Serrano-López. Recurrent germline mutations in RAD51D and PALB2 are present in Colombian hereditary breast and ovarian cancer families [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1211.
Abstract 1225: Co-inhibition of autophagy and MAPK signaling in RAS-driven cancers
Authors: Foth Mona , Kinsey Conan , Schuman Sophia , Battistone Benjamin , Sanchez Emilio Cortes , Kircher David , Welm Bryan , Holmen Sheri , McMahon Martin 
Published: September 2020

Abstract
RASis mutated in a number of cancers, including KRAS-driven colorectal and pancreatic cancer, HRAS-driven bladder cancer, and NRAS-driven melanoma, all of which result in downstream activation of the RAF&gt;MEK&gt;ERK (MAPK) and PI3K&gt;AKT signaling pathways. Most RAS GTPases cannot be targeted directly, and strategies blocking both MAPK and PI3K signaling simultaneously are limited by high toxicity and compensatory signaling mechanisms. Interestingly, oncogene-activated MAPK or PI3K signaling pathways are reasonably well described orchestrators of metabolic transformation through multiple pathways. Our lab has recently shown that autophagy,a conserved metabolic process of self-digestion that recycles intracellular components, is increased in KRAS-driven pancreatic ductal adenocarcinoma (PDA) upon MAPK pathway inhibition. We further showed that co-inhibition of autophagy and MEK1/2, a MAPK component, leads to tumor regression of patient-derived PDA xenografts in mice. Our proposed combination therapy has recently been translated into a phase I/II clinical trial for PDA patients with advanced disease. Our most recent data show that inhibition of RAS&gt;RAF&gt;MEK&gt;ERK signaling also results in induction of autophagy in other RAS-driven cancers, including KRAS-driven colorectal cancer, HRAS-driven bladder cancer and NRAS-driven melanoma. Furthermore, ourin vivodata demonstrate a robust regression of tumors upon combined inhibition of autophagy and MEK1/2 in engrafted KRAS-driven colorectal cancer cells xenografted in mice. Patient data from two KRAS-driven colorectal cancer patients, who were recently treated off-label, indicated clinical responses to the combination treatment co-targeting autophagy and MEK1/2. Altogether, these data suggest that co-inhibition of autophagy and oncogenic signaling may represent a potential new treatment strategy for multiple RAS-driven cancer types. Future experiments aim for a better mechanistic understanding of the combination treatment co-targeting autophagy and oncogenic signaling, with the objective to propose novel therapeutic strategies for cancer patients with RASmutations.
Citation Format: Mona Foth, Conan Kinsey, Sophia Schuman, Benjamin Battistone, Emilio Cortes Sanchez, David Kircher, Bryan Welm, Sheri Holmen, Martin McMahon. Co-inhibition of autophagy and MAPK signaling in RAS-driven cancers [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1225.
Abstract 1272: Enhancer RNA cell line database reveals new associations between TF activity and cancer subtype
Authors: Azofeifa Joseph , Basken Joel , Lai Maria , Langendorf Ryan , Norris Laura , Read Tim , Robbins-Pianka Adam 
Published: September 2020

Abstract
Cell type and lineage is driven, in large part, by changes in transcription factor activity. Particularly in cancer, misregulation of transcription factor binding can lead to de-differentiated states and overproliferation. Recent work suggests that enhancer RNAs are a highly predictive readout of transcription factor activity, however, measuring them is an arduous process. We developed an automated strategy to measure nascent RNAs for over 50 different cancer cell line models. By a modified PRO-seq assay, we annotated enhancer RNAs and transcription factors unique to specific cancer backgrounds. Examples include: ESR1 activity in ER+ breast cancer models, AR activity in castration-sensitive prostate models and GATA3 in AML. This database is the first standardized collection of enhancer RNAs and and can be used in conjunction with the BROAD's CCLE and DepMap consortiums to help expedite treatment options.
Citation Format: Joseph Azofeifa, Joel Basken, Maria Lai, Ryan Langendorf, Laura Norris, Tim Read, Adam Robbins-Pianka. Enhancer RNA cell line database reveals new associations between TF activity and cancer subtype [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1272.
Abstract 1400: An additive effect of ebv-miR-BART5-5p and hsa-miR18a-5p in the downregulation of CDH1 transcript in Epstein-Barr virus associated gastric cancer
Authors: Torres Keila , Landeros Natalia , Wichmann Ignacio , Peñaloza-Otárola Allan , Polakovicova Iva , Maracaja-Coutinho Vinicius , Maturana Maria Jose , Villaroel-Espindola Franz , Corvalan Alejandro 
Published: September 2020

Abstract
Background. Nine percent of Gastric Cancer (GC) is associated with Epstein-Barr virus (EBV-associated GC), with significant variations in the global prevalence rates. Emerging evidence shows that, in addition to cellular miRNAs, viral miRNAs can also bind human mRNAs. EBV miRNAs are examples of this binding and are associated with oncogenic capacities of EBV. ebv-miR-BART5-5p shares the exact seed sequence with hsa-miR-18a-5p. However, common mRNA targets have not been fully described. The aim of this study is to determine predicted targets shared by both miRNAs in EBV-associated GC.
Methodology. By in house method we identified predicted mRNA targets for ebv-miR-BART5-5p and hsa-miR-18a-5p. These targets were queried in published results from the supplementary files of the STAD TCGA study and miRwalk 2.0 software. Validation was performed in 7 EBV-associated GC (cases) and 6 EBV-negative GC (controls) samples by miQ-PCR (ebv-miR-BART5-5p and hsa-miR-18a-5p) and qRT-PCR (predicted targets).
Results. We identified 25 downregulated and 11 upregulated mRNAs in EBV-associated GC cases compared with EBV-negative tumors in validated databases. Interestingly CDH1, which has been associated with diffuse and hereditary GC, was among the predicted targets by miRwalk 2.0. In clinical samples of EBV-associated GC, ebv-miR-BART5-5p and hsa-miR-18a-5p were overexpressed compared with control samples (p=0.0253 and p=0.0205, respectively). Furthermore, CDH1 was downregulated in EBV-associated tumors (p=0.0290).
Conclusion: We identified a common human mRNA target, the CDH1 transcript for ebv-miR-BART5-5p and hsa-miR-18a-5p in EBV-associated GC. An additive effect can be suggested between both miRNAs, which may explain the unique downregulation of CDH1 in EBV-associated GC. This work warrants future validation in vitro, as well as in a larger cohort of EBV-associated GC.
Grant support: CONICYT-FONDAP-15130011, Fondecyt Regular-1191928 and Fondecyt PostDoc-3201028
Citation Format: Keila Torres, Natalia Landeros, Ignacio Wichmann, Allan Peñaloza-Otárola, Iva Polakovicova, Vinicius Maracaja-Coutinho, Maria Jose Maturana, Franz Villaroel-Espindola, Alejandro Corvalan. An additive effect of ebv-miR-BART5-5p and hsa-miR18a-5p in the downregulation of CDH1 transcript in Epstein-Barr virus associated gastric cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1400.
Abstract 1444: c-FLIP antagonizes the survival of extracellular matrix detached cancer cells
Authors: Tsegaye Matyas Abel , McGeehan Kyle , Nemera Mati , Schafer Zachary T. 
Published: September 2020

Abstract
The metastasis of cancer cells to distant sites accounts for over 90% of cancer related deaths. In order to metastasize, cancer cells must be able to survive during extracellular matrix (ECM) detachment, namely by blocking anoikis – caspase dependent cell death – and restoring metabolic deficiencies. Such barriers during tumorigenesis are abrogated through activation of oncogenes, and/or inhibition of tumor suppressors. Elucidating the signaling pathways involved in cancer cell metastasis is a crucial step in designing effective therapeutic interventions. Surprisingly, our investigation has revealed that cellular FLICE-like Inhibitory Protein (c-FLIP), a protein known for its anti-apoptotic function, antagonizes the survival of ECM-detached cancer cells. Additionally, we demonstrated that oncogenic signaling results in the downregulation of c-FLIP expression further suggesting that cancer cells can benefit from diminished FLIP levels. We observed that this repression of c-FLIP expression is a consequence of MEK-ERK signaling. Our study also suggests that the mechanism underlying this paradoxical c-FLIP pathway involves the induction of β-catenin degradation through inhibition of GSK-3β phosphorylation by p38 MAPK. This results in the ubiquitination and subsequent degradation of β-catenin which could contribute to reduced proliferation and migration.
Citation Format: Matyas Abel Tsegaye, Kyle McGeehan, Mati Nemera, Zachary T. Schafer. c-FLIP antagonizes the survival of extracellular matrix detached cancer cells [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1444.
Abstract 1452: Hypoxia-induced MIG-6 promotes glucose metabolic reprogramming and tumorigenesis in triple-negative breast cancer
Authors: He Jiabei , Li Chien-Feng , Lee Hong-Jen , Shin Dong-Hui , De Carvalho Bruno , Chan Chia-Hsin 
Published: September 2020

Abstract
Treatment of triple-negative breast cancer (TNBC) remains challenging due to a lack of effective targeted therapies. Dysregulated glucose uptake and metabolism are essential for TNBC growth. Identifying the molecular drivers and mechanisms underlying the metabolic vulnerability of TNBC is the key to exploiting dysregulated cancer metabolism for therapeutic applications. Mitogen-inducible gene-6 (MIG-6) has long been thought as a feedback inhibitor that targets activated EGFR and suppresses the growth of tumors driven by constitutive activated mutant EGFR. Here, our bioinformatics and histological analyses uncovered that MIG-6 is upregulated in TNBC and that MIG-6 upregulation is positively correlated with poorer clinical outcomes in TNBC. Metabolic arrays and functional assays revealed that MIG-6 drives glucose metabolism reprogramming toward glycolysis. We found that hypoxia-induced MIG-6 promotes HIF1α protein stabilization and the subsequent upregulation of GLUT1 and other HIF1α-regulated glycolytic genes, substantiating the comprehensive regulation of MIG-6 in glucose metabolism. Moreover, our animal studies demonstrated that MIG-6 regulates GLUT1 expression in tumors and subsequent tumor growth in vivo. Collectively, this work reveals that MIG-6 is a novel prognosis biomarker, metabolism regulator, and molecular driver of TNBC.
Citation Format: Jiabei He, Chien-Feng Li, Hong-Jen Lee, Dong-Hui Shin, Bruno De Carvalho, Chia-Hsin Chan. Hypoxia-induced MIG-6 promotes glucose metabolic reprogramming and tumorigenesis in triple-negative breast cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1452.