bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 5214: Stage IV colorectal cancer sub-site and patterns of distant metastases
Authors: Robinson Jamaica R. , Newcomb Polly A. , Hardikar Sheetal , Cohen Stacey A. , Phipps Amanda I. 
Published: July 2016

Abstract
Approximately 20% of individuals diagnosed with colorectal cancer (CRC) in the United States are found to have distant metastases at the time of their diagnosis, indicating an extremely poor prognosis. Although it is well known that primary CRC typically metastasizes to the liver and/or lungs, little is known regarding which factors might explain the anatomic pattern of CRC metastatic spread. Using population-based registry data from the Surveillance, Epidemiology and End Results (SEER) cancer registry of the Seattle-Puget Sound region, we assessed the relationship between primary CRC sub-site and the presence of synchronous metastases in the liver, lungs, and both the liver and lungs. All individuals with stage IV CRC who were diagnosed between 2010-2014 in the 13-county catchment area and who also had complete data on site of metastasis at diagnosis were included in analyses (N = 1287). In total, 703 (55%) patients had distant metastases confined to the liver at the time of diagnosis, 78 (6%) had lung-only metastases, 190 (15%) had metastases in both the liver and lungs but not at other sites, and 316 (25%) exhibited different patterns of metastatic spread, including to the bone, brain, and other anatomic sites. Using multiple logistic regression models, we compared individuals with different patterns of metastatic spread at diagnosis with respect to primary CRC site and with separate models comparing cases with liver-only metastases to all other metastatic cases, comparing cases with lung-only metastases to all other metastatic cases, and comparing cases with metastases to both the liver and lungs to all other metastatic CRC cases. All models were adjusted for age at diagnosis and sex, as well as for depth of primary tumor growth within the colorectum (T-stage) and extent of cancer spread to lymph nodes (N-stage). The odds of having a primary CRC tumor in the rectum, versus proximal colon, were significantly lower among patients with liver-only synchronous metastases relative to those with other patterns of metastatic spread at diagnosis [odds ratio (OR): 0.62, 95% confidence interval (CI): 0.46 - 0.82]. Conversely, the odds of having a primary CRC located in the rectum were significantly higher among those with metastatic disease confined to the lungs (OR: 2.48, 95% CI: 1.38 - 4.47) and those with metastases to the liver and lungs (OR: 1.97, 95% CI: 1.29 - 3.01). Our findings suggest that a patient's site of primary CRC may be informative with respect to possible pattern of metastatic spread.
Citation Format: Jamaica R. Robinson, Polly A. Newcomb, Sheetal Hardikar, Stacey A. Cohen, Amanda I. Phipps. Stage IV colorectal cancer sub-site and patterns of distant metastases. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5214.
Abstract 5228: Estrogen receptor expression is associated with DNA repair capacity in breast cancer
Authors: Matta Jaime L. , Morales Luisa , Ortiz Carmen , Adams Damian , Vargas Wanda , Casbas Patricia , Dutil Julie , Echenique Miguel , Suarez Erick 
Published: July 2016

Abstract
Estrogen receptor (ER) status is an established therapeutic and prognostic biomarker for breast cancer (BC). ER signaling has a propensity to increase proliferation, which can lead to mutations when DNA repair is dysregulated. Deficiencies in DNA repair capacity (DRC) is a hallmark of BC. Recent studies have documented interactions between ER and DNA damage response/repair. Moreover, our previous work showed that DRC in BC patients is approximately 50% less than in women without the disease (p&lt;0.001), and a deficiency in the Nucleotide excision repair (NER) pathway figures prominently in the pathobiology of sporadic BC. Estrogen-receptor-positive (ER+) tumors employ complex signaling that engages in crosstalk with multiple pathways through genomic and non-genomic regulation. A greater understanding of these pathways is important for developing improved biomarkers that can better determine treatment choices, risk of recurrence, and cancer progression. In this study, we aimed to determine whether ER signaling influences DRC. DRC, in terms of the NER pathway, was measured in lymphocytes by means of a host cell reactivation assay with a luciferase reporter gene. A multivariate linear regression model (MLRM) was used to estimate the mean of the DRC and analyze the association between ER positivity (% receptor activation) obtained from pathological reports and DRC in 270 BC patients. These were further stratified by HER2 receptor status. An ordinal logistic regression model (OLRM) was used to confirm the relationship between DRC and ER status using the maximum likelihood method for parameters estimation. Our results show an association between ER status and mean DRC values in BC patients who have HER2-negative (HER-) tumors: that is, the mean DRC value in ER-/HER2- tumors was significantly lower as compared with ER-/HER2+ tumors (p&lt;0.05). In contrast, the mean DRC among patients with ER+/HER2+ tumors did not significantly differ from ER-/HER2+ tumors (p&gt;0.05). The data followed similar patterns when DRC was categorized in tertiles. In conclusion, there is an association between DRC levels and ER status, and this association is modified by HER2 receptor status. Supported by grants from the NCI Center to Reduce Health Disparities and NIH-NIGMS MBRS SCORE and RISE Programs grants # S06 GM008239-20, 9SC1CA182846-04 GM082406 and PSM-MCC Partnership grant # 5U54CA163071-04.
Citation Format: Jaime L. Matta, Luisa Morales, Carmen Ortiz, Damian Adams, Wanda Vargas, Patricia Casbas, Julie Dutil, Miguel Echenique, Erick Suarez. Estrogen receptor expression is associated with DNA repair capacity in breast cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5228.
Abstract 5238: The chemopreventive potential of silver nanoparticles against UVB-induced skin carcinogenesis in mouse model
Authors: Tyagi Nikhil , Arora Sumit , Srivastava Sanjeev K. , Carter James E. , Singh Ajay P. , Singh Seema 
Published: July 2016

Abstract
Solar ultraviolet (UV) radiation, particularly its UVB component, is an established cause of human skin carcinogenesis due to its ability to cause DNA damage in skin cells. Although several sunscreen formulations have been developed and commercialized to limit or minimize UVB exposure to skin cells, incidence of skin cancer has continued to increase suggesting their limited or no efficacy in preventing UV-induced skin cancer occurrence. Recently, we revealed the potential of silver nanoparticles (AgNPs; ≤ 50 nm) against UVB radiation-induced DNA damage in human keratinocytes (HaCaT). Here we performed preclinical evaluation of chemopreventive efficacy of AgNPs against UVB-induced skin tumorigenesis in SKH-1 hairless mouse model. The different concentrations (20 and 40 mg/kg) of AgNPs mixed with hydrophilic cream base were uniformly applied topically onto the dorsal area of mouse skin prior to UVB-irradiation to assess chemopreventive efficacy for several weeks. The UVB treatment group showed tumor formation within 13 weeks, and had high incidence (93.3%) rate by the end of the study (29 weeks). Interestingly, the pretreatment of mice with AgNPs significantly increased the latency period (6-9 weeks) of UVB-induced tumor formation. Moreover, overall tumor incidence was found to be significantly decreased (50 and 78%; in 20 and 40 mg/kg respectively) as compared to AgNPs-untreated mice. Tumor multiplicity and average tumor volume/tumor-bearing mouse were also observed to be significantly reduced in AgNPs-treated mice. Additionally, AgNPs treatment alone for 29 weeks did not induce any apparent signs of toxicity and changes in the body weight suggesting the safety of AgNPs. Altogether, these findings suggest that AgNPs are potential chemopreventive agents against UVB radiation-induced skin carcinogenesis and thus opening the ways for human applications.
Citation Format: Nikhil Tyagi, Sumit Arora, Sanjeev K. Srivastava, James E. Carter, Ajay P. Singh, Seema Singh. The chemopreventive potential of silver nanoparticles against UVB-induced skin carcinogenesis in mouse model. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5238.
Abstract 525: Higher mutation rate is associated with more frequent expression of cancer/testis antigens in human tumors
Authors: Jing Junping , Mayes Patrick , Degenhardt Yan , Brown James R. , Sanseau Philippe 
Published: July 2016

Abstract
Tumors with high mutation rate such as those of melanoma and non-small cell lung cancers (NSCLC) have shown greatest response to the emerging immune therapies. These tumors harbor a large number of somatic mutations, some of which could be translated into neoantigens, potentially evoking host immune response. To what degree self antigens, many of which are cancer testis (CT) antigens, contribute to enhanced immune response in these tumors has never been systematically studied. Here we show that cancers with higher mutation rate frequently express a larger number of CT antigens than cancers with fewer mutations. In NSCLC, tumors with more than 300 non-synonymous mutations (75th percentile, n = 158) express more than 3 times as many CT antigens as those tumors with fewer than 100 mutations (25th percentile, n = 162), with a P-value of 1.6e-13. In head and neck cancers, tumors with more than 140 non-synonymous mutations (75th percentile, n = 79) express nearly twice as many CT antigens as those tumors with fewer than 60 mutations (25th percentile, n = 80), with a P-value of 0.004. Additionally, in NSCLC, tumors with high mutation rate are associated with higher expression of CD8B and granzyme B, markers representing cytotoxic lymphocytes. Tumors with more expressed CT antigens are also associated with higher expression of these markers. These data suggest that CT antigens, along with neoantigens, may contribute to a stronger host immune response in these hypermutative tumors.
Citation Format: Junping Jing, Patrick Mayes, Yan Degenhardt, James R. Brown, Philippe Sanseau. Higher mutation rate is associated with more frequent expression of cancer/testis antigens in human tumors. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 525.
Abstract 5251: Chemoprevention of cadmium induced prostate carcinogenesis
Authors: Suman Suman , Das Trinath P. , Alatassi Houda , Ankem Murali K. , Damodaran Chendil 
Published: July 2016

Abstract
Cadmium is known carcinogen that causes damages to multiple organs. Cadmium acts as an agonist and activates androgen receptor (AR) in prostate epithelial cells which in turn promotes the carcinogenesis of prostate. Studies have indicated that occupational exposure of cadmium is a risk factor for prostate cancer and hence there is an immediate need to prevent cadmium induced prostate cancer in occupational workers. Various reports have shown that inhibition of AR signaling by AR inhibitors suppressed cadmium induced prostate carcinogenesis. So, the present study focuses to identify dietary agent which can effectively prevent cadmium induced prostate cancer and to dissect the mechanism of action on malignant transformed cells. We have disclosed one such compound, 6-(3, 9-dihydroxy-2-prenylcoumestan (Psoralidin) (Pso) a non-toxic, orally bioavailable compound, which effectively targets only prostate cancer cells and innocuous to healthy cells. Our results have shown cadmium transformed prostate epithelial cells (CTPE) exhibits high proliferative and high colony forming ability in soft agar assays. However, treatment of CTPE cells with Pso resulted in growth inhibition, without causing toxicity to normal prostate epithelial cells (RWPE-1). Finally, in vivo experiments showed that oral administration of Pso (20 mg/kg/BW) effectively suppresses the growth in CTPE xenografts, at physiologically achievable doses without any toxicity. The pathological findings suggest that CTPE tumors exhibits epithelial and mesenchymal transition (EMT) phenotype and infiltrating margins into the surrounding muscle and adipose tissue. However, Psoralidin treated tumors showed a decrease in tumor size with a significant central necrosis (up to 60% of the tumor size). More specifically, margins of Psoralidin treated tumors are less infiltrative and becoming more well circumscribed. We have also noticed that the mesenchymal component is not present and the only viable tumor is the epithelial one after Pso treatment. Altogether, our results confirm that consumption of natural compounds such as Psoralidin may play an important role in the chemoprevention for cadmium induced prostate carcinogenesis.
Citation Format: Suman Suman, Trinath P. Das, Houda Alatassi, Murali K. Ankem, Chendil Damodaran. Chemoprevention of cadmium induced prostate carcinogenesis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5251.
Abstract 5254: Andrographolide prevents prostate cancer by targeting CXCR3/CXCR7 and regulators of cell cycle
Authors: Mir Hina , Kapur Neeraj , Singh Rajesh , Sonpavde Guru , Lillard James W. , Singh Shailesh 
Published: July 2016

Abstract
Despite state of the art cancer diagnostics and therapies offered in clinics, prostate cancer (PCa) remains the second leading cause of cancer-related deaths in men. Hence, more robust therapeutic/preventive regimes are required to combat this lethal disease. In the current study, we have tested the efficacy of andrographolide (AG), a bioactive diterpenoid isolated from Andrographis paniculata, against PCa. This natural agent selectively affects PCa cell viability in a dose and time-dependent manner, without affecting primary prostate epithelial cells. Furthermore, AG showed differential effect on phases of cell cycle in LNCaP, C4-2b and PC3 cell lines compared to retinoblastoma protein (RB-/-) lacking DU-145 cells. This agent blocked the G2/M transition in LNCaP, C4-2b and PC3 whereas DU-145 cells failed to transit G1/S phase. This difference was primarily due to switching of the activation states of cell cycle regulators in these cell lines. AG induced its effect mainly via cyclin A2 and B1 in LNCaP, C4-2b and PC3 cell lines; whereas, cyclin E related regulation was affected in DU-145 cells. Phosphorylation status of Wee1, a nuclear kinase belonging to the Ser/Thr family and CDC2 was also affected by AG. Intriguingly, AG affected cell viability and the ability of PCa cells to migrate via modulating CXCL11 and CXCR3 and CXCR7 expression. The significant impact of AG on cellular and molecular processes involved in PCa progression suggest this agent has potential to be used as a therapeutic and/or preventive modality.
Citation Format: Hina Mir, Neeraj Kapur, Rajesh Singh, Guru Sonpavde, James W. Lillard, Shailesh Singh. Andrographolide prevents prostate cancer by targeting CXCR3/CXCR7 and regulators of cell cycle. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5254.
Abstract 5261: Novel resveratrol analogue, HS-1793, inhibits hypoxia-induced HIF-1 and VEGF expressions and inhibits tumor growth of human breast cancer cells in a nude mouse xenograft model
Authors: Kim Dong Hwan , Kim Min Jeong , Sung Bokyung , Kang Yong Jung , Hwang Seong Yeon , Hwang Na Lam , Kim Nam Deuk 
Published: July 2016

Abstract
Taking phytochemicals provide various benefits for human health. Among them, resveratrol, from the blueberry, is well known for its beneficial effects for human. However, resveratrol has photosensitive and easily decomposition by digestive enzyme. Thus we synthesized several synthetic analogues of resveratrol with potent activity. One of them, 4-(6-hydroxy-2-naphtyl)-1, 3-benzenediol (HS-1793) treatment showed potent antitumor activity in various human cancer cells. In this study, we investigated the effects of a novel analogue of resveratrol, HS-1793 on the expressions of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in MCF-7 with MDA-MB-231 human breast cancer cells. We found that HS-1793 inhibited hypoxia (1.0% oxygen) induced HIF-1α protein level and its downstream target, vascular endothelial growth factor (VEGF) expression dose-dependently in both cell lines. Decreased HIF-1α by HS-1793 modulated through 26S proteasome pathway. We also found that HS-1793 suppressed tumor growth in tumor xenograft mice model. Treatment with 10 mg/kg of HS-1793 suppressed Ki-67 and CD31 expressions in tumor tissues. Above all, HS-1793 shows more powerful effects than resveratrol. Taken together, these results implied that HS-1793, a novel analogue of resveratrol might be a new potent chemopreventive agent and anticancer therapy in human breast cancer.
Citation Format: Dong Hwan Kim, Min Jeong Kim, Bokyung Sung, Yong Jung Kang, Seong Yeon Hwang, Na Lam Hwang, Nam Deuk Kim. Novel resveratrol analogue, HS-1793, inhibits hypoxia-induced HIF-1 and VEGF expressions and inhibits tumor growth of human breast cancer cells in a nude mouse xenograft model. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5261.
Abstract 5266: Fast and accurate fusion transcript detection using the Trinity Cancer Transcriptome Analysis Toolkit
Authors: Haas Brian , Tickle Timothy , Pochet Nathalie , Sun Jing , Hsu Peggy , Stewart Chip , Ganote Carrie , Fulton Ben , Wu Catherine , Regev Aviv 
Published: July 2016

Abstract
Chromosomal rearrangements leading to fusion transcripts represent a class of oncogenic aberrations that are of high interest for understanding cancer biology, treating cancer patients, and as targets for the development of new therapies. Transcriptome sequencing via RNA-Seq coupled with downstream bioinformatics software applications offers an effective method for identifying candidate fusion transcripts, and is more targeted and cost-effective than whole genome sequencing. Although many such fusion detection software tools have recently been made available, they often differ greatly in prediction accuracy, execution times, computational requirements, installation complexity, and in not being readily accessible to non-bioinformatician cancer researchers.
Here we present the Trinity Cancer Transcriptome Analysis Toolkit (CTAT), a newly developed suite of RNA-Seq targeted fusion detection tools leveraging a combination of reference genome read-mapping and de novo transcriptome assembly, coupled to in silico fusion transcript validation, annotation, and visualization. We show that components of our Trinity CTAT fusion detection toolkit, including STAR-Fusion and FusionInspector, yield improved accuracy and run times as compared to alternative leading tools. As a demonstration of the utility of Trinity CTAT, we explore fusion transcript discovery in a large cohort of ∼300 chronic lymphocytic leukemia (CLL) patient samples. We identify several novel recurrent fusions that may represent drivers of CLL etiology and provide new avenues to therapies.
In addition to fusion transcript identification, Trinity CTAT aims to provide cancer researchers with easy access to methods for analyzing cancer RNA-Seq, including transcript reconstruction, identification of mutations, expression analysis, and tumor heterogeneity. Trinity CTAT is freely available open source software and readily accessible to all cancer researchers via our public Galaxy web portal: https://galaxy.ncgas-trinity.indiana.edu/.
Citation Format: Brian Haas, Timothy Tickle, Nathalie Pochet, Jing Sun, Peggy Hsu, Chip Stewart, Carrie Ganote, Ben Fulton, Catherine Wu, Aviv Regev. Fast and accurate fusion transcript detection using the Trinity Cancer Transcriptome Analysis Toolkit. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5266.
Abstract 5281: Fast and scalable software for comparative variant analysis and visualization of massive next-generation sequencing data
Authors: Katainen Riku , Mäkinen Veli , Aaltonen Lauri A. , Pitkänen Esa 
Published: July 2016

Abstract
Next-generation sequencing (NGS) techniques produce high quantities of DNA and RNA sequencing data, enabling variation analysis at a whole genome level. Due to the massive availability of NGS data, the processing and analysis now constitute a serious challenge for research in life sciences. This necessitates the development of novel, user-friendly and scalable software tools, which are able to jointly handle large NGS data sets in order to break the bottleneck that has already moved from data generation to data analysis in high-throughput biology.
Here we introduce a highly efficient NGS analysis and visualization software tool (Rikurator), which is designed for researchers who are struggling with NGS data analysis and may not have access to a dedicated bioinformatics team. Rikurator can be applied to a multitude of genomic analysis tasks, including discovery of pathogenic mutations in familial or sporadic sample sets, analysis of structural variants and somatic characterization of cancer genomes. To these ends the software implements interactive variant filtering and annotation methods based on sample comparison, control data (e.g. ExAC), amino acid changes and quality scores, which provide an intuitive view at the studied samples. Shared candidate genes in a set of dozens of individuals can be discovered in a matter of minutes with an ordinary laptop computer. Importantly, the software is able to analyze hundreds of whole-genome sequenced samples using only a modest amount of RAM. The tool also visualizes and integrates genes, variants (VCF file format), sequence reads (BAM) and user defined features (BED/GFF). In addition, Rikurator is not limited to human studies, supporting reference genomes and genome annotations in standard formats. The software supports targeted (e.g. exome), whole-genome, RNA, Oxford Nanopore and PacBio sequencing data.
Rikurator can be run on Windows, Linux and Mac, and it will be freely available after publication.
Citation Format: Riku Katainen, Veli Mäkinen, Lauri A. Aaltonen, Esa Pitkänen. Fast and scalable software for comparative variant analysis and visualization of massive next-generation sequencing data. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5281.