bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4823: Serum level of urokinase plasminogen activator receptor is suggested as diagnostic and prognostic biomarker in prostate cancer
Authors: Wach Sven , Al-Janabi Omar , Weigelt Katrin , Fischer Kersten , Greither Thomas , Marcou Marios , Theil Gerit , Nolte Elke , Holzhausen Hans-Juergen , Stoehr Robert , Huppert Verena , Hartmann Arndt , Fornara Paolo , Wullich Bernd , Taubert Helge W. 
Published: August 2015

Abstract
Background: This study aimed to assess the applicability of the soluble urokinase plasminogen activator receptor (suPAR) protein as a diagnostic and/or prognostic biomarker for prostate cancer (PCa) patients.
Material and Methods: SuPAR levels were evaluated by ELISA in serum samples from 146 PCa patients, 35 benign prostate hyperplasia (BPH) patients and 18 healthy controls.
Results: Antigen levels of suPAR differed between healthy controls and PCa or BPH patients (P&lt;0.001). Additionally, suPAR levels differed between the Gleason sum groups GS = 7 vs. GS&gt;7, with higher levels in the latter group (P = 0.011). For further statistical analysis, patients and proband cohorts were separated according to their serum expression of suPAR in a group with low/intermediate level (≤66% percentile) and a group with high levels (&gt;66% percentile). A significant difference in the disease-specific survival was detected between the low/intermediate and the high suPAR level groups (191.4 vs. 144.5 months; P = 0.039; log rank test). The high level group showed a 3.91-fold increased risk of tumor-related death compared to the low/intermediate suPAR level group but this was not significant (P = 0.055; univariate Cox's regression hazard analysis). Therefore, future studies with larger cohorts of PCa patients as well as prospective surveys are necessary.
Conclusion: The differences between the PCa/BPH/healthy control cohorts for suPAR in conjunction with the association of high suPAR antigen levels in the serum with a poor prognosis suggest a diagnostic and prognostic impact of this biomarker for PCa patients.
Citation Format: Sven Wach, Omar Al-Janabi, Katrin Weigelt, Kersten Fischer, Thomas Greither, Marios Marcou, Gerit Theil, Elke Nolte, Hans-Juergen Holzhausen, Robert Stoehr, Verena Huppert, Arndt Hartmann, Paolo Fornara, Bernd Wullich, Helge W. Taubert. Serum level of urokinase plasminogen activator receptor is suggested as diagnostic and prognostic biomarker in prostate cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4823. doi:10.1158/1538-7445.AM2015-4823
Abstract 4824: Pancreatic adenocarcinoma: Comparative analysis of cancer stem cell markers between neoadjuvant and treatment naïve specimens
Authors: Horsley Whitney , Stanley Melissa , O'Neil Bert , Shahda Safi , Sandusky George 
Published: August 2015

Abstract
To better understand the effect of neoadjuvant therapy on the presence of stem cell within pancreatic adenocarcinoma, CD24 and ALDH1 expression levels were compared between surgical specimens that received neoadjuvant therapy and those that did not. ALDH1+ and CD24+ cells have been implicated as markers for cancer stem cells in various cancers. For this study, paraffin-embedded tissues slides were obtain from Indiana University Simon Cancer Center Tissue Procurement and Indiana University Health Pathology Laboratory under approved IRB protocols. The tissues were then stained with immunohistochemical stains for CD24 and ALDH1, scanned using Aperio Imaging System and analyzed using the positive-pixel algorithm in ImageScope giving a percentage of tumor tissue expressing each marker. The results showed that the neoadjuvant tissues (avg. 42.1%) expressed a higher level of ALDH1 (p&lt;0.001) than the treatment naïve tissue (avg. 24.9%); and that the treatment naïve tissues (avg. 30.1%) expressed a higher level of CD24 (p = 0.01) than the neoadjuvant tissue (avg. 17.9%). This indicates that neoadjuvant therapy may be effectively eliminating non-stem cells but not as effective at targeting stem cells expressing ALDH1, though somewhat effective at targeting CD24+ cells.
Citation Format: Whitney Horsley, Melissa Stanley, Bert O'Neil, Safi Shahda, George Sandusky. Pancreatic adenocarcinoma: Comparative analysis of cancer stem cell markers between neoadjuvant and treatment naïve specimens. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4824. doi:10.1158/1538-7445.AM2015-4824
Abstract 4825: Association between genetic profiles and histological classifications of 18 Japanese pseudomyxoma peritonei
Authors: Noguchi Rei , Yano Hideaki , Gohda Yoshimasa , Suda Ryuichiro , Igari Toru , Ohta Yasunori , Yamashita Naohide , Yamaguchi Kiyoshi , Terakado Yumi , Ikenoue Tsuneo , Furukawa Yoichi 
Published: August 2015

Abstract
Pseudomyxoma peritonei (PMP) is a rare disease occurring in 1-2 / 1000,000 and shows a distinct clinical feature caused by cancerous cells that produce mucin or gelatinous fluid in the abdominal cavity. Tumor cells are the most frequently originated from appendiceal mucinous cancer, and less frequently from mucinous tumors of the ovary. PMP is histologically classified into two types; disseminated peritoneal adenomucinosis (DPAM) showing milder phenotype, and peritoneal mucinous adenocarcinomas (PMCA) exhibiting more aggressive phenotype. Several molecular studies have shown frequent mutations in the KRAS and GNAS genes. However molecular profiles associated with different histological and/or clinical characteristics remain largely unknown. To elucidate molecular mechanisms underlying PMP, we analyzed 18 Japanese PMP tumors comprising of 10 DPAMs and 8 PMCAs. DNA was extracted from tumor tissues and their matched normal samples, and was subjected to amplicon sequencing using Ion AmpliSeq Cancer Panel v2 (Life Technologies) containing 49 cancer-related genes. In the 18 tumors, we identified a total of 42 somatic mutations (34 missense, 1 deletion, 1 insertion, 2 intron, 1 splice site mutations, and 3 synonymous mutations) in 13 genes. Of the 42 mutations, 35 were judged as pathogenic, and the remaining seven as non-pathogenic by the search of public databases and reports, or by in silico analysis. KRAS and GNAS mutations were found in 14 (77.8%) and 8 (44.4%) tumors, respectively. Interestingly, no mutations were detected in APC or CTNNB1. Notably, TP53 mutation was found in 3 of the 8 PMCAs, but not in the 10 DPAMs. Two of the 8 PMCAs carried mutation in either PIK3CA or AKT1. These data suggest that KRAS and/or GNAS mutations play a vital role in the development of both types of PMP, and that inactivation of Wnt signaling pathway may not be involved in the tumorigenesis. Furthermore, mutations in TP53 and/or genes related to PIK3CA-AKT pathway may be associated with malignant properties of PMCA. Further studies will facilitate the elucidation of molecular mechanism underlying PMP, and contribute to the development of effective therapeutic and preventive strategies to this disease.
Citation Format: Rei Noguchi, Hideaki Yano, Yoshimasa Gohda, Ryuichiro Suda, Toru Igari, Yasunori Ohta, Naohide Yamashita, Kiyoshi Yamaguchi, Yumi Terakado, Tsuneo Ikenoue, Yoichi Furukawa. Association between genetic profiles and histological classifications of 18 Japanese pseudomyxoma peritonei. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4825. doi:10.1158/1538-7445.AM2015-4825
Abstract 4832: Independent prognostic role of chromosome 12p deletion in prostate cancer
Authors: Minner Sarah Jane Pauline , Ahray Ramin , Kluth Martina , Schlomm Thorsten , Simon Ronald , Sauter Guido , Tsourlakis Maria Christina 
Published: August 2015

Abstract
Deletion of chromosome 12p is a recurrent alteration in prostate cancer, but the prevalence and clinical significance of this alteration is unclear. More than 7,000 prostate cancers with clinical follow-up data in a tissue microarray (TMA) format were analyzed by dual labeling fluorescence in situ hybridization (FISH) using probes for 12p13 (CDKN1B; p27) and for centromere 12 as a reference. CDKN1B was selected as a probe because this gene is located in the center of the deletion, which spans &gt;10 Mb and includes &gt;50 genes in 80% of cancers with 12p deletion. In 13.7% of prostate cancers a deletion of 12p was found (13.5% hemizygeous; 0.2% homozygeous deletions). 12p deletions were linked to advanced tumor stage (p&lt;0.0001), high Gleason grade (p&lt;0.0001), lymph node metastasis (p = 0.0004), rapid tumor cell proliferation (p&lt;0.0001), and early biochemical recurrence (BCR) (p = 0.0027). Multivariate analysis including pT stage (p&lt;0.0001), Gleason grade (p&lt;0.0001), pN status (p = 0.0001), preoperative PSA levels (p = 0.0001), and resection margin status (p = 0.0001) revealed an independent prognostic value of 12p deletion (p = 0.0014). There was no association with ERG fusion status. Deletion of 12p deletion was only minimally linked to p27 expression status, which by itself was unrelated to clinical outcome. This argues against p27 as the key target gene of 12p deletions. Since none of the involved 12p genes is recurrently mutated in next generation sequencing studies, simultaneous dosage reduction of multiple genes may exert a relevant biological effect in 12p deleted cancers. In summary, the results of our study demonstrate that 12p deletion is frequent and provides independent prognostic information in prostate cancer.
Citation Format: Sarah Jane Pauline Minner, Ramin Ahray, Martina Kluth, Thorsten Schlomm, Ronald Simon, Guido Sauter, Maria Christina Tsourlakis. Independent prognostic role of chromosome 12p deletion in prostate cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4832. doi:10.1158/1538-7445.AM2015-4832
Abstract 4846: Automated RNA and DNA purification from FFPE samples
Authors: Mandrekar Michelle , Horejsh Douglas , Lewis Samantha , Moreland Chris , Urh Marjeta 
Published: August 2015

Abstract
Formalin-fixed, paraffin-embedded (FFPE) samples are commonly used for archiving pathology samples for use by many researchers including clinical research labs. These samples provide a valuable tool for retrospective studies of diseases such as cancer. Traditional methods for the purification of DNA or RNA from FFPE tissue samples are often labor intensive, include the use of hazardous organic reagents, and involve difficult pre-processing steps. Here, we describe development of automated methods for the purification of RNA or DNA from FFPE tissue sections using the Maxwell® RSC Instrument, which can process between 1 and 16 samples. DNA was purified from FFPE mouse brain, liver, lung, skin and spleen as well as FFPE human colon. RNA was purified from FFPE mouse brain, liver, lung, skin and spleen as well as FFPE human breast tissue. Eluates were tested for inhibition in qPCR or RT-qPCR. A comparison with another automated method was performed with FFPE mouse spleen and skin and a human tissue. The Maxwell RSC methods produced high quality amplifiable DNA or RNA from a variety of sample types with little or no inhibition. In addition, these methods simplified pre-processing, minimized hands-on time, and did not use hazardous organics.
Citation Format: Michelle Mandrekar, Douglas Horejsh, Samantha Lewis, Chris Moreland, Marjeta Urh. Automated RNA and DNA purification from FFPE samples. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4846. doi:10.1158/1538-7445.AM2015-4846
Abstract 4855: DBGC: database of gastric cancer
Authors: Yu Yingyan 
Published: August 2015

Abstract
DBGC is a comprehensive database, integrating various gastric cancer related data resources. In this database, gastric cancer related transcriptomics projects, proteomics projects, mutations, biomarkers and drug sensitive genes from different sources were collected and unified. Besides, follow-up information and clinicopathological information of gastric cancer patients in Shanghai, China, were also integrated through ID-mapping. We believe that this database will greatly facilitate the research work of gastric cancer researchers.
Database URL: http://bminfor.tongji.edu.cn/dbgc/index.do
Note: This abstract was not presented at the meeting.
Citation Format: Yingyan Yu. DBGC: database of gastric cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4855. doi:10.1158/1538-7445.AM2015-4855
Abstract 4856: ITD Assembler: An algorithm for internal tandem duplication discovery from short-read sequencing data
Authors: Hampton Oliver A. , Rustagi Navin , Li Jie , Xi Liu , Gibbs Richard A. , Plon Sharon E. , Kimmel Marek , Wheeler David A. 
Published: August 2015

Abstract
Tandem duplication of coding sequence is an important mechanism of somatic mutation capable of activating oncogenes such as fms-related tyrosine kinase 3 (FLT3) as well as the potential for underlying constitutional or germline disease. Detection of internal tandem duplication (ITD) in short-read sequencing data remains challenging due to deficiencies in short-read alignment where reads carrying signatures of ITD are often unmapped. Assembly based approaches collapse repetitive sequences, resulting in reduced or lost genomic complexity. The majority of structural variation detection tools are limited to finding insertions that are contained entirely within individual read alignments, and are unable to detect read-spanning duplications. Tools designed to detect large structural variation from paired-end reads that map discordantly based on expected fragment size and orientation do not provide the precision needed to detect ITDs. Only tools that consider the characteristic alignment features that signal the presence of ITDs will be able to detect them; these alignment features include: an excess of reads with unaligned, soft-clipped bases, read pairs where one end is unmapped located near the site of insertion, and read pairs where both ends are unmapped.
We introduce ITD Assembler, a novel approach that searches all unmapped reads from exome capture or whole genome sequencing data to identify duplications. From the entire set of unmapped reads plus subset of mapped reads harboring soft-clipped bases, de Bruijn graph assembly is applied to select reads that form cycles, indicative of duplicated sequence structures. Reads from de Bruijn graph cycles are then assembled using an Overlap Layout Consensus (OLC) methodology thereby alleviating the collapse of repeat sequences affecting de Bruijn graph assembly approaches. Resulting OLC assembled contigs are locally aligned to the reference sequence to annotate the position of ITDs.
ITD Assembler was run on The Cancer Genome Atlas (TCGA) acute myeloid leukemia (AML) dataset, and FLT3-ITD detection rates were compared against orthogonal algorithms. ITD Assembler identified the highest percentage of TCGA FLT3-ITDs, reported significantly higher allele fractions, and discovered additional ITDs in the KIT, CEBPA and WT1 cancer genes.
Citation Format: Oliver A. Hampton, Navin Rustagi, Jie Li, Liu Xi, Richard A. Gibbs, Sharon E. Plon, Marek Kimmel, David A. Wheeler. ITD Assembler: An algorithm for internal tandem duplication discovery from short-read sequencing data. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4856. doi:10.1158/1538-7445.AM2015-4856
Abstract 4875: HIVE Proteomics: Integrated, cloud-based RNA-Seq and proteomics analysis of prostate adenocarcinoma samples
Authors: Dingerdissen Hayley , Mazumder Raja 
Published: August 2015

Abstract
Automated bottom-up proteomics workflows implemented with modern mass-spectrometry instrumentation can readily generate millions of peptide fragmentation spectra from cell-lines and clinically derived samples. The tandem mass-spectra promise to reveal wild-type and somatic mutations, insertions, and deletions and alternatively spliced isoforms translated to functional protein isoforms in tumor samples. However, the available reference proteomes represent a poor analysis substrate for the observation of protein evidence of genomic and transcript variation. The advent of cheap and fast RNA sequencing (RNA-Seq) provides an elegant solution to the lack of sample-specific reference proteomes. We anticipate that the falling cost of RNA-Seq will prompt an increasing number of proteomics labs to use contract next-gen sequencing (NGS) services to obtain RNA-Seq data to derive sample-specific reference proteomes. In contrast to public repositories of genomic variation, sample-specific RNA-Seq data captures transcribed rare, individual, cell-type, and sample-specific genomic variation. RNA-Seq-based transcripts also provide sample-specific information on observable proteins. Furthermore, paired RNA-Seq and proteomics data links gene expression and protein abundance, enabling the study of gene regulation linked to protein abundance dynamics. However, the analysis of multi-gigabyte paired mass-spectra and RNA-Seq datasets pose significant scientific and logistical challenges. Few proteomics labs have the personnel, archival data storage, computational resources, or informatics pipelines needed. The cloud-based genomics analysis platform High-performance Integrated Virtual Environment (HIVE) will provide turn-key integrated proteomics and RNA-Seq analyses to the wider proteomics community in a secure, trackable, sharable, and scalable computing platform. We will then use this integrated proteomics_RNA-Seq analysis pipeline to identify high-value mutations in prostate adenocarcinoma samples, thereby demonstrating the utility of the platform while also generating key data for future investigations.
Citation Format: Hayley Dingerdissen, Raja Mazumder. HIVE Proteomics: Integrated, cloud-based RNA-Seq and proteomics analysis of prostate adenocarcinoma samples. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4875. doi:10.1158/1538-7445.AM2015-4875
Abstract 4882: Megabase-scale phased haplotypes of genetic aberrations from whole cancer genome sequencing of primary colorectal tumors
Authors: Lau Billy , Bell John M. , Schnall-Levin Michael , Jarosz Mirna , Hopmans Erik , Wood Christina M. , Zheng Grace X. , Giorda Kristina , Ji Hanlee P. 
Published: August 2015

Abstract
Cancer genomes contain multiple types of genetic aberrations that include mutations, deletions, copy number variants and chromosomal rearrangements. Despite advances in next generation sequencing, it remains a major challenge to delineate many of these somatic genomic alterations because of intrinsic complexity of cancer genomes. Haplotyping involves the assignment of genetic variants such as mutations and structural variants to specific segment of homologous chromosomes. Experimentally determined phasing of cancer genomes offers an opportunity to resolve complex genomic structures such as somatic rearrangements, aneuploidy composition and ongoing evolutionary changes. However, contiguous phasing of cancer genomes on a megabase (Mb) scale remains difficult to achieve with sequencing-based approaches.
In this proof-of-concept study, we experimentally determined Mb-scale haplotypes of primary tumor samples via whole genome sequencing. To generate haplotypes, we employed an automated instrument that partitions long DNA fragments into hundreds of thousands of reactions, each of which incorporates a unique, nonrandom barcode into indexed sequencing libraries. Given need to amplify from sparse numbers of molecules and the high efficiency of the automated sequencing library construction process, the DNA requirements for each sample are less than 5 ng.
We sequenced the genomes of primary colorectal cancer samples and their matched normal diploid DNA with an Illumina sequencer. We used the single nucleotide variants to generate Mb-scale haplotype blocks (N50 of 1.2 Mb) with phased haplotype block size of up to 11.3 Mb. We were able to delineate cancer genome haplotypes that cover allelic imbalances, copy number variations such as deletions and other genomic instability events. Structural variants were identified in the context of their position in specific chromosome homologues. Thus, we improved the characterization of somatic genetic aberrations using contiguity mapping and cancer genome haplotypes in the context of whole cancer genome sequencing. Overall, we demonstrated the feasibility and potential utility of conducting contiguous phased haplotypes in whole cancer genome sequencing from primary tumor samples.
Citation Format: Billy Lau, John M. Bell, Michael Schnall-Levin, Mirna Jarosz, Erik Hopmans, Christina M. Wood, Grace X. Zheng, Kristina Giorda, Hanlee P. Ji. Megabase-scale phased haplotypes of genetic aberrations from whole cancer genome sequencing of primary colorectal tumors. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4882. doi:10.1158/1538-7445.AM2015-4882