bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1487: Rotating 3D projections of prostate lesions imaged by Cu-64-VPAC1 ligand PET and CT
Authors: Wampole Matthew E. , Paudyal Bishnuhari , Trabulsi Edouard J. , Thakur Mathew L. , Wickstrom Eric 
Published: August 2015

Abstract
Surgeons are obliged to examine multiple planar images of fine needle biopsies, CT, and PET images for diagnosis and evaluation of prostate cancer. We hypothesize that optimal comprehension of prostate lesions in the prostate, as they present in the surrounding tissue, will be achieved by 3D registration and presentation of all available images. In particular, PET imaging of a cancer cell surface marker maximizes specificity, relative to imaging of F-18-deoxyglucose uptake. We have demonstrated specific PET imaging in patients of vasoactive intestinal peptide and pituitary adenylate cyclase activating peptide receptor 1 (VPAC1), which is overexpressed on breast cancer and prostate cancer cells. Our PET agent is Cu-64-TP3805, a peptide derived from vasoactive intestinal peptide. From our ongoing prostate cancer patient imaging study, we segmented and co-registered CT image slices and TP3805 PET image slices, then created moving 3D images. Viewing the rotating 3D images from all sides revealed clear delineation of prostate lesions from the adjoining bladder. The lesion images colocalized in space with intraprostatic tumor foci identified from H&E staining of whole mount slices after prostatectomy. Thus, rapid 3D presentation of anatomical, histological, and molecular images could be a useful preparative tool to minimize complications during prostate cancer surgery. This result supports proceeding to 3D analysis of a larger prostate cancer cohort.
Citation Format: Matthew E. Wampole, Bishnuhari Paudyal, Edouard J. Trabulsi, Mathew L. Thakur, Eric Wickstrom. Rotating 3D projections of prostate lesions imaged by Cu-64-VPAC1 ligand PET and CT. [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 1487. doi:10.1158/1538-7445.AM2015-1487
Abstract 150: Long non-coding RNA are differentially expressed in breast cancer clinical subtypes
Authors: Kumar Surendra , Seiler Michael , Bjørklund Sunniva , Børresen-Dale Anne-Lise , Kristensen Vessela , Bhanot Gyan , Ganesan Shridar 
Published: August 2015

Abstract
A primary benefit of RNA-Seq over traditional DNA microarrays is the ability to interrogate expression in unannotated areas of the transcriptome. Methods for identifying novel genes in genomic DNA sequence can use features such as an open reading frame and conserved functional protein elements. Non-coding RNA structures are more difficult to detect, and most of our knowledge of them comes from expressed sequence tags (ESTs), which are large, sequenced contigs from transcriptome cDNA libraries. Carninci et al. showed that over half of these sequences appear to originate from non-coding sources, though very few are annotated. Moreover, many of these non-coding sources are poorly conserved over multiple species indicating that these transcripts may not be functional, but instead, may be the result of “random” transcription. As more studies focus on these “non-coding” regions of the genome evidence of conservation and functionality is emerging. To identifying possibly functional transcripts, we took the approach of identifying only non-coding transcripts which were differentially expressed between breast cancer tumor subtypes, and tumor versus non-tumor samples by RNAseq analysis. We reason that such ncRNA transcription is more likely to be functional because of its association with a specific disease phenotype and the possibility that they affect some regulatory pathway. We have identified known long-non coding tumor suppressors, such as H19 and MEG3, as expressed exclusively in non-tumor samples. In addition we have identified 59 intergenic regions representing a total of 132 300 bp which were differentially expressed between ER+/HER2- and ER-/HER2- breast tumor subtypes. This resulted in 4 potential non-coding regions associated with ER-/HER2- tumors, and 6 potential non-coding regions associated with ER+/HER2- tumors. These transcripts are of great interest, and should be studied in more detail to elucidate the function of these non-coding RNA molecules.
Citation Format: Surendra Kumar, Michael Seiler, Sunniva Bjørklund, Anne-Lise Børresen-Dale, Vessela Kristensen, Gyan Bhanot, Shridar Ganesan. Long non-coding RNA are differentially expressed in breast cancer clinical subtypes. [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 150. doi:10.1158/1538-7445.AM2015-150
Abstract 152: The long non-coding RNA HOTAIR affects exosome-mediated bladder cancer progression
Authors: Berrondo Claudia , Flax Jonathan , Messing Edward M. , Beckham Carla 
Published: August 2015

Abstract
Exosomes are 30-100nM membrane-bound vesicles that participate in intercellular communication and facilitate tumor microenvironments. The mechanisms by which exosomes modify tumor niches are not fully understood. One possibility is that exosomes deliver biologically active molecules like mRNA, protein, miRNA and long non coding RNA (lncRNA) that alter the metabolism of recipient cells to produce pathological phenotypes. Exosomes may also activate the expression of genes involved in tumor progression in recipient cells. Overexpression of the lncRNA HOTAIR is associated with poor prognosis and affects tumor progression, in part, by recruiting PRC2 and LSD1 chromatin modifying complexes to thousands of target genes involved in tumor progression processes such as epithelial-to-mesenchyme transition (EMT). We show that HOTAIR is enriched in bladder cancer (BC) patient tumors and urinary exosomes. BC cell lines also express elevated levels of HOTAIR. Knockdown of HOTAIR in BC cell lines significantly reduces migration and invasion in trans-well and 3D culture, which correlates with EMT gene expression changes in these cells. Exosomes isolated from shHOTAIR vs shScramble cells fail to facilitate migration and invasion in 3D culture of a recipient BC cell line. Selected bands were isolated from a coomassie gel of shHOTAIR and shScramble exosomes and sent for mass spectrometry. Hundreds of putative proteins were identified including proteins involved in RNA binding, apoptosis, vesicle trafficking and integrins. These data support HOTAIR as an important player in exosome-mediated BC tumor progression possibly through affects on gene expression in exosome producer cells. For example, in shHOTAIR cells the loss of PRC2 and/or LSD1 complexes from key genes may ultimately affect the proteins available for packaging into exosomes. Exosomes have important roles in the tumor microenvironment and these data support a role for HOTAIR in the modulation of exosome-mediated tumor progression.
Citation Format: Claudia Berrondo, Jonathan Flax, Edward M. Messing, Carla Beckham. The long non-coding RNA HOTAIR affects exosome-mediated bladder cancer progression. [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 152. doi:10.1158/1538-7445.AM2015-152
Abstract 1522: Survival of skin cancer tumor initiating cells requires the Ezh2 polycomb group protein
Authors: Adhikary Gautam , Grun Dan , Kerr Candace , Balasubramanian Sivaprakasam , Rorke Ellen , Xu Wen , Eckert Richard 
Published: August 2015

Abstract
Epidermal squamous cell carcinoma is among the most common cancers in humans. These tumors are comprised of phenotypically diverse of cells that display varying potential for proliferation and differentiation. Polycomb group (PcG) proteins, including Ezh2, are important candidate stem cell maintanence proteins. Our previous study showed that Ezh2-enriched epidermal cancer stem cells (ECS cells) represent a minority of cells in tumors, yet drive aggressive tumor formation. In the present study, we show that Ezh2 is required for ECS cell survival, migration, invation and tumor formatiom and this is associated with increased histone H3 trimethylationon lysine 27, a mark of Ezh2 action. We also show that Ezh2 knockdown or treatment with Ezh2-selective inhibitors, GSK126 or EP-6438, reduce Ezh2 level and activity, leading to reduced spheroid formation, migration, invasion and tumor formation. Use of these inhibitors was associated with reduced ECS cell vaibility and induction of apoptosis. These studies indicate that epidermal squamous cell carcinoma cells contain a subpopulation of cancer stem cells-like tumor initiating cells that are enriched in Ezh2 expression and that Ezh2 is required for optimal survival of these cells and tumor formation. These studies suggest that treatment with Ezh2 inhibitors may be a strategy for reducing epidermal cancer stem cell survival and supressing tumor formation.
Citation Format: Gautam Adhikary, Dan Grun, Candace Kerr, Sivaprakasam Balasubramanian, Ellen Rorke, Wen Xu, Richard Eckert. Survival of skin cancer tumor initiating cells requires the Ezh2 polycomb group protein. [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 1522. doi:10.1158/1538-7445.AM2015-1522
Abstract 1534: The microbiome of cancer as seen through the lens of public genome sequence data
Authors: Robinson Kelly M. , Sieber Karsten B. , Anderson Kathleen E. , Riley David R. , Dunning Hotopp Julie C. 
Published: August 2015

Abstract
There are 10 times more bacterial cells in the human body than human cells and various bacteria are known to influence carcinogenesis. Therefore we sought to investigate if publicly available whole genome and whole transcriptome sequencing data generated by large public cancer genome efforts, like The Cancer Genome Atlas (TCGA), could be used to examine the microbial composition of tumors. The Burrows-Wheeler Aligner (BWA) was used to align a selection of Illumina paired-end sequencing data from TCGA data to the human reference genome and all complete bacterial genomes in the RefSeq database. Reads were filtered for low complexity and duplicates and then assigned an Operational Taxonomic Unit (OTU). Through careful consideration of all of the bacterial taxa present in the cancer types investigated, we found an increased abundance of Acinetobacter spp. in acute myeloid leukemia (AML) samples, Mycobacterium tuberculosis complex in ovarian serous cystadenocarcinomas (OV), and Pseudomonas spp. in stomach adenocarcinoma (STAD) samples. Further investigation prompted us to conclude that Mycobacterium tuberculosis complex read pairs were found in the OV samples due to sequencing center batch effects. The same analysis of the AML and STAD samples suggests that Acinetobacter spp. are truly present in AML samples and that Pseudomonas spp. are actually present in the STAD samples investigated. Upon completion of this analysis, we determined that it is possible to identify bacteria in human tumor samples. However, care must be taken to assess bacteria that arrived in the sample via various forms of contamination. It is also important to note that the sequencing library method heavily biases the bacterial taxa identified. One sample sequenced with RNA-Sequencing, whole exome sequencing (WXS), and whole genome sequencing (WGS) had extensively different bacteria reflected in the RNA-Seq data compared to that of WGS and WXS. In the future, a comprehensive approach should be used when evaluating the microbiome of tumor samples via sequencing data. The methods used in this study are valid and useful for identifying the presence of bacteria in human samples, but may not be an exhaustive picture. More weight should be given to this approach in the future when bacterial associations with diseases are suspected.
Citation Format: Kelly M. Robinson, Karsten B. Sieber, Kathleen E. Anderson, David R. Riley, Julie C. Dunning Hotopp. The microbiome of cancer as seen through the lens of public genome sequence 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 1534. doi:10.1158/1538-7445.AM2015-1534
Abstract 1535: Omentin: A novel adipokine linking visceral obesity to ovarian cancer progression
Authors: Au Yeung Chi Lam , Co Ngai Na , Onstad Michaela , Yeung Tsz-Lun , Leung Cecilia S. , Schmandt Rosemarie , Lu Karen H. , Mok Samuel C. 
Published: August 2015

Abstract
Advanced stage serous ovarian cancer metastasizes preferentially to the omentum, which is a major site of intra-abdominal fat accumulation, suggesting that the omental microenvironment is a favorable niche for ovarian cancer cells. The 5-year survival drops to below 50% for the cancer cases that spread beyond the pelvis to the omentum. It has also become apparent that obesity contributes to a poor clinical outcome. The mechanisms by which omental adipose tissue promotes tumor growth and disease progression are not entirely clear.
Using transcriptome profiling analysis on the microdissected adipose tissue from patients with benign gynecologic diseases and from patients with advanced high-grade serous ovarian cancer (HGSOC), we found that a novel adipokine called omentin (Intestinal Lactoferrin Receptor ITLN1) was significantly down-regulated in ovarian cancer associated adipose tissue compared with the normal adipose tissue. Survival correlation studies demonstrated that patients with serum ITLN1 levels of &gt;350 ng/mL at the time of first treatment experienced longer survival times than those with lower levels of ITLN1. We showed that ITLN1 suppressed the ovarian cancer cell migration ability and invasion potential in vitro. To delineate the underlying molecular mechanisms, RNA sequencing and pathway analyses were performed on ITLN1 treated ovarian cancer cells and we identified MMP1 as one of the potential mediators. It has been shown that MMP1 expression was induced by lactoferrin, which is abundant in ascites. We hypothesized ITLN1 could abrogate the effect of lactoferrin on ovarian cancer motility and invasion potential. Our preliminary data suggested that secreted ITLN1 may sequester lactoferrin in the ascites, thereby preventing it from binding to the low-density-lipoprotein-receptor-related-protein-1 (LRP-1) on ovarian cancer cell surface and thus inactivate downstream signaling pathways that control MMP1 expression.
The study provides the first evidence that ovarian cancer cells modify the visceral adipose tissue through down-regulation of omentin to facilitate their growth in the omental microenvironment.
Citation Format: Chi Lam Au Yeung, Ngai Na Co, Michaela Onstad, Tsz-Lun Yeung, Cecilia S. Leung, Rosemarie Schmandt, Karen H. Lu, Samuel C. Mok. Omentin: A novel adipokine linking visceral obesity to ovarian cancer progression. [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 1535. doi:10.1158/1538-7445.AM2015-1535
Abstract 1547: The clinical implication of MMP-1 and TIMP-1 on prognosis in patients with non-small cell lung cancer
Authors: An Ho Jung , Kang Jin-Hyoung , Lee Yoon-Jin , Hong Soon Uk , Lee Kyo Young , Kim Jeong-Oh 
Published: August 2015

Abstract
Introduction: The interaction between tumor cells and tumor micro-environment (TME) plays important role in tumor initiation, progression, treatment resistance, and prognosis in solid tumors including non-small cell lung cancer (NSCLC). The aim of this study is to evaluate the prognostic role of TME-related molecules in NSCLC patients who received surgical resection. To find out a possibility of a potential serum biomarker, protein expression in tissue from surgical specimen and pre-operative serum were investigated together.
Methods: For 85 NSCLC patients who underwent surgical resection from August 2006 to September 2010 and had pre-operative serum samplings, we screened the serum levels of 60 TME-related molecules with angiogenesis array kit for 8 patients who had recurrences and 4 patients who did not. For matrix metalloproteinase (MMP)-1 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 in which significant difference was observed between recurrence and recurrence-free groups, protein expressions were investigated using ELISA in serum and immunohistochemistry in tumor tissue.
Results: High serum MMP-1 was related to carcinoembryonic antigen (CEA) level≥5 at diagnosis (P = 0.034), higher frequency of the presence of vascular invasion (P = 0.041). High expression of MMP-1 in tumor cells (intensity score≥2) was related to tumor differentiation (P = 0.057), whereas high MMP-1 expression in stroma was significantly associated with lymph node metastasis and TNM stage (P = 0.021 and P = 0.022, respectively). In the case of TIMP-1, expression in tumor cells was higher for adenocarcinoma but higher in stromal cells for squamous cell carcinoma (P = 0.046). There was no correlation between the tissue and serum levels of MMP-1 and TIMP-1. High serum MMP-1 showed a trend for short overall survival (P = 0.080). When serum MMP-1 was combined with CEA level or presence of vascular invasion, the prognostic implication for overall survival was statistically significant. Neither tumor nor stromal positivity for MMP-1 and TIMP-1 was associated with survival outcome; however, a tumor/stroma TIMP-1 intensity ratio≥1 was strongly associated with early recurrence in multivariate analysis (HR = 13.1, P = 0.008).
Conclusion: In surgically resected NSCLC patients, serum MMP-1 showed a possibility as a prognostic biomarker. In addition, the tumor/stroma TIMP-1 ratio (≥1) in tissue may be a useful to predict tumor recurrence.
Citation Format: Ho Jung An, Jin-Hyoung Kang, Yoon-Jin Lee, Soon Uk Hong, Kyo Young Lee, Jeong-Oh Kim. The clinical implication of MMP-1 and TIMP-1 on prognosis in patients with non-small cell lung 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 1547. doi:10.1158/1538-7445.AM2015-1547
Abstract 1562: Proteomic changes observed in colon cancer tumors by label-free differential profiling of paired tumor versus normal FFPE samples
Authors: Agrawal Lokesh , McAlister Fiona , Roy Sushmita , Unger Florian , David Kerstin , Juhl Harmut , Chelsky Daniel , Moore Helen 
Published: August 2015

Abstract
Colorectal cancer (CRC) is the third most common cancer and if caught early enough has a good prognosis. Mass screening of the adult population is advisable to reduce CRC mortality rate as well as reduce the cost of treating advanced CRC cases. A blood-based biomarker panel with the ability to diagnose CRC as well as determine prognosis and predict the response to drug therapy is desired. However, blood biomarker discovery is hampered by problems of complexity and dynamic range of protein abundance.
Formalin-fixed and paraffin-embedded (FFPE) tissue is an ideal sample type for cancer biomarker analysis due to its ubiquitous use in cancer diagnosis in the clinic and consequent availability in oncology hospitals and clinics as well as biobanks. Biomarker discovery to date using FFPE have used only very few patient samples, making clinically relevant biomarker discovery difficult due to large patient-to-patient variation. As a part of our Biospecimen Research Network (BRN) program we funded a proteomic biomarker study of a large number of colorectal cancer and adjacent normal tissue samples. The investigators employed two platforms for biomarker discovery: label-free intensity based discovery using high resolution tandem mass spectrometry and targeted quantitation using multiple reaction monitoring. These two techniques allowed them to dig deeper into the proteome and to profile phosphopeptides. Paired tissue from 40 patients was profiled and of the 2875 proteins quantified, 367 proteins changed significantly in patients whose tumor size was greater than 50%. Large changes in secreted proteins were observed and many of these proteins were also observed in blood, offering promise for a potential blood-based biomarker for colorectal cancer. A blood-based biomarker assay for colorectal cancer could ultimately reduce the number of colonoscopies required, reducing cost and discomfort.
Citation Format: Lokesh Agrawal, Fiona McAlister, Sushmita Roy, Florian Unger, Kerstin David, Harmut Juhl, Daniel Chelsky, Helen Moore. Proteomic changes observed in colon cancer tumors by label-free differential profiling of paired tumor versus normal 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 1562. doi:10.1158/1538-7445.AM2015-1562
Abstract 1563: Stool proteomics reveals novel candidate biomarkers for colorectal cancer screening
Authors: Bosch Linda JW , de Wit Meike , Hiemstra Annemieke C. , Piersma Sander , Pham Thang , Oudgenoeg Gideon , Scheffer George , Mongera Sandra , Komor Malgorzata , Terhaar Sive Droste Jochim , Oort Frank A. , van Turenhout Sietze , Ben Larbi Ilhame , Mulder Chris JJ , Carvalho Beatriz , Fijneman Remond JA , Jimenez Connie , Meijer Gerrit A. 
Published: August 2015

Abstract
Introduction and objectives: Early detection of colorectal cancer (CRC) and its precursor lesions is an effective approach to reduce CRC mortality rates. The fecal immunochemical test (FIT) is a non-invasive CRC screening test that detects small traces of the blood protein hemoglobin. Although beneficial in its current form, the FIT test characteristics leave room for improvement. The aim of the present study was to identify and validate novel protein biomarkers in stool that complement or outperform the current hemoglobin-based test, to improve its diagnostic accuracy.
Methods: Proteins isolated from stool from 10 subjects without any signs of colorectal neoplasia (controls) at colonoscopy and from 12 CRC patients were analyzed by GeLC-MS/MS (discovery set). Data were analyzed by comparing protein abundancies, measured as spectral counts. Analysis of differential proteins was performed using the beta-binomial test. Findings were validated by mass spectrometry (Q-Exactive) in an independent series of 292 stool samples obtained from control subjects (n = 109) and subjects with adenomas (n = 55), advanced adenomas (n = 53), or CRCs (n = 75).
Results and Discussion: In total 830 human proteins were identified in the discovery set, of which 134 were significantly enriched in CRC. These included 78 proteins that were significantly more enriched in FIT-negative CRC stool samples compared to controls. Preliminary analysis of the validation set indicates that more than half of these markers are significantly more abundant in CRC samples compared to controls.
Conclusion: Proteome profiling of stool samples revealed novel candidate biomarkers to improve current CRC screening tests. More data analysis is currently ongoing to select most promising protein biomarkers for clinical assay development.
Citation Format: Linda JW Bosch, Meike de Wit, Annemieke C. Hiemstra, Sander Piersma, Thang Pham, Gideon Oudgenoeg, George Scheffer, Sandra Mongera, Malgorzata Komor, Jochim Terhaar Sive Droste, Frank A. Oort, Sietze van Turenhout, Ilhame Ben Larbi, Chris JJ Mulder, Beatriz Carvalho, Remond JA Fijneman, Connie Jimenez, Gerrit A. Meijer. Stool proteomics reveals novel candidate biomarkers for colorectal cancer screening. [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 1563. doi:10.1158/1538-7445.AM2015-1563