tbuckley/cabot-search huggingface dataset:
CHARACTERISTICS AND DISTRIBUTION OF POLYPS FOUND IN BOWEL CANCER SCREENING COLONOSCOPY
Authors: W Lai, M Fung, J Vatish, R Pullan, M Feeney
Journal: Gut (2013)

<h3>Introduction</h3> Bowel Cancer Screening Programme (BCSP) in the UK achieved nationwide coverage in 20101. We collected data from a local endoscopy unit that performs bowel cancer screening colonoscopy between 2010 and 2011. <h3>Aims/Background</h3> This audit aims to look at the characteristics and distribution of polyps found in screening as well as surveillance colonoscopies performed under the BCSP. <h3>Method</h3> Patients aged between 60 and 75 who underwent bowel cancer screening colonoscopy (first and surveillance) in Torbay endoscopy unit from January 2010 to December 2011 were identified from the BCSP database (Oracle BI Interactive Dashboards). Endoscopy reports were drawn from Scorpio© reporting system and corresponding histology results using Cyberlab© integrated pathology system. <h3>Results</h3> 887 procedures were performed in the 2 year period. 794 polyps were found in 354 procedures, giving a polyp detection rate of 39.9% in this series. Of which 6% contained focus/were of high grade dysplasia. Majority of polyps was found in the sigmoid colon (40.8%) and rectum (13.5%). 669 polyps had histology results, of which 51.8% were Tubular adenomas, 34.7% Tubulovillous adenomas and 7.6% Hyperplastic polyps. There was a 9.6% increase (95% CI 18.5%–0.7%) in the proportion of Tubular adenomas in the over 70s compare with the 60–65 age group (57% vs. 47.4%) (Table&nbsp;1). There was also an apparent shift from Hyperplastic polyps and Tubulovillous adenoma to Tubular adenoma with increasing age (Figure&nbsp;1). <h3>Conclusion</h3> The most common benign polyp found was Tubular adenomas, and more common amongst the elderly (statistically significant), but further study such as a national BCSP evaluation is needed.
Consortium Closing in on Neurofibromatosis Type 1 Gene
Authors: M. E. Newman
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Consortium Closing in on Neurofibromatosis Type 1 Gene Get access Michael E. Newman Michael E. Newman Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 19, 4 October 1989, Pages 1444–1445, https://doi.org/10.1093/jnci/81.19.1444 Published: 04 October 1989
Abstract 2222: Identify and evaluate novel biomarker CIP2A for cervical cancer diagnostics
Authors: Lisa P. Huang, Erika Libby, Jason Trama
Journal: Cancer Research (2011)

Abstract Early detection of cervical cancer is critical for a favorable prognosis. HPV infection is not a reliable marker for predicting the malignancy potential of cervical lesions. Standard cytological detection methods such as Pap smear are highly subjective. As a result, there remains a very high demand for a diagnostic assay capable of determining which early stage cervical lesions will progress to cervical cancer. We sought to identify cervical cancer biomarkers and to test the hypothesis that the small percentage of HPV positive patients who progress to cervical cancer have aberrant expression of the cell signaling component, c-myc and its regulators, including protein phosphatase 2A (PP2A) and cancerous inhibitor of PP2A (CIP2A). In this study, Bio-Plex liquid microarray analysis was used to determine the HPV status cervical specimens (NNon-tumor=28, NTumor=30). qRT-PCR, Western blotting, flow cytometry, and ELISA analysis were used to access expression levels of CIP2A, c-myc, PP2A, Ki67, TOP2A, MCM2, MCM5, p14ARF, and p16INK4a. Our studies indicate CIP2A was abundantly expressed in cervical cancer cell lines and it was not expressed in normal epithelial cells. CIP2A mRNA levels were higher in cervical tissues from stage I, II, and III cervical cancer patients in comparison to the level of CIP2A mRNA in normal tissue. CIP2A protein was specifically expressed in cervical cancer tissues at different cancer stages, and not in non-cancer or adjacent non-tumor cervical tissue. Our data showed that CIP2A mRNA detection had a sensitivity of 80% and specificity of 91% and CIP2A protein expression detection had a sensitivity of 80% and specificity of 100%, similar to that of p16INK4a biomarker. Although CIP2A/PP2A/c-myc pathway may work together in the development of cervical cancer, our data strongly indicate that only CIP2A (but not PP2A or c-myc) is a reliable biomarker for detection of cervical cancer. In this study, we also examined the combined use of at least two biomarkers as a tool to detect cervical cancer. Our studies also suggest there was no strong correlation of CIP2A expression with HPV subtype, age, ethnical background, or other patient characteristics. In conclusion, our clinical studies suggest that CIP2A is a reliable and sensitive biomarker for detection of cervical cancer. CIP2A mRNA or protein can both serve as reliable markers. A combined use of CIP2A with at least on additional marker selected from the group consisting of Ki67, TOP2A, MCM2, MCM5, and p16 will improve the assay sensitivity and specificity. CIP2A is a novel biomarker for early detection of cervical cancer in humans. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2222. doi:10.1158/1538-7445.AM2011-2222
Abstract 1226: Lapatinib could not prevent heregulin-induced HER2-HER3 signalling, and addition of pertuzumab to lapatinib increases drug sensitivity and inhibition of HER signalling
Authors: Wing Yin Leung, Anthony H. Kong
Journal: Cancer Research (2012)

Abstract Lapatinib is an EGFR/HER2 tyrosine kinase inhibitor (TKI) that has been approved for clinical use in HER2 positive breast cancer patients who have progressed on previous Trastuzumab containing regimens. However, lapatinib monotherapy only delays tumour growth in HER2 positive xenograft models and has only modest clinical activity in breast cancer patients. There is a further need to understand its mechanisms of action and resistance. We aimed to assess the acute effect of lapatinib on HER2 phosphorylation in HER2 positive breast cancer cells since previous work from our lab showed that inadequate suppression of HER2 phosphorylation by gefitinib and trastuzumab may lead to acquired drug resistance. Traditionally, the phosphorylation status of HER proteins is determined by phosphor-tyrosine western blotting followed by immunoprecipitation. The limitation of this technique includes false positive due to signals from co-precipitated proteins of the same size as target, which is even more prominent with the HER family of protein. With the use of phosphorylated protein-specific antibody, we found that, contrary to general belief, lapatinib could not abolish HER2 phosphorylation in HER2 over-expressed breast cancer cell lines under serum-supplemented condition. It was thought that the growth factors in the serum activate other HER receptors to maintain HER2 phosphorylation. Indeed, Lapatinib could reduce phospho-HER2 level in serum-starved breast cancer cell lines; however, it failed to reverse heregulin-induced HER signalling activation and downstream MAPK and AKT signalling. The combination of lapatinib and pertuzumab drastically inhibited ligand-induced HER family phosphorylation and downstream signalling. HER3 was reported as an important biomarker for resistance in HER family targeted therapy. This novel combination could inhibit HER3 phosphorylation and its downstream AKT pathway more than lapatinib or pertuzumab alone; this finding also correlated with cancer cell viability, as the combination of lapatinib and pertuzumab reduced cell viability more than either drug alone. These results might indicate a new strategy of drug combination to tackle resistance in HER2 targeted therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1226. doi:1538-7445.AM2012-1226
AB0031 Anti-inflammatory property of hdl in nod1 ligand induced kawasaki arteritis in mice
Authors: H. Kono, T. Yanagida, H. Kikuchi, K. Asako, M. Takayama
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Atherosclerosis is a chronic metabolic disease of inflammatory processes. Immune cells including monocytes are recruited to the subintimal lesion of the vascular wall and store lipids to transform themselves to the foam cells. The lipid profiles in the serum are shown to be risk factors for developing atherosclerosis, such as high LDL (low density lipoprotein) or low HDL (high density lipoprotein) concentration. In addition to deliver cholesterol from vascular wall to liver, HDL is supposed to exert antiinflammatory properties which are not well characterized. We recently indentified that HDL exert an antiinflammatory property which is not ascribed to it’s capacity to lower the cholesterol level of the peripheral tissue. <h3>Objectives</h3> To investigate the antiinflammatory function of reconstituted HDL (rHDL) in the Kawasaki arteritis murine model in vivo. <h3>Methods</h3> Coronary arteritis mimicking Kawasaki disease was induced by administrating 20 microgram of lipopolysaccharide followed by weekly injection of 500 microgram of the nucleotide-binding oligomerization domain 1 (NOD1) ligand FK-565 for 4 times. 2 mg of rHDL or control PBS was injected 4 times along with FK-565 administration. After a week after the last injection of FK-565 or control PBS, the severity of coronary arteritis was quantified by measuring the inflammation area surrounding the coronary arteries on the microscopic images. The cytokine levels of the serum were determined by multiplex. <h3>Results</h3> The rHDL treatment reduced the inflammatory area of coronary arteries compared with the control PBS treated groups, showing statistically significance (P=0.008 with Student t-test, 0.29±0.24 mm<sup>2</sup> (PBS control group) and 0.13±0.07 mm<sup>2</sup> (rHDL group)). Serum level of IL-12p40 was decreased in mice treated with rHDL. <h3>Conclusions</h3> The data indicate that rHDL exert an antiinflammatory activity in the NOD1 ligand induced Kawasaki arteritis model in vivo. <h3>References</h3> Nishio H et al. <i>Arterioscler Thromb Vasc Biol</i>. 2011, 31: 1093-9 <h3>Disclosure of Interest</h3> None Declared
Abstract 3423: The role of PGC1-α and KLF4 in inhibiting the progression of human hepatoma cells
Authors: Chin-Wen Chi, Ming-Ta Sung, Ann-Tin Ho, Chin-Chun Lee, Wei-Shan Tu, Peng-Nein Yin, Pen-Hui Yin, Hsin-Chen Lee, Wing-Yiu Lui
Journal: Cancer Research (2011)

Abstract Hepatocellular carcinoma (HCC) is one of the most common cancers with high mortality worldwide. Hypoxia is considered as a driving force to trigger the progression of malignancy, such as epithelial-mesenchymal transition (EMT) process, tumor metastasis, and recurrence. Because of the high recurrence rate caused by frequent metastasis and the lack of effective systemic treatment, development of new biomarkers and therapeutic targets for HCC treatment is urgently needed. Loss of E-cadherin is an early and critical step in EMT process and tumor metastasis. Consequently, modulation of the expression of E-cadherin may be a potential way to prevent tumor metastasis. Recently, we have demonstrated that overexpression of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) not only down-regulated the cyclin D1 expression and inhibited growth of hepatoma HepG2 cells, but also up-regulated the E-cadherin expression and concomitantly down-regulated the mesenchymal marker, and decreased the vimentin expression as well as the migration of HepG2 cells. In this study, we observed a significant increase in the expression level of Kruppel-like factor 4 (KLF4) in HepG2 cells when PGC-1α was overexpressed by adenovirus mediated gene transfer. Using wound healing assay and Western blotting, we further observed increased cell migration and decreased expression of KLF4 in HepG2, Hep3B, and HA22T/VGH hepatoma cell lines under hypoxia condition. Moreover, the KLF4 expression level in HepG2 cells under hypoxia and combined with drug treatment was also examined. We found that treatment of sodium nitroprusside, a nitric oxide donor, can protect HepG2 cells from hypoxia- and glucose depletion-induced cytotoxicity through repressing the KLF4 and Bip/Grp78 expression. After treatment with a cytotoxic dose (1 μM) of doxorubicin, the KLF4 expression of HepG2 cells was decreased under normoxia while it was increased under hypoxia. These results together suggest that PGC-1α may regulate the expression of E-cadherin via KLF4, and the KLF4 expression correlated with the response of HepG2 cells to doxorubicin under hypoxia. PGC-1α and KLF4 may serve as potential targets to inhibit the growth and metastasis of hepatoma cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3423. doi:10.1158/1538-7445.AM2011-3423
Efficient Purification and Release of Circulating Tumor Cells by Synergistic Effect of Biomarker and SiO<sub>2</sub>@Gel‐Microbead‐Based Size Difference Amplification
Authors: Qinqin Huang, Bo Cai, Bolei Chen, Lang Rao, Zhaobo He, Rongxiang He, Feng Guo, Libo Zhao, Kiran Kumar Kondamareddy, Wei Liu, Shishang Guo, Xing‐Zhong Zhao
Journal: Advanced Healthcare Materials (2016)

Microfluidics-based circulating tumor cell (CTC) isolation is achieved by using gelatin-coated silica microbeads conjugated to CTC-specific antibodies. Bead-binding selectively enlarges target cell size, providing efficient high-purity capture. CTCs captured can be further released non-invasively. This stratagem enables high-performance CTC isolation for subsequent studies. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Abstract 328: Complex oligonucleotide libraries enable high-resolution cytogenetic analysis of human and mouse genomes with fluorescence <i>in situ</i> hybridization (FISH)
Authors: Robert A. Ach, N. Alice Yamada, Peter Tsang, Kristina Aleksic, Yvonne Begus-Nahrmann, Alicia Scheffer-Wong, Stephen Laderman, Andre Lechel, K. Lenhard Rudolph, Michael Speicher, Laurakay Bruhn
Journal: Cancer Research (2010)

Abstract Cytogenetic analysis of chromosomes using Fluorescence in situ Hybridization (FISH) is a powerful method for the study of chromosome structure, organization, and stability. However, to date, the utility of FISH has largely depended upon access to cloned template DNA used to generate probes. Clones for specific regions are often unavailable, or the genomic template may contain repetitive and other non-informative sequences which can confound FISH analysis. We have leveraged our ability to chemically synthesize oligonucleotides in massively parallel reactions to produce DNA libraries that can be used to generate FISH probes. The sequences of the oligonucleotides in these libraries are selected in silico using empirically determined criteria so as to target only the most informative elements in the genomic region to be analyzed and avoiding any repetitive elements or regions homologous to other non-targeted loci. Our FISH protocol is similar to ones used for FISH with BAC probes. Using our methods, human chromosomal regions as small as 1.8 kb and as large as chromosome arms were successfully visualized in both metaphase and interphase cells. Using our probe design methods, we readily obtained specific and robust signals for chromosomal regions rich in repeats and/or GC content. We also investigated the utility of these probes for studies of mouse chromosomes by generating probes for over ten loci in the mouse genome. All the probes hybridized well using cytologic and cryosectioned samples. In addition, FFPE samples showed promising preliminary results. We have also applied our FISH methods to develop chromosome-specific enumeration probes for the mouse genome at pericentromeric regions. These enumeration probes should be useful for detecting aneuploidies, polyploidies, and other genomic rearrangements that were previously difficult to study at single-cell resolution, particularly in tissue samples. Successful co-hybridization of chromosome enumeration probes and loci-specific probes in mouse intestinal crypt cells allowed for accurate copy number analyses in tissue samples. We are also continuing to explore other breakthrough applications that are enabled by our oligonucleotide-based FISH methodology. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 328.
HOW TO SELECT THE CANDIDATES OF VENTRICULAR ASSIST DEVICE IMPLANTATION AMONG PATIENTS WITH INTERMACS PROFILE 4-7? A COMPARISON OF TWO SCORING SYSTEMS
Authors: Teruhiko Imamura, Koichiro Kinugawa, Daisuke Nitta, Osamu Kinoshita, Kan Nawata, Minoru Ono
Journal: Journal of the American College of Cardiology (2016)
Abstract 2096: The role of microRNA-1 as a candidate tumor suppressor in cutaneous squamous cell carcinoma
Authors: Dustin L. Gable, Jessica L. Fleming, Amanda Ewart Toland
Journal: Cancer Research (2010)

Abstract Cutaneous squamous cell carcinoma (SCC) is the second most common form of skin cancer, affecting over 250,000 people in the United States annually. Using miRNA expression arrays, we identified lower levels of microRNA-1 (miR-1) expression in skin from FVB/NJ mice, which are susceptible to chemically-induced skin cancer, compared to skin from Spr/EiJ mice, which are resistant to chemically-induced skin cancer. Additionally, murine SCC cell lines showed greatly reduced levels of miR-1 compared to normal skin. We hypothesize that decreased expression of miR-1 in susceptible mice and SCC cell lines suggests a possible role of miR-1 as a tumor suppressor in skin. To test this hypothesis, we transfected a precursor for miR-1 into a murine SCC cell line, A5, and measured proliferation and cell viability via an MTT assay at 24, 48, and 72 hours post-transfection. The growth rate for cells transfected with miR-1 was significantly decreased at 48 to 72 hours post-transfection relative to those mock-transfected cells and corresponded to miR-1 expression levels. These data are consistent with our hypothesis that miR-1 may act as a tumor suppressor in the skin. Using in silico prediction programs, we identified a number of putative targets of miR-1. The transcription factor oncogene, Ets1, emerged as an interesting potential direct target of miR-1. Ets1 has three predicted target binding sites for miR-1. Quantitative PCR and Western analyses revealed decreased Ets1 mRNA and protein expression in A5 cells transfected with miR-1 compared to mock-transfected A5 control cells. Ets1 mRNA expression is also decreased in a normal keratinocyte cell line, C5N, compared to A5 cells. From these experiments we showed that Ets1 expression shows an inverse correlation with miR-1 levels. These results suggest Ets1 is regulated by miR-1. Future studies will determine whether Ets1 is a direct target of miR-1. We will also clarify the role of Ets1 in SCC cell proliferation and migration and identify other tumor-related phenotypes associated with miR-1. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2096.
Irinotecan monotherapy as second-line treatment in advanced pancreatic cancer
Authors: Y. Park, S. Yi, H. Kim, S. Lee, I. Hwang, S. Park, B. Park, J. Park, H. Lim, W. Kang
Journal: Journal of Clinical Oncology (2007)

15111 Background: The aim of this phase II study was to determine whether second line therapy with single agent irinotecan could provide any clinical benefit in patients with gemcitabine- pretreated advanced pancreatic cancer. Methods: From January 2004 to October 2006, patients with advanced pancreatic cancer previously treated with gemcitabine alone or combination were treated with single agent irinotecan(150 mg/m 2 , biweekly), until unacceptable toxicity or disease progression. Primary endpoint was response rate with single stage design. Results: Twenty-eight patients were enrolled(22 male, 6 female, median age : 54.5 years (39–76)). Nine patients are still alive and 3 remain on therapy with stable disease. The median number of cycles was 3.5(1–12). Twenty-four patients were assessable for toxicity and 21 for response. The most common toxicities was diarrhea (grade 3, 12.5%). Grade 3 neutropenia in 1 patient was observed. Other hematological and non-hematological toxicities were mild and manageable. Partial responses were observed in 3 patients (3/21, 14%). An additional 9 patients (9/21, 43%) had stable disease as their best response. 12 patients have progressed with a median time-to-progression of 4.0 months. Conclusions: Single-agent irinotecan was tolerated with manageable toxicity, offering encouraging activity as second-line treatment of patients with advanced pancreatic cancer, refractory to gemcitabine. No significant financial relationships to disclose.
Endocardium Minimally Contributes to Coronary Endothelium in the Embryonic Ventricular Free Walls
Authors: Hui Zhang, Wenjuan Pu, Guang Li, Xiuzhen Huang, Lingjuan He, Xueying Tian, Qiaozhen Liu, Libo Zhang, Sean M. Wu, Henry M. Sucov, Bin Zhou
Journal: Circulation Research (2016)

Rationale: There is persistent uncertainty regarding the developmental origins of coronary vessels, with 2 principal sources suggested as ventricular endocardium or sinus venosus (SV). These 2 proposed origins implicate fundamentally distinct mechanisms of vessel formation. Resolution of this controversy is critical for deciphering the programs that result in the formation of coronary vessels and has implications for research on therapeutic angiogenesis. Objective: To resolve the controversy over the developmental origin of coronary vessels. Methods and Results: We first generated nuclear factor of activated T cells (Nfatc1)-Cre and Nfatc1-Dre lineage tracers for endocardium labeling. We found that Nfatc1 recombinases also label a significant portion of SV endothelial cells in addition to endocardium. Therefore, restricted endocardial lineage tracing requires a specific marker that distinguishes endocardium from SV. By single-cell gene expression analysis, we identified a novel endocardial gene natriuretic peptide receptor 3 (Npr3). Npr3 is expressed in the entirety of the endocardium but not in the SV. Genetic lineage tracing based on Npr3-CreER showed that endocardium contributes to a minority of coronary vessels in the free walls of embryonic heart. Intersectional genetic lineage tracing experiments demonstrated that endocardium minimally contributes to coronary endothelium in the embryonic ventricular free walls. Conclusions: Our study suggested that SV, but not endocardium, is the major origin for coronary endothelium in the embryonic ventricular free walls. This work thus resolves the recent controversy over the developmental origin of coronary endothelium, providing the basis for studying coronary vessel formation and regeneration after injury.