Identification of Ovarian Cancer Gene Expression Patterns Associated
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Combined Human Epididymis 4 and Carbohydrate Antigen 125 Serum Protein Levels Diagnostic Value in Ovarian Cancer
ISSN: 2640-5180 Madridge Journal of Cancer Study & Research Research Article Open Access Combined Human Epididymis 4 and Carbohydrate Antigen 125 Serum Protein Levels Diagnostic value in Ovarian Cancer Salwa Hassan Teama1*, Reham El Shimy2 and Hebatallah Gamal3 1Department of Molecular Biology, Medical Ain Shams Research Institute (MASRI), Faculty of Medicine, Ain Shams University, Cairo, Egypt 2Department of Clinical and Chemical Pathology, National Cancer Institute, Faculty of Medicine, Cairo University, Cairo, Egypt 3Departement of Surgical Oncology, National Cancer Institute, Faculty of Medicine, Cairo University, Cairo, Egypt Article Info Abstract *Corresponding author: Objective: Human Epididymis 4 (HE-4) protein, a new candidate for ovarian cancer Salwa Hassan Teama detection shows promising diagnostic value for ovarian cancer diagnosis, this study aimed Department of Molecular Biology Medical Ain Shams Research Institute to assess the diagnostic significance of combined Human Epididymis 4 and Carbohydrate (MASRI) Antigen 125 (CA-125) serum protein levels in ovarian cancer detection. Faculty of Medicine Ain Shams University Subjects and Methods: A clinical case control study include; forty nine subjects; patients Abbasia, Cairo with ovarian cancer (n=33), non-cancer control group (n=16). Serum protein levels of Egypt HE-4 were measured using an enzyme linked immune sorbent assay (ELISA). All data were Tel: 0020-1005293116 E-mail: [email protected] analyzed by SPSS software (version 21.0.0; IPM SPSS, Chicago, IL, USA). Results: The results showed that increased serum protein concentration of HE-4 (pMol/L) and Received: July 25, 2018 CA-125 (U/ml) in the ovarian cancer group mean (SD)/median (range) 329.61±336.55/199 Accepted: August 13, 2018 Published: August 17, 2018 (28.72-1064) and 521.36±572.60/287 (10.50-2377), than non-cancer control group 64.80±38.51/54.53 (21 -160) and 28.35±10.80/28 (10-50) respectively (p<0.05). -
WFDC2 Control Peptide
AP10066CP-N OriGene Technologies Inc. OriGene EU Acris Antibodies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] WFDC2 control peptide Alternate names: ESPE4, Epidydimal Secretory Protein E4, HE4, Major Epididymis-Specific protein E4, WAP four-disulfide core domain protein 2, WAP5, WFDC2 Catalog No.: AP10066CP-N Quantity: 0.25 mg Concentration: 2.5 mg/ml Background: The whey acidic protein (WAP) domain is a conserved motif, containing eight cysteines found in a characteristic 4-disulphide core arrangement, that is present in a number of otherwise unrelated proteins. One of these proteins, which contains two WAP domains, is HE4 (also known as WFDC2), originally described as an epididymis specific protein but more recently suggested to be a putative serum tumour marker for ovarian cancer and a presumptive role in natural immunity. The HE4 protein expression is not only confined to epidydimis but is expressed in a number of normal human tissues out side the reproductive system, including regions of the respiratory tract and nasopharynx and in a subset of lung tumor cell lines. HE4 gene expression was highest in normal human trachea and salivary gland, and to a lesser extent, lung, prostate, pituitary gland, thyroid, and kidney. Highest level of expression of ESPE4 was observed in adenocarcinomas of the lung, and occasional breast, transitional cell and pancreatic carcinomas (1). The WFDC2 gene under goes extensive splicing in malignant tissues that give rise to five WAP domain containing iso forms (2). -
Three Dact Gene Family Members Are Expressed During Embryonic Development
Three Dact Gene Family Members are Expressed During Embryonic Development and in the Adult Brains of Mice Daniel A Fisher, Saul Kivimäe, Jun Hoshino, Rowena Suriben, Pierre -Marie Martin, Nichol Baxter, Benjamin NR Cheyette Department of Psychiatry & Gra duate Programs in Developmental Biology and Neuroscience, University of California, San Francisco, 94143-2611 Correspondence: Benjamin NR Cheyette [email protected] 415.476.7826 Running Title: Mouse Dact Gene Family Expression Key Words: mouse, Dpr, Frodo, Thyex, Dact, Wnt, Dvl, expression, embryo, brain Supported by: NIH: MH01750 K08; NARSAD Young Investigator Award; NAAR award #551. Abstract Members of the Dact protein family were initially identified through binding to Dishevelled (Dvl), a cytoplasmic protein central to Wnt signaling. During mouse development, Dact1 is detected in the presomitic mesoderm and somites during segmentation, in the limb bud mesenchyme and other mesoderm-derived tissues, and in the central nervous system (CNS). Dact2 expression is most prominent during organogenesis of the thymus, kidneys, and salivary glands, with much lower levels in the somites and in the developing CNS. Dact3, not previously described in any organism, is expressed in the ventral region of maturing somites, limb bud and branchial arch mesenchyme, and in the embryonic CNS; of the three paralogs it is the most highly expressed in the adult cerebral cortex. These data are consistent with studies in other vertebrates showing that Dact paralogs have distinct signaling and developmental roles, and suggest they may differentially contribute to postnatal brain physiology. Introduction Signaling downstream of secreted Wnt ligands is a conserved process in multicellular animals that plays important roles during development and, when misregulated, contributes to cancer and other diseases (Polakis, 2000; Moon et al., 2002). -
Systematic Cpg Islands Methylation Profiling of Genes in the Wnt Pathway in Epithelial Ovarian Cancer Identifies Biomarkers of Progression-Free Survival
Published OnlineFirst April 1, 2011; DOI: 10.1158/1078-0432.CCR-10-3021 Clinical Cancer Imaging, Diagnosis, Prognosis Research Systematic CpG Islands Methylation Profiling of Genes in the Wnt Pathway in Epithelial Ovarian Cancer Identifies Biomarkers of Progression-Free Survival Wei Dai1, Jens M. Teodoridis1, Constanze Zeller1, Janet Graham1, Jenny Hersey3, James M. Flanagan1, Euan Stronach2, David W. Millan4, Nadeem Siddiqui5, Jim Paul6, and Robert Brown1,3 Abstract Purpose: Wnt pathways control key biological processes that potentially impact on tumor progression and patient survival. We aimed to evaluate DNA methylation at promoter CpG islands (CGI) of Wnt pathway genes in ovarian tumors at presentation and identify biomarkers of patient progression-free survival (PFS). Experimental Design: Epithelial ovarian tumors (screening study n ¼ 120, validation study n ¼ 61), prospectively collected through a cohort study, were analyzed by differential methylation hybridization at 302 loci spanning 189 promoter CGIs at 137 genes in Wnt pathways. The association of methylation and PFS was examined by Cox proportional hazards model. Results: DNA methylation is associated with PFS at 20 of 302 loci (P < 0.05, n ¼ 111), with 5 loci significant at false discovery rate (FDR) less than 10%. A total of 11 of 20 loci retain significance in an independent validation cohort (n ¼ 48, P 0.05, FDR 10%), and 7 of these loci, at FZD4, DVL1, NFATC3, ROCK1, LRP5, AXIN1, and NKD1 genes, are independent from clinical parameters (adjusted P < 0.05). Increased methylation at these loci associates with increased hazard of disease progression. A multivariate Cox model incorporates only NKD1 and DVL1, identifying two groups differing in PFS [HR ¼ 2.09; 95% CI (1.39–3.15); permutation test P < 0.005]. -
VU Research Portal
VU Research Portal Genetic architecture and behavioral analysis of attention and impulsivity Loos, M. 2012 document version Publisher's PDF, also known as Version of record Link to publication in VU Research Portal citation for published version (APA) Loos, M. (2012). Genetic architecture and behavioral analysis of attention and impulsivity. General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal ? Take down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. E-mail address: [email protected] Download date: 28. Sep. 2021 Genetic architecture and behavioral analysis of attention and impulsivity Maarten Loos 1 About the thesis The work described in this thesis was performed at the Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, The Netherlands. This work was in part funded by the Dutch Neuro-Bsik Mouse Phenomics consortium. The Neuro-Bsik Mouse Phenomics consortium was supported by grant BSIK 03053 from SenterNovem (The Netherlands). -
Human Epididymis Protein 4 (HE4)
Human Epididymis Protein 4 (HE4) Monitoring Patients With Epithelial Ovarian Carcinoma Introduction cancer patients.5 This group found that measurement Human epididymis protein 4 (HE4), or WAP four- of HE4 showed sensitivity and specificity comparable disulphide core domain protein 2 (WFDC2), was first to that of CA125 for differentiating postmenopausal identified in the epithelium of the distal epididymis women with ovarian cancer from normal controls.5 They and was originally predicted to be a protease inhibitor suggested that the HE4 assay may have an advantage involved in sperm maturation.1,2 HE4 is the gene over CA125 in that it is less frequently positive in product of the WFDC2 gene that is located on patients with nonmalignant disease.5 chromosome 20q12-13.1.3 The WFDC2 gene is one of 14 homologous genes on this chromosome that encode Expression of HE4 in EOC proteins with WAP-type four-disulphide core (WFDC2) Drapkin and colleagues used immunohistochemical domains.3 techniques to show that cortical inclusion cysts (CIC) lined by metaplastic Mullerian epithelium abundantly HE4 belongs to the family of whey acidic four-disulfide expresses HE4 relative to normal surface epithelium.3 core (WFDC2) proteins with suspected trypsin inhibitor Using tissue microarrays, they showed that HE4 properties3,4; however, no biological function has so far expression was restricted to certain histologic subtypes been identified for HE4.5,6 The HE4 gene codes for a of epithelial ovarian carcinomas (EOC).3 13-kD protein, although in its mature glycosylated -
Effects and Mechanisms of Eps8 on the Biological Behaviour of Malignant Tumours (Review)
824 ONCOLOGY REPORTS 45: 824-834, 2021 Effects and mechanisms of Eps8 on the biological behaviour of malignant tumours (Review) KAILI LUO1, LEI ZHANG2, YUAN LIAO1, HONGYU ZHOU1, HONGYING YANG2, MIN LUO1 and CHEN QING1 1School of Pharmaceutical Sciences and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, Yunnan 650500; 2Department of Gynecology, Yunnan Tumor Hospital and The Third Affiliated Hospital of Kunming Medical University; Kunming, Yunnan 650118, P.R. China Received August 29, 2020; Accepted December 9, 2020 DOI: 10.3892/or.2021.7927 Abstract. Epidermal growth factor receptor pathway substrate 8 1. Introduction (Eps8) was initially identified as the substrate for the kinase activity of EGFR, improving the responsiveness of EGF, which Malignant tumours are uncontrolled cell proliferation diseases is involved in cell mitosis, differentiation and other physiological caused by oncogenes and ultimately lead to organ and body functions. Numerous studies over the last decade have demon- dysfunction (1). In recent decades, great progress has been strated that Eps8 is overexpressed in most ubiquitous malignant made in the study of genes and signalling pathways in tumours and subsequently binds with its receptor to activate tumorigenesis. Eps8 was identified by Fazioli et al in NIH-3T3 multiple signalling pathways. Eps8 not only participates in the murine fibroblasts via an approach that allows direct cloning regulation of malignant phenotypes, such as tumour proliferation, of intracellular substrates for receptor tyrosine kinases (RTKs) invasion, metastasis and drug resistance, but is also related to that was designed to study the EGFR signalling pathway. Eps8 the clinicopathological characteristics and prognosis of patients. -
Identification of Genomic Organisation, Sequence Variants and Analysis of the Role of the Human Dishevelled 1 Gene in Late Onset Alzheimer's Disease
Molecular Psychiatry (2002) 7, 104–109 2002 Nature Publishing Group All rights reserved 1359-4184/02 $15.00 www.nature.com/mp ORIGINAL RESEARCH ARTICLE Identification of genomic organisation, sequence variants and analysis of the role of the human dishevelled 1 gene in late onset Alzheimer’s disease C Russ, S Lovestone and JF Powell Department of Neuroscience, Institute of Psychiatry, London SE5 8AF, UK Keywords: polymorphism; genomic; DVL1; association; kinases, such as c-Jun N-terminal kinase (JNK), and SNP glycogen synthase kinase 3 beta (GSK3) have been Alzheimer’s disease (AD) is a disorder characterised by shown to phosphorylate tau in vitro, in cell at sites that a progressive deterioration in memory and other cogni- are phosphorylated in PHF.4–7 JNK and GSK3 are tive functions. Neurofibrillary tangles (NFT) are a major regulated by the dishevelled 1 gene (DVL1), the latter pathological hallmark of AD, these are aggregations of as part of the wnt signalling pathways.8–11 Activation paired helical filaments (PHF) comprised of the hyper- of the wnt signalling pathway is thought to cause DVL1 phosphorylated microtubule associated protein tau. to inactivate GSK3 through complex-formation with Several kinases, such as glycogen synthase kinase 3   adenomatous poliposis coli (APC), axin and -catenin beta (GSK3 ) and c-Jun N-terminal kinase (JNK), phos- proteins,8 whereas JNK is activated by DVL1.10,11 The phorylate tau at sites that are phosphorylated in PHF. Dishevelled 1 (DVL1) is thought to act as a positive mechanism by which this JNK activation occurs is regulator of the wnt signalling pathway, and inhibits unclear, however, it has been demonstrated that a DEP GSK3 activity preventing -catenin degradation and (dishevelled, egl-10 and pleckstrin) protein binding thus allowing wnt target gene expression. -
The DNA Sequence and Comparative Analysis of Human Chromosome 20
articles The DNA sequence and comparative analysis of human chromosome 20 P. Deloukas, L. H. Matthews, J. Ashurst, J. Burton, J. G. R. Gilbert, M. Jones, G. Stavrides, J. P. Almeida, A. K. Babbage, C. L. Bagguley, J. Bailey, K. F. Barlow, K. N. Bates, L. M. Beard, D. M. Beare, O. P. Beasley, C. P. Bird, S. E. Blakey, A. M. Bridgeman, A. J. Brown, D. Buck, W. Burrill, A. P. Butler, C. Carder, N. P. Carter, J. C. Chapman, M. Clamp, G. Clark, L. N. Clark, S. Y. Clark, C. M. Clee, S. Clegg, V. E. Cobley, R. E. Collier, R. Connor, N. R. Corby, A. Coulson, G. J. Coville, R. Deadman, P. Dhami, M. Dunn, A. G. Ellington, J. A. Frankland, A. Fraser, L. French, P. Garner, D. V. Grafham, C. Grif®ths, M. N. D. Grif®ths, R. Gwilliam, R. E. Hall, S. Hammond, J. L. Harley, P. D. Heath, S. Ho, J. L. Holden, P. J. Howden, E. Huckle, A. R. Hunt, S. E. Hunt, K. Jekosch, C. M. Johnson, D. Johnson, M. P. Kay, A. M. Kimberley, A. King, A. Knights, G. K. Laird, S. Lawlor, M. H. Lehvaslaiho, M. Leversha, C. Lloyd, D. M. Lloyd, J. D. Lovell, V. L. Marsh, S. L. Martin, L. J. McConnachie, K. McLay, A. A. McMurray, S. Milne, D. Mistry, M. J. F. Moore, J. C. Mullikin, T. Nickerson, K. Oliver, A. Parker, R. Patel, T. A. V. Pearce, A. I. Peck, B. J. C. T. Phillimore, S. R. Prathalingam, R. W. Plumb, H. Ramsay, C. M. -
ID AKI Vs Control Fold Change P Value Symbol Entrez Gene Name *In
ID AKI vs control P value Symbol Entrez Gene Name *In case of multiple probesets per gene, one with the highest fold change was selected. Fold Change 208083_s_at 7.88 0.000932 ITGB6 integrin, beta 6 202376_at 6.12 0.000518 SERPINA3 serpin peptidase inhibitor, clade A (alpha-1 antiproteinase, antitrypsin), member 3 1553575_at 5.62 0.0033 MT-ND6 NADH dehydrogenase, subunit 6 (complex I) 212768_s_at 5.50 0.000896 OLFM4 olfactomedin 4 206157_at 5.26 0.00177 PTX3 pentraxin 3, long 212531_at 4.26 0.00405 LCN2 lipocalin 2 215646_s_at 4.13 0.00408 VCAN versican 202018_s_at 4.12 0.0318 LTF lactotransferrin 203021_at 4.05 0.0129 SLPI secretory leukocyte peptidase inhibitor 222486_s_at 4.03 0.000329 ADAMTS1 ADAM metallopeptidase with thrombospondin type 1 motif, 1 1552439_s_at 3.82 0.000714 MEGF11 multiple EGF-like-domains 11 210602_s_at 3.74 0.000408 CDH6 cadherin 6, type 2, K-cadherin (fetal kidney) 229947_at 3.62 0.00843 PI15 peptidase inhibitor 15 204006_s_at 3.39 0.00241 FCGR3A Fc fragment of IgG, low affinity IIIa, receptor (CD16a) 202238_s_at 3.29 0.00492 NNMT nicotinamide N-methyltransferase 202917_s_at 3.20 0.00369 S100A8 S100 calcium binding protein A8 215223_s_at 3.17 0.000516 SOD2 superoxide dismutase 2, mitochondrial 204627_s_at 3.04 0.00619 ITGB3 integrin, beta 3 (platelet glycoprotein IIIa, antigen CD61) 223217_s_at 2.99 0.00397 NFKBIZ nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, zeta 231067_s_at 2.97 0.00681 AKAP12 A kinase (PRKA) anchor protein 12 224917_at 2.94 0.00256 VMP1/ mir-21likely ortholog -
The Ancestor of Extant Japanese Fancy Mice Contributed to the Mosaic Genomes of Classical Inbred Strains
Downloaded from genome.cshlp.org on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press Revised Resources The ancestor of extant Japanese fancy mice contributed to the mosaic genomes of classical inbred strains 1, 8 2, 3 3 4 Toyoyuki Takada, Toshinobu Ebata, Hideki Noguchi, Thomas M. Keane, David 4 2 2, 3 5, 8 3 J. Adams, Takanori Narita, Tadasu Shin-I, Hironori Fujisawa, Atsushi Toyoda, 6 6 7 6 Kuniya Abe, Yuichi Obata, Yoshiyuki Sakaki, Kazuo Moriwaki, Asao Fujiyama, 3 2 1, 8* Yuji Kohara and Toshihiko Shiroishi 1 Mammalian Genetics Laboratory, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan 2 Genome Biology Laboratory, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan 3 Comparative Genomics Laboratory, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan 4 The Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, CB10 1SA, UK 5 The Institute of Statistical Mathematics, 10-3 Midori-cho, Tachikawa, Tokyo 190-8562, Japan 6 BioResource Center, RIKEN Tsukuba Institute, Tsukuba, Ibaraki 305-0074, Japan 1 Downloaded from genome.cshlp.org on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press 7 Genome Science Center, RIKEN Yokohama Institute, Yokohama, Kanagawa 230-0045, Japan; present address, Toyohashi University of Technology, Hibarigaoka, Tempaku, Toyohashi, Aichi 441-8580, Japan 8 Transdisciplinary Research Integration Center, Research Organization of Information and Systems, Minato-ku, Tokyo 105-0001, Japan *Corresponding author. E-mail: [email protected] Mammalian Genetics Laboratory, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan TEL: +81-55-981-6818, FAX: +81-55-981-6817 Keywords: mouse genome, MSM/Ms, JF1/Ms, inter-subspecific genome difference Running title: Mus musculus molossinus genome 2 Downloaded from genome.cshlp.org on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press Abstract Commonly used classical inbred mouse strains have mosaic genomes with sequences from different subspecific origins. -
Robles JTO Supplemental Digital Content 1
Supplementary Materials An Integrated Prognostic Classifier for Stage I Lung Adenocarcinoma based on mRNA, microRNA and DNA Methylation Biomarkers Ana I. Robles1, Eri Arai2, Ewy A. Mathé1, Hirokazu Okayama1, Aaron Schetter1, Derek Brown1, David Petersen3, Elise D. Bowman1, Rintaro Noro1, Judith A. Welsh1, Daniel C. Edelman3, Holly S. Stevenson3, Yonghong Wang3, Naoto Tsuchiya4, Takashi Kohno4, Vidar Skaug5, Steen Mollerup5, Aage Haugen5, Paul S. Meltzer3, Jun Yokota6, Yae Kanai2 and Curtis C. Harris1 Affiliations: 1Laboratory of Human Carcinogenesis, NCI-CCR, National Institutes of Health, Bethesda, MD 20892, USA. 2Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo 104-0045, Japan. 3Genetics Branch, NCI-CCR, National Institutes of Health, Bethesda, MD 20892, USA. 4Division of Genome Biology, National Cancer Center Research Institute, Tokyo 104-0045, Japan. 5Department of Chemical and Biological Working Environment, National Institute of Occupational Health, NO-0033 Oslo, Norway. 6Genomics and Epigenomics of Cancer Prediction Program, Institute of Predictive and Personalized Medicine of Cancer (IMPPC), 08916 Badalona (Barcelona), Spain. List of Supplementary Materials Supplementary Materials and Methods Fig. S1. Hierarchical clustering of based on CpG sites differentially-methylated in Stage I ADC compared to non-tumor adjacent tissues. Fig. S2. Confirmatory pyrosequencing analysis of DNA methylation at the HOXA9 locus in Stage I ADC from a subset of the NCI microarray cohort. 1 Fig. S3. Methylation Beta-values for HOXA9 probe cg26521404 in Stage I ADC samples from Japan. Fig. S4. Kaplan-Meier analysis of HOXA9 promoter methylation in a published cohort of Stage I lung ADC (J Clin Oncol 2013;31(32):4140-7). Fig. S5. Kaplan-Meier analysis of a combined prognostic biomarker in Stage I lung ADC.