DOCSLIB.ORG

PDF Output of CLIC (Clustering by Inferred Co-Expression)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
PDF Output of CLIC (Clustering by Inferred Co-Expression) PDF Output of CLIC (clustering by inferred co-expression) Dataset: Num of genes in input gene set: 14 Total number of genes: 16493 CLIC PDF output has three sections: 1) Overview of Co-Expression Modules (CEMs) Heatmap shows pairwise correlations between all genes in the input query gene set. Red lines shows the partition of input genes into CEMs, ordered by CEM strength. Each row shows one gene, and the brightness of squares indicates its correlations with other genes. Gene symbols are shown at left side and on the top of the heatmap. 2) Details of each CEM and its expansion CEM+ Top panel shows the posterior selection probability (dataset weights) for top GEO series datasets. Bottom panel shows the CEM genes (blue rows) as well as expanded CEM+ genes (green rows). Each column is one GEO series dataset, sorted by their posterior probability of being selected. The brightness of squares indicates the gene's correlations with CEM genes in the corresponding dataset. CEM+ includes genes that co-express with CEM genes in high-weight datasets, measured by LLR score. 3) Details of each GEO series dataset and its expression profile: Top panel shows the detailed information (e.g. title, summary) for the GEO series dataset. Bottom panel shows the background distribution and the expression profile for CEM genes in this dataset. Overview of Co-Expression Modules (CEMs) with Dataset Weighting Scale of average Pearson correlations Num of Genes in Query Geneset: 14. Num of CEMs: 1. 0.0 0.2 0.4 0.6 0.8 1.0 H2-K1 Fcgrt Hfe H2-Bl H2-Q2 H2-Q10 C920025E04Rik H2-M3 B2m Mr1 Azgp1 Ulbp1 Procr H2-D1 H2-K1 Fcgrt Hfe H2-Bl H2-Q2 H2-Q10 C920025E04Rik CEM 1 (14 datasets) H2-M3 B2m Mr1 Azgp1 Ulbp1 Procr H2-D1 C920025E04Rik Symbol Num ofCEMGenes:14.Predicted1049.SelectedDatasets:Strength:0.2 CEM 1,Geneset"[G]MHCclassIproteincomplex",Page1 AA467197 Lgals3bp Hsd11b1 H2-Q10 Ifi27l2a Phf11d Psmb8 Psmb9 Dram1 Casp1 Casp4 Tapbp Azgp1 H2-M3 H2-Q2 Fxyd5 H2-Aa H2-D1 H2-K1 Icam1 Parp3 Pilrb1 Ulbp1 P2ry6 Irgm2 Tor3a Ifitm3 Procr H2-Bl Gbp2 Emr1 Fcgrt Slfn8 Cd74 Cd44 Cd68 Lcn2 Rtp4 B2m Ifi47 Ifi27 C1s Igtp Grn Ifit3 Mr1 Hfe Irf7 Irf8 0.0 1.0 GSE5891 [6] GSE30488 [52] GSE45619 [6] Only showingfirst200datasets-Seetxtoutputforfulldetails. GSE43899 [12] GSE28389 [20] GSE24793 [8] GSE21137 [16] GSE23895 [18] GSE15794 [6] GSE38831 [7] GSE6223 [13] GSE19194 [14] GSE13103 [8] GSE29241 [6] GSE9330 [8] GSE18460 [16] GSE51213 [16] GSE15872 [18] GSE38074 [39] GSE33134 [31] GSE40260 [6] GSE5298 [8] GSE4029 [10] GSE23925 [6] GSE32386 [13] GSE34423 [40] GSE26299 [108] GSE22381 [12] GSE16675 [72] GSE16496 [102] GSE13753 [10] GSE6837 [8] GSE18586 [9] GSE3554 [6] GSE8039 [32] GSE14395 [24] GSE19616 [16] GSE42548 [29] GSE7342 [12] GSE43242 [10] GSE25286 [10] GSE17256 [8] GSE20577 [12] GSE13149 [25] GSE21576 [10] GSE25257 [6] GSE10965 [8] GSE17266 [59] GSE5334 [19] GSE33726 [48] GSE4926 [12] GSE15580 [14] GSE13526 [6] GSE27159 [8] GSE20954 [14] GSE1986 [17] GSE12730 [24] GSE5041 [8] GSE41759 [14] GSE9763 [20] GSE6285 [24] GSE29648 [10] GSE13874 [14] GSE18281 [33] GSE34765 [6] GSE9038 [24] GSE18660 [10] GSE10871 [32] GSE16874 [12] GSE19076 [12] GSE45618 [6] GSE35160 [6] GSE9443 [24] GSE39621 [51] GSE7897 [60] GSE31972 [6] GSE4535 [6] GSE11201 [18] GSE22005 [23] GSE9441 [36] GSE11358 [8] GSE4323 [6] GSE52542 [9] GSE28559 [30] GSE42264 [26] GSE17794 [44] GSE8295 [16] GSE30160 [6] GSE42601 [6] GSE11386 [15] GSE2019 [12] GSE47196 [6] GSE55356 [6] GSE17796 [39] GSE57543 [6] GSE30855 [6] GSE35734 [6] GSE16925 [15] GSE15624 [12] GSE14344 [6] GSE8249 [46] GSE41084 [6] GSE38224 [12] GSE32265 [6] GSE7333 [6] GSE27114 [6] GSE8726 [7] GSE19181 [6] GSE7424 [8] GSE3861 [6] GSE13071 [15] GSE10913 [6] GSE31744 [8] GSE10176 [6] GSE37975 [8] GSE33308 [10] GSE7694 [12] GSE25767 [6] GSE6210 [12] GSE51608 [6] GSE29318 [9] GSE48790 [8] GSE53951 [10] GSE16679 [8] GSE7767 [6] GSE6591 [15] GSE20302 [12] GSE52357 [8] GSE2250 [18] GSE17985 [8] GSE35396 [24] GSE31598 [12] GSE4193 [8] GSE6998 [32] GSE54653 [6] GSE4749 [6] GSE36336 [6] GSE19272 [30] GSE14481 [12] GSE15772 [8] GSE43381 [26] GSE54785 [6] GSE15155 [12] GSE35785 [10] GSE49346 [6] GSE12454 [13] GSE20372 [6] GSE27811 [9] GSE56777 [8] GSE36384 [12] GSE32598 [11] GSE9338 [42] GSE33770 [8] GSE23923 [8] CEM+ CEM GSE10528 [6] GSE23398 [7] GSE19885 [9] GSE34902 [6] GSE6065 [100] GSE23119 [9] 0.0 GSE21836 [8] GSE22006 [19] GSE19729 [14] Scale ofaveragePearsoncorrelations GSE7764 [10] GSE23182 [12] GSE50603 [12] GSE55855 [6] GSE8828 [6] GSE24121 [9] 0.2 GSE19979 [6] GSE8044 [6] GSE22841 [12] GSE46875 [10] GSE52474 [154] GSE37658 [6] GSE38335 [9] GSE10813 [12] GSE9725 [16] 0.4 GSE23600 [10] GSE50824 [19] GSE51385 [8] GSE22927 [38] GSE18326 [8] GSE35091 [11] GSE11259 [9] GSE51628 [15] GSE43620 [8] 0.6 GSE7069 [8] GSE11723 [9] GSE19204 [6] GSE19657 [21] GSE42103 [9] GSE28093 [6] GSE42018 [8] GSE31208 [8] GSE35219 [6] 0.8 GSE51365 [28] GSE1983 [6] GSE17879 [6] GSE16684 [6] Score 6.15 6.17 6.18 6.19 6.20 6.20 6.22 6.24 6.28 6.30 6.32 6.34 6.34 6.37 6.49 6.50 6.51 6.61 6.64 6.65 6.67 6.79 6.91 6.92 6.96 6.99 7.06 7.07 7.16 7.42 7.44 7.98 8.40 8.55 8.98 9.32 1.0 Notes Symbol Num ofCEMGenes:14.Predicted1049.SelectedDatasets:Strength:0.2 CEM 1,Geneset"[G]MHCclassIproteincomplex",Page2 Serpina3n Cyp27a1 Themis2 S100a13 Psmb10 Ms4a6d Hsd3b7 S100a1 Tyrobp Akr1c6 Ptpn18 P2ry13 Adssl1 Ube2l6 Fcer1g Clec7a Cxcl10 Mpeg1 Tcirg1 Parp9 Oasl2 Fcgr1 Itgam Isg20 Gbp3 Gbp7 Gbp6 Cd86 Dtx3l Cd53 Stat6 Lpxn Lcp1 Tap1 Lyz2 Ctsd Ctsb Ctsh Pilra Ctss Ccl6 Ccl9 Pld4 Fgl2 Mlkl Ang Tlr2 Hck Tlr1 Ifit1 0.0 1.0 GSE5891 [6] GSE30488 [52] GSE45619 [6] Only showingfirst200datasets-Seetxtoutputforfulldetails. GSE43899 [12] GSE28389 [20] GSE24793 [8] GSE21137 [16] GSE23895 [18] GSE15794 [6] GSE38831 [7] GSE6223 [13] GSE19194 [14] GSE13103 [8] GSE29241 [6] GSE9330 [8] GSE18460 [16] GSE51213 [16] GSE15872 [18] GSE38074 [39] GSE33134 [31] GSE40260 [6] GSE5298 [8] GSE4029 [10] GSE23925 [6] GSE32386 [13] GSE34423 [40] GSE26299 [108] GSE22381 [12] GSE16675 [72] GSE16496 [102] GSE13753 [10] GSE6837 [8] GSE18586 [9] GSE3554 [6] GSE8039 [32] GSE14395 [24] GSE19616 [16] GSE42548 [29] GSE7342 [12] GSE43242 [10] GSE25286 [10] GSE17256 [8] GSE20577 [12] GSE13149 [25] GSE21576 [10] GSE25257 [6] GSE10965 [8] GSE17266 [59] GSE5334 [19] GSE33726 [48] GSE4926 [12] GSE15580 [14] GSE13526 [6] GSE27159 [8] GSE20954 [14] GSE1986 [17] GSE12730 [24] GSE5041 [8] GSE41759 [14] GSE9763 [20] GSE6285 [24] GSE29648 [10] GSE13874 [14] GSE18281 [33] GSE34765 [6] GSE9038 [24] GSE18660 [10] GSE10871 [32] GSE16874 [12] GSE19076 [12] GSE45618 [6] GSE35160 [6] GSE9443 [24] GSE39621 [51] GSE7897 [60] GSE31972 [6] GSE4535 [6] GSE11201 [18] GSE22005 [23] GSE9441 [36] GSE11358 [8] GSE4323 [6] GSE52542 [9] GSE28559 [30] GSE42264 [26] GSE17794 [44] GSE8295 [16] GSE30160 [6] GSE42601 [6] GSE11386 [15] GSE2019 [12] GSE47196 [6] GSE55356 [6] GSE17796 [39] GSE57543 [6] GSE30855 [6] GSE35734 [6] GSE16925 [15] GSE15624 [12] GSE14344 [6] GSE8249 [46] GSE41084 [6] GSE38224 [12] GSE32265 [6] GSE7333 [6] GSE27114 [6] GSE8726 [7] GSE19181 [6] GSE7424 [8] GSE3861 [6] GSE13071 [15] GSE10913 [6] GSE31744 [8] GSE10176 [6] GSE37975 [8] GSE33308 [10] GSE7694 [12] GSE25767 [6] GSE6210 [12] GSE51608 [6] GSE29318 [9] GSE48790 [8] GSE53951 [10] GSE16679 [8] GSE7767 [6] GSE6591 [15] GSE20302 [12] GSE52357 [8] GSE2250 [18] GSE17985 [8] GSE35396 [24] GSE31598 [12] GSE4193 [8] GSE6998 [32] GSE54653 [6] GSE4749 [6] GSE36336 [6] GSE19272 [30] GSE14481 [12] GSE15772 [8] GSE43381 [26] GSE54785 [6] GSE15155 [12] GSE35785 [10] GSE49346 [6] GSE12454 [13] GSE20372 [6] GSE27811 [9] GSE56777 [8] GSE36384 [12] GSE32598 [11] GSE9338 [42] GSE33770 [8] GSE23923 [8] CEM+ CEM GSE10528 [6] GSE23398 [7] GSE19885 [9] GSE34902 [6] GSE6065 [100] GSE23119 [9] 0.0 GSE21836 [8] GSE22006 [19] GSE19729 [14] Scale ofaveragePearsoncorrelations GSE7764 [10] GSE23182 [12] GSE50603 [12] GSE55855 [6] GSE8828 [6] GSE24121 [9] 0.2 GSE19979 [6] GSE8044 [6] GSE22841 [12] GSE46875 [10] GSE52474 [154] GSE37658 [6] GSE38335 [9] GSE10813 [12] GSE9725 [16] 0.4 GSE23600 [10] GSE50824 [19] GSE51385 [8] GSE22927 [38] GSE18326 [8] GSE35091 [11] GSE11259 [9] GSE51628 [15] GSE43620 [8] 0.6 GSE7069 [8] GSE11723 [9] GSE19204 [6] GSE19657 [21] GSE42103 [9] GSE28093 [6] GSE42018 [8] GSE31208 [8] GSE35219 [6] 0.8 GSE51365 [28] GSE1983 [6] GSE17879 [6] GSE16684 [6] Score 4.95 4.96 4.96 4.97 4.97 4.99 4.99 4.99 5.03 5.07 5.08 5.09 5.12 5.15 5.17 5.19 5.21 5.21 5.22 5.22 5.22 5.23 5.24 5.25 5.30 5.32 5.45 5.45 5.45 5.47 5.48 5.48 5.52 5.56 5.58 5.59 5.66 5.68 5.68 5.70 5.71 5.73 5.74 5.75 5.76 6.03 6.03 6.09 6.10 6.12 1.0 Notes 5430435G22Rik Symbol Num ofCEMGenes:14.Predicted1049.SelectedDatasets:Strength:0.2 CEM 1,Geneset"[G]MHCclassIproteincomplex",Page3 Adamdec1 Tnfrsf13b Tnfrsf1b Alox5ap Nckap1l Slc37a2 Slc11a1 Cyp4v3 Rnase4 H2-Ab1 S100a4 Gsdmd Parp12 Rnf213 Col5a3 Pyhin1 Mocos Nucb1 Oas1a Selplg Anxa4 Abcc3 Wdfy4 Fxyd1 Agmo Erap1 Fcgr3 Il15ra Ifi204 Nnmt Nlrc5 Oas2 Cd84 Bag3 Cd14 Phyh Slfn2 Sdc4 Tspo Tap2 Ly6a Ccr1 Ctsc Ncf4 Ifih1 Aif1 Xdh Tlr4 Clu 0.0 1.0 GSE5891 [6] GSE30488 [52] GSE45619 [6] Only showingfirst200datasets-Seetxtoutputforfulldetails. GSE43899 [12] GSE28389 [20] GSE24793 [8] GSE21137 [16] GSE23895 [18] GSE15794 [6] GSE38831 [7] GSE6223 [13] GSE19194 [14] GSE13103 [8] GSE29241 [6] GSE9330 [8] GSE18460 [16] GSE51213 [16] GSE15872 [18] GSE38074 [39] GSE33134 [31] GSE40260 [6] GSE5298 [8] GSE4029 [10] GSE23925 [6] GSE32386 [13] GSE34423 [40] GSE26299 [108] GSE22381 [12] GSE16675 [72] GSE16496 [102] GSE13753 [10] GSE6837 [8] GSE18586 [9] GSE3554 [6] GSE8039 [32] GSE14395 [24] GSE19616 [16] GSE42548
Load more

Recommended publications
  • The Rise and Fall of the Bovine Corpus Luteum
    University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Spring 5-6-2017 The Rise and Fall of the Bovine Corpus Luteum Heather Talbott University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Biochemistry Commons, Molecular Biology Commons, and the Obstetrics and Gynecology Commons Recommended Citation Talbott, Heather, "The Rise and Fall of the Bovine Corpus Luteum" (2017). Theses & Dissertations. 207. https://digitalcommons.unmc.edu/etd/207 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. THE RISE AND FALL OF THE BOVINE CORPUS LUTEUM by Heather Talbott A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor John S. Davis University of Nebraska Medical Center Omaha, Nebraska May, 2017 Supervisory Committee: Carol A. Casey, Ph.D. Andrea S. Cupp, Ph.D. Parmender P. Mehta, Ph.D. Justin L. Mott, Ph.D. i ACKNOWLEDGEMENTS This dissertation was supported by the Agriculture and Food Research Initiative from the USDA National Institute of Food and Agriculture (NIFA) Pre-doctoral award; University of Nebraska Medical Center Graduate Student Assistantship; University of Nebraska Medical Center Exceptional Incoming Graduate Student Award; the VA Nebraska-Western Iowa Health Care System Department of Veterans Affairs; and The Olson Center for Women’s Health, Department of Obstetrics and Gynecology, Nebraska Medical Center.
    [Show full text]
  • Targeting EZH2 Reactivates a Breast Cancer Subtype-Specific Anti-Metastatic Transcriptional Program
    ARTICLE DOI: 10.1038/s41467-018-04864-8 OPEN Targeting EZH2 reactivates a breast cancer subtype-specific anti-metastatic transcriptional program Alison Hirukawa1,2, Harvey W. Smith1, Dongmei Zuo1, Catherine R. Dufour1, Paul Savage 1, Nicholas Bertos 1, Radia M. Johnson1, Tung Bui1,2, Guillaume Bourque3,4, Mark Basik5,6, Vincent Giguère 1,2,6, Morag Park1,2,6 & William J. Muller1,2,6 1234567890():,; Emerging evidence has illustrated the importance of epigenomic reprogramming in cancer, with altered post-translational modifications of histones contributing to pathogenesis. However, the contributions of histone modifiers to breast cancer progression are unclear, and how these processes vary between molecular subtypes has yet to be adequately addressed. Here we report that genetic or pharmacological targeting of the epigenetic modifier Ezh2 dramatically hinders metastatic behaviour in both a mouse model of breast cancer and patient-derived xenografts reflective of the Luminal B subtype. We further define a subtype- specific molecular mechanism whereby EZH2 maintains H3K27me3-mediated repression of the FOXC1 gene, thereby inactivating a FOXC1-driven, anti-invasive transcriptional program. We demonstrate that higher FOXC1 is predictive of favourable outcome specifically in Luminal B breast cancer patients and establish the use of EZH2 methyltransferase inhibitors as a viable strategy to block metastasis in Luminal B breast cancer, where options for targeted therapy are limited. 1 Goodman Cancer Research Centre, McGill University, Montréal, QC H3A 1A3, Canada. 2 Department of Biochemistry, McGill University, Montréal, QC H3G 1Y6, Canada. 3 McGill University, Génome Québec Innovation Centre, Montréal, QC H3A 0G1, Canada. 4 Department of Human Genetics, McGill University, Montréal, QC H3A 1A3, Canada.
    [Show full text]
  • Identification and Characterization of the Forkhead Box
    IDENTIFICATION AND CHARACTERIZATION OF THE FORKHEAD BOX FAMILY OF TRANSCRIPTIONAL REGULATORS IN PARASITIC SCHISTOSOMES by MELISSA M. VARRECCHIA Submitted in partial fulfillment of the requirements for the degree of Doctor of philosophy Department of Biology CASE WESTERN RESERVE UNIVERSITY August 2017 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the dissertation of Melissa M. Varrecchia candidate for the degree of Doctor of Philosophy Committee Chair Michael F. Benard Committee Member Emmitt R. Jolly Committee Member Christopher A. Cullis Committee Member Claudia M. Mizutani Committee Member Brian M. McDermott Date of Defense June 6, 2017 *We also certify that written approval has been obtained for any proprietary material contained therein. ii Dedication I would like to dedicate this dissertation to my Mom and Dad. Mom, thank you for your endless love, support and encouragement throughout the years. Dad, I miss you and I know that you are with me always, cheering me on in spirit. iii Table of Contents Table of Contents………………………………………………………………………...1 List of Tables……………………………………………………………………………..6 List of Figures…………………………………………………………………………....8 Acknowledgements…………………………………………………………………..…11 List of Abbreviations…………………………………………………………………...13 Abstract…………………………………………………………………………………15 Chapter 1: Introduction………………………………………………………………..17 1.1 Schistosomiasis………………………………………………………………17 1.2 Pathogenesis and treatment…………………………………………………..18 1.3 Schistosome life cycle………………………………………………………..20 1.4 Schistosome morphology
    [Show full text]
  • Research Progress on the Forkhead Box C1
    www.impactjournals.com/oncotarget/ Oncotarget, 2018, Vol. 9, (No. 15), pp: 12471-12478 Review Research progress on the forkhead box C1 Jinhua Wang1,2, Wan Li2, Xiangjin Zheng2, Xiaocong Pang2 and Guanhua Du1,2 1The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing 100050, China 2Key Laboratory of Drug Target Research and Drug Screen, Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, China Correspondence to: Jinhua Wang, email: [email protected] Guanhua Du, email: [email protected] Keywords: FOX family; FOXC1; cancer; drug resistance; stem cell Received: July 29, 2017 Accepted: November 01, 2017 Published: November 20, 2017 Copyright: Wang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT FOXC1 is a vital member of FOX families which play important roles in biological processes including proliferation, differentiation, apoptosis, migration, invasion, metabolism, and longevity. Here we are focusing on roles of FOXC1 and their mechanisms in cancers. FOXC1 promoted progress of many cancers, such as breast cancer (especially basal-like breast cancer), hepatocellular carcinoma, gastric cancer and so on. FOXC1 was also found to be associated with drug resistance of cancers. FOXC1 promoted metastasis of cancers by increasing expression of MMP7, NEDD9 and Snail. Proliferation and invasion of cancers were increased by FOXC1 by mediating NF-κB, MST1R and KLF4 expression. FOXC1 was associated with development by regulating expression of FGF19 and MSX1.
    [Show full text]
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
    [Show full text]
  • Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene
    Hodgkin Lymphoma SUPPLEMENTARY APPENDIX Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene Melissa Rotunno, 1 Mary L. McMaster, 1 Joseph Boland, 2 Sara Bass, 2 Xijun Zhang, 2 Laurie Burdett, 2 Belynda Hicks, 2 Sarangan Ravichandran, 3 Brian T. Luke, 3 Meredith Yeager, 2 Laura Fontaine, 4 Paula L. Hyland, 1 Alisa M. Goldstein, 1 NCI DCEG Cancer Sequencing Working Group, NCI DCEG Cancer Genomics Research Laboratory, Stephen J. Chanock, 5 Neil E. Caporaso, 1 Margaret A. Tucker, 6 and Lynn R. Goldin 1 1Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 2Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 3Ad - vanced Biomedical Computing Center, Leidos Biomedical Research Inc.; Frederick National Laboratory for Cancer Research, Frederick, MD; 4Westat, Inc., Rockville MD; 5Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; and 6Human Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA ©2016 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2015.135475 Received: August 19, 2015. Accepted: January 7, 2016. Pre-published: June 13, 2016. Correspondence: [email protected] Supplemental Author Information: NCI DCEG Cancer Sequencing Working Group: Mark H. Greene, Allan Hildesheim, Nan Hu, Maria Theresa Landi, Jennifer Loud, Phuong Mai, Lisa Mirabello, Lindsay Morton, Dilys Parry, Anand Pathak, Douglas R. Stewart, Philip R. Taylor, Geoffrey S. Tobias, Xiaohong R. Yang, Guoqin Yu NCI DCEG Cancer Genomics Research Laboratory: Salma Chowdhury, Michael Cullen, Casey Dagnall, Herbert Higson, Amy A.
    [Show full text]
  • Mechanisms Acting on Hedgehog-Gli Pathway and Their Therapeutic Potential
    From the Department of Biosciences and Nutrition Karolinska Institutet, Stockholm, Sweden MECHANISMS ACTING ON HEDGEHOG-GLI PATHWAY AND THEIR THERAPEUTIC POTENTIAL Ani Azatyan Stockholm 2020 All previously published papers were reproduced with permission from the publisher. Published by Karolinska Institutet. Printed by Universitetsservice US-AB © Ani Azatyan, 2020 ISBN 978-91-7831-880-3 Mechanisms acting on Hedgehog-GLI pathway and their therapeutic potential THESIS FOR DOCTORAL DEGREE (Ph.D.) By Ani Azatyan Principal Supervisor: Opponent: Prof. Peter Zaphiropoulos Prof. Matthias Lauth Karolinska Institutet Philipps-University Marburg, Germany Department of Biosciences and Nutrition Center for Tumor Biology and Immunology Co-supervisor(s): Examination Board: Prof. Karl Ekwall Doc. Ning Xu Landén Karolinska Institutet Karolinska Institutet Department of Biosciences and Nutrition Department of Medicine, Division of Dermatology Doc. Vladimir Bykov Prof. Sonia Lain Karolinska Institutet Karolinska Institutet Department of Oncology-Pathology Department of Microbiology, Tumor and Cell Biology Prof. Ann-Kristin Östlund Farrants Stockholm University Department of Molecular Biosciences “I am among those who think that science has great beauty” - Marie Curie Abstract Hedgehog signaling is crucial for diverse aspects of animal development, essential in regulating many cellular processes and is largely implicated in various forms of human cancer. However, many aspects of Hedgehog signaling are not completely understood. This thesis aims to contribute towards a better understanding of the mechanisms acting on Hedgehog-GLI signaling and explore their possible therapeutic potential. PAPER I. We demonstrate that the small molecule RITA, a p53 activator, downregulates Hedgehog signaling in human medulloblastoma and rhabdomyosarcoma cells via JNK kinase and irrespective of p53. In vitro RITA enhanced the anti-proliferative effects of the GLI antagonist GANT61.
    [Show full text]
  • Human Pluripotent Stem Cell-Derived Ectomesenchymal Stromal Cells Promote More Robust Functional Recovery Than Umbilical Cord-De
    Human pluripotent stem cell-derived ectomesenchymal stromal cells promote more robust functional recovery than umbilical cord-derived mesenchymal stromal cells after hypoxic- ischaemic brain damage Jiawei Huang1,3*, Kin Pong U1,3*, Fuyuan Yang1, Zeyuan Ji1, Jiacheng Lin1,3, Zhihui Weng1, Lai Ling Tsang1,3, Tobias D Merson5, Ye Chun Ruan6, Chao Wan1,3, Gang Li2, Xiaohua Jiang1,3,4 1School of Biomedical Sciences, 2Department of Orthopaedics and Traumatology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, PR China. 3School of Biomedical Sciences Core Laboratory, Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, PR China. 4Sichuan University – The Chinese University of Hong Kong Joint Laboratory for Reproductive Medicine, West China Second University Hospital, Sichuan University, Chengdu 610041, Sichuan, China. 5Australian Regenerative Medicine Institute, Monash University, Clayton, VIC, Australia. 6Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China. Running Title: Human ectomesenchymal stromal cells promote functional recovery in a rat HIE model *Corresponding author: Prof. Xiaohua JIANG, Email: [email protected] Address: Room 409A, Lo Kwee Seong Integrated Biomedical Sciences Building, Area 39, The Chinese University of Hong Kong, Shatin. Keywords: HIE, ectomesenchymal stromal cells, brain damage, regeneration, paracrine, ERK Abstract: Aims: Hypoxic-ischaemic encephalopathy (HIE) is one of the most serious complications in neonates and infants. Mesenchymal stromal cell (MSC)-based therapy is emerging as a promising treatment avenue for HIE. However, despite its enormous potential, the clinical application of MSCs is limited by cell heterogeneity, low isolation efficiency and unpredictable effectiveness. In this study, we examined the therapeutic effects and underlying mechanisms of human pluripotent stem cell-derived ectomesenchymal stromal cells (hPSC-EMSCs) in a rat model of HIE.
    [Show full text]
  • Sox2 Promotes Malignancy in Glioblastoma by Regulating
    Volume 16 Number 3 March 2014 pp. 193–206.e25 193 www.neoplasia.com Artem D. Berezovsky*, Laila M. Poisson†, Sox2 Promotes Malignancy in ‡ ‡ David Cherba , Craig P. Webb , Glioblastoma by Regulating Andrea D. Transou*, Nancy W. Lemke*, Xin Hong*, Laura A. Hasselbach*, Susan M. Irtenkauf*, Plasticity and Astrocytic Tom Mikkelsen*,§ and Ana C. deCarvalho* Differentiation1,2 *Department of Neurosurgery, Henry Ford Hospital, Detroit, MI; †Department of Public Health Sciences, Henry Ford Hospital, Detroit, MI; ‡Program of Translational Medicine, Van Andel Research Institute, Grand Rapids, MI; §Department of Neurology, Henry Ford Hospital, Detroit, MI Abstract The high-mobility group–box transcription factor sex-determining region Y–box 2 (Sox2) is essential for the maintenance of stem cells from early development to adult tissues. Sox2 can reprogram differentiated cells into pluripotent cells in concert with other factors and is overexpressed in various cancers. In glioblastoma (GBM), Sox2 is a marker of cancer stemlike cells (CSCs) in neurosphere cultures and is associated with the proneural molecular subtype. Here, we report that Sox2 expression pattern in GBM tumors and patient-derived mouse xenografts is not restricted to a small percentage of cells and is coexpressed with various lineage markers, suggesting that its expression extends beyond CSCs to encompass more differentiated neoplastic cells across molecular subtypes. Employing a CSC derived from a patient with GBM and isogenic differentiated cell model, we show that Sox2 knockdown in the differentiated state abolished dedifferentiation and acquisition of CSC phenotype. Furthermore, Sox2 deficiency specifically impaired the astrocytic component of a biphasic gliosarcoma xenograft model while allowing the formation of tumors with sarcomatous phenotype.
    [Show full text]
  • Chromosomal Microarray Analysis in Turkish Patients with Unexplained Developmental Delay and Intellectual Developmental Disorders
    177 Arch Neuropsychitry 2020;57:177−191 RESEARCH ARTICLE https://doi.org/10.29399/npa.24890 Chromosomal Microarray Analysis in Turkish Patients with Unexplained Developmental Delay and Intellectual Developmental Disorders Hakan GÜRKAN1 , Emine İkbal ATLI1 , Engin ATLI1 , Leyla BOZATLI2 , Mengühan ARAZ ALTAY2 , Sinem YALÇINTEPE1 , Yasemin ÖZEN1 , Damla EKER1 , Çisem AKURUT1 , Selma DEMİR1 , Işık GÖRKER2 1Faculty of Medicine, Department of Medical Genetics, Edirne, Trakya University, Edirne, Turkey 2Faculty of Medicine, Department of Child and Adolescent Psychiatry, Trakya University, Edirne, Turkey ABSTRACT Introduction: Aneuploids, copy number variations (CNVs), and single in 39 (39/123=31.7%) patients. Twelve CNV variant of unknown nucleotide variants in specific genes are the main genetic causes of significance (VUS) (9.75%) patients and 7 CNV benign (5.69%) patients developmental delay (DD) and intellectual disability disorder (IDD). were reported. In 6 patients, one or more pathogenic CNVs were These genetic changes can be detected using chromosome analysis, determined. Therefore, the diagnostic efficiency of CMA was found to chromosomal microarray (CMA), and next-generation DNA sequencing be 31.7% (39/123). techniques. Therefore; In this study, we aimed to investigate the Conclusion: Today, genetic analysis is still not part of the routine in the importance of CMA in determining the genomic etiology of unexplained evaluation of IDD patients who present to psychiatry clinics. A genetic DD and IDD in 123 patients. diagnosis from CMA can eliminate genetic question marks and thus Method: For 123 patients, chromosome analysis, DNA fragment analysis alter the clinical management of patients. Approximately one-third and microarray were performed. Conventional G-band karyotype of the positive CMA findings are clinically intervenable.
    [Show full text]
  • FOXS1 Is Regulated by GLI1 and Mir-125A-5P and Promotes Cell
    www.nature.com/scientificreports OPEN FOXS1 is regulated by GLI1 and miR-125a-5p and promotes cell proliferation and EMT in gastric Received: 21 November 2018 Accepted: 14 March 2019 cancer Published: xx xx xxxx Sen Wang1,2, Longke Ran2,3, Wanfeng Zhang 2,3, Xue Leng1,2, Kexin Wang4, Geli Liu1,2, Jing Song2,3, Yujing Wang1,2, Xianqin Zhang1,2, Yitao Wang1,2, Lian Zhang1,2, Yan Ma5, Kun Liu1,2, Haiyu Li6, Wei Zhang7, Guijun Qin8 & Fangzhou Song1,2 Gastric cancer (GC) is the fourth most common malignant neoplasm and the second leading cause of cancer death. Identifcation of key molecular signaling pathways involved in gastric carcinogenesis and progression facilitates early GC diagnosis and the development of targeted therapies for advanced GC patients. Emerging evidence has revealed a close correlation between forkhead box (FOX) proteins and cancer development. However, the prognostic signifcance of forkhead box S1 (FOXS1) in patients with GC and the function of FOXS1 in GC progression remain undefned. In this study, we found that upregulation of FOXS1 was frequently detected in GC tissues and strongly correlated with an aggressive phenotype and poor prognosis. Functional assays confrmed that FOXS1 knockdown suppressed cell proliferation and colony numbers, with induction of cell arrest in the G0/G1 phase of the cell cycle, whereas forced expression of FOXS1 had the opposite efect. Additionally, forced expression of FOXS1 accelerated tumor growth in vivo and increased cell migration and invasion through promoting epithelial–mesenchymal transition (EMT) both in vitro and in vivo. Mechanistically, the core promoter region of FOXS1 was identifed at nucleotides −660~ +1, and NFKB1 indirectly bind the motif on FOXS1 promoters and inhibit FOXS1 expression.
    [Show full text]
  • Molecular Genetic Characterization of Retinoblastoma Tumors Lacking Rb1 Mutations
    MOLECULAR GENETIC CHARACTERIZATION OF RETINOBLASTOMA TUMORS LACKING RB1 MUTATIONS by Jennifer Yvonne Kennett B.Sc., Simon Fraser University, 2005 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE in The Faculty Of Graduate Studies (Pathology and Laboratory Medicine) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) December 2012 © Jennifer Yvonne Kennett, 2012 Abstract Retinoblastoma is a rare childhood cancer of the retina and is the most common intraocular tumor in children. Classically, retinoblastoma results from biallelic loss of the RB1 tumor suppressor gene. As with other cancer types, dysregulation of a single gene alone is not considered sufficient for complete transformation to malignancy. Frequent regions of genetic alteration harbouring additional genes, implicated in retinoblastoma oncogenesis and progression, include chromosomes 1q, 2p, 6p, 13q and 16q. Sensitive molecular genetic screening techniques are capable of identifying RB1 mutations in 98% of unilateral retinoblastoma tumors. The remaining 2% harbour no identifiable RB1 inactivating alterations, and therefore molecular interrogation of these cases would likely reveal alternative genetic events driving retinoblastoma tumorigenesis in the absence of RB1 inactivation. Towards this objective, in this thesis work, I describe genetic alterations identified by tiling path array comparative genomic hybridization in a rare sample set composed of 23 RB1+/+ tumors. In addition to gene disruption by copy number alteration, mechanisms of gene disruption resulting in no overall change in copy number or change in copy number with allelic imbalance were also investigated utilizing genome-wide SNP array analysis on five of the RB1+/+ tumors. The most striking recurrent genetic alteration identified in retinoblastoma tumors lacking RB1 inactivating mutations, was focal high-level MYCN amplification, which occurred at a frequency of approximately 48%.
    [Show full text]