about
Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumoursCloning of a novel human ELF-1-related ETS transcription factor, ELFR, its characterization and chromosomal assignment relative to ELF-1Ewing's sarcoma family of tumors: current managementIntercohort gene expression co-analysis reveals chemokine receptors as prognostic indicators in Ewing's sarcomaCommon variants near TARDBP and EGR2 are associated with susceptibility to Ewing sarcoma[Cytogenetic and molecular genetic changes in malignant primary bone tumors]Single-chain antibodies to the EWS NH(2) terminus structurally discriminate between intact and chimeric EWS in Ewing's sarcoma and interfere with the transcriptional activity of EWS in vivo.CD133 expression in chemo-resistant Ewing sarcoma cellsThe Ewing family of tumors and the search for the Achilles' heel.Hypoxia modulates EWS-FLI1 transcriptional signature and enhances the malignant properties of Ewing's sarcoma cells in vitro.Redirecting T cells to Ewing's sarcoma family of tumors by a chimeric NKG2D receptor expressed by lentiviral transduction or mRNA transfection.EWS-FLI1 target genes recovered from Ewing's sarcoma chromatin.Epigenome mapping reveals distinct modes of gene regulation and widespread enhancer reprogramming by the oncogenic fusion protein EWS-FLI1.EZH2 is a mediator of EWS/FLI1 driven tumor growth and metastasis blocking endothelial and neuro-ectodermal differentiation.EWS-FLI1 employs an E2F switch to drive target gene expression.Potentials for RNAi in sarcoma research and therapy: Ewing's sarcoma as a model.The first European interdisciplinary ewing sarcoma research summitContext matters: the hen or egg problem in Ewing's sarcoma.Variability of nm23-H1/NDPK-A expression in human lymphomas and its relation to tumour aggressivenessYK-4-279 effectively antagonizes EWS-FLI1 induced leukemia in a transgenic mouse model.EWS-FLI1 suppresses NOTCH-activated p53 in Ewing's sarcomaA molecular function map of Ewing's sarcoma.Variability in functional p53 reactivation by PRIMA-1(Met)/APR-246 in Ewing sarcoma.Targeted therapies in bone sarcomas.Blocking the road, stopping the engine or killing the driver? Advances in targeting EWS/FLI-1 fusion in Ewing sarcoma as novel therapy.Ewing Sarcoma: Current Management and Future Approaches Through Collaboration.Progress in the molecular biology of ewing tumors.Overexpression of HOX genes is prevalent in Ewing sarcoma and is associated with altered epigenetic regulation of developmental transcription programs.Suppression of deacetylase SIRT1 mediates tumor-suppressive NOTCH response and offers a novel treatment option in metastatic Ewing sarcoma.Development of curative therapies for Ewing sarcomas by interdisciplinary cooperative groups in Europe.Suppression of FOXO1 is responsible for a growth regulatory repressive transcriptional sub-signature of EWS-FLI1 in Ewing sarcoma.Downstream EWS/FLI1 - upstream Ewing's sarcomaCaveolin-1 (CAV1) is a target of EWS/FLI-1 and a key determinant of the oncogenic phenotype and tumorigenicity of Ewing's sarcoma cells.Dr. Jekyll and Mr. Hyde: The Two Faces of the FUS/EWS/TAF15 Protein Family.ESF-EMBO Symposium "Molecular Biology and Innovative Therapies in Sarcomas of Childhood and Adolescence" Sept 29-Oct 4, Polonia Castle Pultusk, Poland.A detailed analysis of duplications appearing during early, high multiplicity infections with polyoma virus.O-GlcNAcylation is involved in the transcriptional activity of EWS-FLI1 in Ewing's sarcoma.CD99 regulates neural differentiation of Ewing sarcoma cells through miR-34a-Notch-mediated control of NF-κB signaling.Mobilization of tumour cells during biopsy in an infant with Ewing sarcoma.Among genes involved in the RB dependent cell cycle regulatory cascade, the p16 tumor suppressor gene is frequently lost in the Ewing family of tumors.
P50
Q24298221-1C1FAEB3-6AD3-4A1B-8D7A-142B26DFF96EQ24320348-6F06F139-4EC9-4F46-A6BA-D0139E1401B0Q28242009-2C7FCE6D-09BD-4257-89D6-724DB64E281EQ28284358-16214F9F-408B-44D7-B24B-537CDE0813B5Q29028729-9E233F3F-57B0-4C1C-9DCA-C805768AF47BQ32040546-579E54AA-D8C4-40CE-834E-0C915A8FD218Q33260657-9C0D5F90-FE34-43BF-9C50-CF59BC620E32Q33546702-11260F8E-D8EF-4E7D-B7D1-0AB9EFEAFC8AQ33693680-1FE25745-4108-4EB7-9B95-0E1BAA531249Q33908885-C1585292-9FFE-4576-B4D4-9FFF062E3942Q34166288-072384B8-DE31-4A7C-BF7E-6CF74B421A0CQ34398493-A82C8547-BDA5-4B7B-A49A-3AF1853294EAQ34464009-4B10B1E1-E7F2-4CE2-8FD7-8B1A508A9C20Q34963463-F2162FFA-0489-47DD-89CC-5362ACE9FC32Q35171620-C35AE1EF-F422-48E1-BB85-4D2C8210BEDBQ35561604-2890595E-E765-4DDF-914F-76952E955AE4Q35993560-D82776A8-C4A2-4F57-A9CF-1DB6EFBAA273Q36096571-02477D11-30A4-444A-AD6D-802808639544Q36141262-B5DD4CFF-A3A4-45F8-99C4-E3ED92BE3FF8Q36545848-91D4D8B3-A6D4-44DC-B53F-78FB67312EA7Q37135628-FBEEFD6A-40D2-4FA7-B7D6-3D90585E2AC8Q37165799-3F5F946E-E4EB-4E60-9E9D-2EC9A8B938A8Q37323049-B5DA8289-CD6A-40CE-AF79-9AD7784D9AF8Q37660434-141D86F7-1849-4C4E-91CE-9FBF51CC077AQ38243878-8D156E8A-F878-4892-9E47-D0B12D19A166Q38573422-69E1D04A-BDA3-483D-8583-F54BBA4C2152Q38612055-9DD249D0-0DB3-4A2D-87DF-41D28B9338C9Q38916006-83F801EF-9336-4421-B581-21B5742E404FQ38950669-D63AC5B4-5FF8-493A-9F8B-1B37FF762E66Q39005440-0976E152-09BB-4EB6-8E69-1ECFFECA843BQ39101609-624386F8-1442-44A6-87A0-AEC7527EE978Q39325942-4806151F-3291-47D9-94E1-CBE3625A2EE3Q40219007-32D412FE-08AC-4405-876B-972EE3678114Q41304204-82A2E57C-DAE7-465F-AD84-B50815C41051Q41462039-EDCD3915-9094-44BA-B783-468E8F123381Q41673091-F136DAFB-2BA3-4029-A157-F697438B0EC7Q42025548-1D5FA62C-4F8C-448B-8C37-FCB596BE12C2Q42392077-FD030F70-F18F-4942-8642-0D7AABA2AFB4Q42635568-50E5B8EA-1C9E-404A-96F7-BA4B8B25B6FBQ42816542-79873088-AB54-4670-9201-27B4B7E1E814
P50
description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Heinrich Kovar
@ast
Heinrich Kovar
@en
Heinrich Kovar
@es
Heinrich Kovar
@nl
Heinrich Kovar
@sl
type
label
Heinrich Kovar
@ast
Heinrich Kovar
@en
Heinrich Kovar
@es
Heinrich Kovar
@nl
Heinrich Kovar
@sl
prefLabel
Heinrich Kovar
@ast
Heinrich Kovar
@en
Heinrich Kovar
@es
Heinrich Kovar
@nl
Heinrich Kovar
@sl
P106
P21
P31
P496
0000-0001-6873-9109