About: Ahmed Idbaih

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

researcher

Attributes	Values
rdf:type	Item
description	forskare (sv) researcher (en) 연구원 (ko) 研究者 (ja) araştırmacı (tr) дослідник (uk) эрдэмтэн (mn) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy) onderzoeker (nl)
rdfs:label	Ahmed Idbaih (en) Ahmed Idbaih (es) Ahmed Idbaih (nl) Ahmed Idbaih (sl) Ahmed Idbaih (ast)
skos:prefLabel	Ahmed Idbaih (en) Ahmed Idbaih (es) Ahmed Idbaih (nl) Ahmed Idbaih (sl) Ahmed Idbaih (ast)
name	Ahmed Idbaih (en) Ahmed Idbaih (es) Ahmed Idbaih (nl) Ahmed Idbaih (sl) Ahmed Idbaih (ast)
Scopus author ID	wds:Q55459195-493B6C99-E589-41C9-ABC2-C23E312281AD
Scopus author ID	22134879200
instance of	wds:Q55459195-E6A77F92-0BEB-4CB8-AB19-C5D8087A1347
instance of	Homo sapiens
occupation	wds:Q55459195-000637BC-B1CC-41E1-B2DC-82FE4A6959B4
employer	wds:Q55459195-292B8C18-3E74-43F2-A2DA-AC3C15B943FA wds:Q55459195-3A44B30C-C3C7-4EA7-B23E-EB5E1589C8BB wds:Q55459195-D9AFAB68-A568-4BF9-A814-D0D775879477
sex or gender	wds:Q55459195-FA47205E-FCCA-41D2-ABE7-6C35821DDA92
ISNI	wds:Q55459195-5FD79B3B-F342-4F28-AEBF-5105B47D4814
VIAF ID	wds:Q55459195-5E23C86C-AEA6-41C7-90D8-B9F7CB9FDFB4
IdRef ID	wds:Q55459195-9B37F423-E17D-432B-83A1-D3E385EDC618
date of birth	wds:Q55459195-648DEB99-C517-46B6-9ED1-7FE0FB0A6980
educated at	wds:Q55459195-20B77B0A-D94A-42B5-88A4-7537A1CC6A3D wds:Q55459195-6466AB20-16D4-45A4-9288-B7F74CDF3348 wds:Q55459195-6B4908B2-A7BC-41DE-9522-3A1A2DAB5302 wds:Q55459195-ACA9A595-F497-41B8-8BB9-CCF9FF53B83D wds:Q55459195-EE46CEA0-8BB5-4F75-91A5-E373EA6511DA
PLWABN ID	wds:Q55459195-59330ED9-3817-4E0E-8FAC-8EAFEB77034D
VIAF ID	http://viaf.org/viaf/315223537
IdRef ID	http://www.idref.fr/114953139/id
occupation	researcher
employer	Dana–Farber Cancer Institute Sorbonne University
sex or gender	male
ISNI	0000000139473946
VIAF ID	315223537
IdRef ID	114953139
date of birth	1975-01-01 00:00:00Z (xsd:dateTime)
educated at	University of Paris-Sud Pierre and Marie Curie University Sorbonne University Medical Faculty
PLWABN ID	9810658806805606
ORCID iD	wds:Q55459195-B862C8EA-5980-4554-894F-E3B3532F064A
ORCID iD	https://orcid.org/0000-0001-5290-1204
ORCID iD	0000-0001-5290-1204
ResearcherID	wds:Q55459195-C7DB4637-4659-4DFF-B826-DD31DFB2890F
ResearcherID	N-8746-2017
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q55459195
is author of	Mitotic index, microvascular proliferation, and necrosis define 3 groups of 1p/19q codeleted anaplastic oligodendrogliomas associated with different genomic alterations Allelic loss of 9p21.3 is a prognostic factor in 1p/19q codeleted anaplastic gliomas Deciphering the 8q24.21 association for glioma [Should elderly patients with glioblastoma be proposed to radiotherapy?] BAC array CGH distinguishes mutually exclusive alterations that define clinicogenetic subtypes of gliomas. CRX is a diagnostic marker of retinal and pineal lineage tumors Maintenance Therapy With Tumor-Treating Fields Plus Temozolomide vs Temozolomide Alone for Glioblastoma: A Randomized Clinical Trial Anaplastic oligodendrogliomas with 1p19q codeletion have a proneural gene expression profile Isocitrate dehydrogenase 1 codon 132 mutation is an important prognostic biomarker in gliomas. Chromosome 7p11.2 (EGFR) variation influences glioma risk Genetic risk profiles identify different molecular etiologies for glioma Association between glioma susceptibility loci and tumour pathology defines specific molecular etiologies Prophylactic intrathecal chemotherapy in primary CNS lymphoma Recurrent mutations of MYD88 and TBL1XR1 in primary central nervous system lymphomas ASPM-associated stem cell proliferation is involved in malignant progression of gliomas and constitutes an attractive therapeutic target Myxoid malignant fibrous histiocytoma and pleomorphic liposarcoma share very similar genomic imbalances IDH1 or IDH2 mutations predict longer survival and response to temozolomide in low-grade gliomas. TP53 mutations but no CHEK2 *1100DelC variant in familial gliomas. Molecular classification of anaplastic oligodendroglioma using next-generation sequencing: a report of the prospective randomized EORTC Brain Tumor Group 26951 phase III trial. French Intensive Care Society, International congress - Réanimation 2016 DNA fragmentation simulation method (FSM) and fragment size matching improve aCGH performance of FFPE tissues Short course of radiation therapy in elderly patients with glioblastoma multiforme Primary brain tumours in adults IDH1 and IDH2 mutations are prognostic but not predictive for outcome in anaplastic oligodendroglial tumors: a report of the European Organization for Research and Treatment of Cancer Brain Tumor Group Two types of chromosome 1p losses with opposite significance in gliomas. Low penetrance susceptibility to glioma is caused by the TP53 variant rs78378222. Tumor genomic profiling and TP53 germline mutation analysis of first-degree relative familial gliomas. Influence of MDM2 SNP309 alone or in combination with the TP53 R72P polymorphism in oligodendroglial tumors. Dramatic response of a BRAF V600E-mutated primary CNS histiocytic sarcoma to vemurafenib. Spatial and temporal evolution of distal 10q deletion, a prognostically unfavorable event in diffuse low-grade gliomas Intrinsic molecular subtypes of glioma are prognostic and predict benefit from adjuvant procarbazine, lomustine, and vincristine chemotherapy in combination with other prognostic factors in anaplastic oligodendroglial brain tumors: a report from EOR Array-based genomics in glioma research Clinical value of chromosome arms 19q and 11p losses in low-grade gliomas Detection, Characterization, and Inhibition of FGFR-TACC Fusions in IDH Wild-type Glioma.

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