{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,13]],"date-time":"2025-09-13T16:12:32Z","timestamp":1757779952027,"version":"3.37.3"},"reference-count":54,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2017,11,23]],"date-time":"2017-11-23T00:00:00Z","timestamp":1511395200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Else \u00dcbelmesser Foundation for Applied Cancer Research, T\u00fcbingen, Germany","award":["D.30.19845"],"award-info":[{"award-number":["D.30.19845"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuropathology Appl Neurobio"],"published-print":{"date-parts":[[2018,2]]},"abstract":"<jats:sec><jats:title>Aims<\/jats:title><jats:p>Previous data suggest that expression of transcription factors FoxG1 and Olig\u20102 can separate hotspot histone H3 family member 3A (H3F3A)\u2010mutant tumours in paediatric glioma. We evaluated their prognostic potential and feasibility for identifying H3F3A\u2010mutant tumours among IDH\u2010mutant\/wild\u2010type gliomas.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Immunohistochemistry of FoxG1\/Olig\u20102 and \u03b1\u2010thalassaemia\/mental\u2010retardation\u2010syndrome\u2010X\u2010linked gene (ATRX) in 471 cases of diffuse gliomas and molecular determination of IDH, H3F3A, MGMT and 1p\/19 codeletion status.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Mean percentage of FoxG1\u2010positive tumour cells increased from 17% in WHO grade II to over 21% in grade III to 37% in grade IV tumours, whereas mean Olig\u20102 indices decreased from 29% to 28% to 17% respectively. FoxG1 indices were similar in astrocytic and oligodendroglial tumours, whereas Olig\u20102 indices were increased in oligodendrogliomas compared to astrocytic tumours (<jats:italic>n<\/jats:italic> = 451, <jats:italic>P<\/jats:italic> &lt; 0.0001). FoxG1\u2010positive nuclei were significantly reduced in IDH and H3F3A K27\u2010mutant tumours, whereas Olig\u20102\u2010positive nuclei were significantly reduced in IDH\u2010wild\u2010type and H3F3A G34\u2010mutant tumours. Among IDH\u2010mutant tumours, mean Olig\u20102 index was significantly higher in 1p\/19q codeleted tumours (mean: 43%) compared to IDH\u2010mutant tumours with ATRX loss (mean: 23%, <jats:italic>P<\/jats:italic> &lt; 0.0001). A significantly better outcome was first suggested for FoxG1<jats:sup>low<\/jats:sup> tumours (<jats:italic>n<\/jats:italic> = 212, log rank <jats:italic>P<\/jats:italic> = 0.0132) and Olig\u20102<jats:sup>high<\/jats:sup> tumours (<jats:italic>n<\/jats:italic> = 203, log\u2010rank <jats:italic>P<\/jats:italic> = 0.0011) based on classification and regression tree determined cutoffs, but this was not confirmed by multivariate analysis including IDH mutation, WHO grade, ATRX status and age.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>While the combined FoxG1\/Olig\u20102 profile may discriminate H3F3A K27\u2010 and G34\u2010mutant tumours and define a prognostically favourable subset in IDH\u2010mutant gliomas, our data show that labelling indices of these transcription factors overlap with adult IDH\u2010mutant and wild\u2010type tumour classes.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nan.12447","type":"journal-article","created":{"date-parts":[[2017,10,20]],"date-time":"2017-10-20T22:10:37Z","timestamp":1508537437000},"page":"207-223","source":"Crossref","is-referenced-by-count":12,"title":["Low FoxG1 and high Olig\u20102 labelling indices define a prognostically favourable subset in isocitrate dehydrogenase (IDH)\u2010mutant gliomas"],"prefix":"10.1111","volume":"44","author":[{"given":"S.","family":"Sch\u00e4fer","sequence":"first","affiliation":[{"name":"Department of Neuropathology Institute of Pathology and Neuropathology University Hospital of Tuebingen Eberhard Karls University of Tuebingen Tuebingen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F.","family":"Behling","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery University Hospital of Tuebingen Eberhard Karls University of Tuebingen Tuebingen Germany"},{"name":"Center for CNS Tumors Comprehensive Cancer 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