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However, occasionally supratentorial ependymomas cannot be readily assigned to any of these groups due to lack of detection of a typical fusion and\/or ambiguous DNA methylation\u2013based classification. An unbiased approach with a cohort of unprecedented size revealed distinct methylation clusters composed of tumors with ependymal but also various other histologic features containing alternative translocations that shared ZFTA as a partner gene. Somatic overexpression of ZFTA-associated fusion genes in the developing cerebral cortex is capable of inducing tumor formation in vivo, and cross-species comparative analyses identified GLI2 as a key downstream regulator of tumorigenesis in all tumors. Targeting GLI2 with arsenic trioxide caused extended survival of tumor-bearing animals, indicating a potential therapeutic vulnerability in ZFTA fusion\u2013positive tumors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>ZFTA\u2013RELA fusions are a hallmark feature of supratentorial ependymoma. We find that ZFTA acts as a partner for alternative transcriptional activators in oncogenic fusions of supratentorial tumors with various histologic characteristics. Establishing representative mouse models, we identify potential therapeutic targets shared by ZFTA fusion\u2013positive tumors, such as GLI2.<\/jats:p>\n                    <jats:p>This article is highlighted in the In This Issue feature, p. 2113<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/2159-8290.cd-20-0963","type":"journal-article","created":{"date-parts":[[2021,4,20]],"date-time":"2021-04-20T18:08:49Z","timestamp":1618942129000},"page":"2230-2247","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":84,"title":["Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA\/C11orf95 Fusion\u2013Positive Supratentorial Ependymomas"],"prefix":"10.1158","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3385-7353","authenticated-orcid":false,"given":"Tuyu","family":"Zheng","sequence":"first","affiliation":[{"name":"1Hopp Children's Cancer Center Heidelberg (KiTZ), Heidelberg, Germany."},{"name":"2Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany."},{"name":"3Faculty of Biosciences, Heidelberg University, Heidelberg, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3844-9933","authenticated-orcid":false,"given":"David R.","family":"Ghasemi","sequence":"additional","affiliation":[{"name":"1Hopp Children's Cancer Center Heidelberg (KiTZ), Heidelberg, Germany."},{"name":"2Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Konstantin","family":"Okonechnikov","sequence":"additional","affiliation":[{"name":"1Hopp Children's Cancer Center Heidelberg (KiTZ), Heidelberg, Germany."},{"name":"2Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ) and German Cancer 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