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Using whole\u2010exome sequencing (<jats:italic>n<\/jats:italic>\u2009=\u2009124), transcriptomic (<jats:italic>n<\/jats:italic>\u2009=\u200978), and methylation (<jats:italic>n<\/jats:italic>\u2009=\u200940) analysis, we identified recurrent mutations in known epigenetic drivers (<jats:italic>TET2, DNMT3A, IDH2<\/jats:italic>\n<jats:sup>\n<jats:italic>R172<\/jats:italic>\n<\/jats:sup>) and novel ones (<jats:italic>TET3, KMT2D<\/jats:italic>). <jats:italic>TET2, IDH2<\/jats:italic>\n<jats:sup>\n<jats:italic>R172<\/jats:italic>\n<\/jats:sup>, <jats:italic>DNMT3A<\/jats:italic> co\u2010mutated AITLs had poor prognosis (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.0001). Genes regulating T\u2010cell receptor (TCR) signaling (<jats:italic>CD28, PLCG1, VAV1<\/jats:italic>, <jats:italic>FYN<\/jats:italic>) or activation (<jats:italic>RHOA<\/jats:italic>\n<jats:sup>\n<jats:italic>G17V<\/jats:italic>\n<\/jats:sup>) or regulators of the PI3K\u2010pathway (PIK(3)C members, <jats:italic>PTEN, PHLPP1, PHLPP2<\/jats:italic>) were mutated. <jats:italic>CD28<\/jats:italic> mutation\/fusion was associated with poor prognosis (<jats:italic>p<\/jats:italic>\u2009=\u20090.02). WES of purified, neoplastic T\u2010cell (CD3<jats:sup>+<\/jats:sup>PD1<jats:sup>+<\/jats:sup>) demonstrated high concordance with whole tumor biopsies and validated the presence of <jats:italic>TET2<\/jats:italic> and <jats:italic>DNMT3A<\/jats:italic> in tumor and non\u2010lymphoid cells, but other mutations (<jats:italic>CD28<\/jats:italic>, <jats:italic>RHOA<\/jats:italic>\n<jats:sup>\n<jats:italic>G17V<\/jats:italic>\n<\/jats:sup>, <jats:italic>IDH2<\/jats:italic>\n<jats:sup>\n<jats:italic>R172<\/jats:italic>\n<\/jats:sup>, <jats:italic>PLCG1<\/jats:italic>) in neoplastic cells. Integrated DNA\u2010methylation and mRNA expression analysis revealed epigenetic alterations in genes regulating TCR, cytokines, PI3K\u2010signaling, and apoptosis. RNA\u2010seq analysis identified fusion transcripts regulating TCR\u2010activation (8%), revealed a restricted TCR\u2010repertoire (\u03b1\u2009=\u200987%, \u03b2\u2009=\u200972%), and showed the presence of Epstein\u2013Barr virus transcriptome (73%). GEP demonstrated the association of B\u2010cells or dendritic cells in the tumor milieu with prognosis (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01). RNA\u2010seq and WES analysis of 12 AITL\u2010patient\u2010derived\u2010xenografts (PDX) showed that bi\u2010allelic <jats:italic>TET2<\/jats:italic> and <jats:italic>DNMT3A<\/jats:italic> mutations or sub\u2010clonal mutations (<jats:italic>PLCG1, PHLPP2<\/jats:italic>) propagated in sequential passages, and gene signatures related to <jats:bold>T<\/jats:bold>\n<jats:sub>FH<\/jats:sub> and <jats:bold>T<\/jats:bold>\n<jats:sub>CM<\/jats:sub> (central\u2010memory) were well\u2010maintained through passages. Gene expression signatures associated with late PDX passages (3rd\u20135th) were enriched with proliferation and metabolic reprogramming\u2010related genes and predicted prognosis in an independent AITL series. Low <jats:italic>PHLPP2<\/jats:italic> mRNA expression predicted poor prognosis (<jats:italic>p<\/jats:italic>\u2009=\u20090.05) and engineered <jats:italic>PHLPP2<\/jats:italic> or <jats:italic>TET2 loss<\/jats:italic> in CD4<jats:sup>+<\/jats:sup> T\u2010cells showed enhanced PI(3)K activation, thus uncovering a therapeutic target for clinical trials.<\/jats:p>","DOI":"10.1002\/ajh.27736","type":"journal-article","created":{"date-parts":[[2025,6,13]],"date-time":"2025-06-13T05:00:18Z","timestamp":1749790818000},"page":"1486-1501","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Integrative Genomic and Transcriptomic Analysis Reveals Targetable Vulnerabilities in Angioimmunoblastic T\u2010Cell Lymphoma"],"prefix":"10.1002","volume":"100","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1324-6678","authenticated-orcid":false,"given":"Alyssa","family":"Bouska","sequence":"first","affiliation":[{"name":"Department 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