Authors

Alyssa Bouska, University of Nebraska Medical CenterFollow
Weiwei Zhang, University of Nebraska Medical CenterFollow
Sunandini Sharma, University of Nebraska Medical Center
Harald Holte, Oslo University Hospital
Rauf Shah, University of Nebraska Medical CenterFollow
Waseem G. Lone, University of Nebraska Medical Center
Mahfuza Afroz Soma, University of Nebraska Medical CenterFollow
Ruimeng Yang, City of Hope National Medical Center
Xuxiang Liu, City of Hope National Medical Center
Syed Mehmood, University of Nebraska Medical CenterFollow
Ravneet Singh Chawla, University of Nebraska Medical CenterFollow
Luca Vincenzo Cappelli, Weil Cornell Medical College
Danilo Fiore, Weil Cornell Medical College
Qiang Gong, City of Hope National Medical Center
Tayla B. Heavican-Foral, University of Nebraska Medical CenterFollow
Jeffrey J. Cannatella, University of Nebraska Medical CenterFollow
Catalina Amador, University of Miami Miller School of Medicine
Aiza Arif, University of Nebraska Medical Center
Lynette M. Smith, University of Nebraska Medical CenterFollow
Soon Thye Lim, National Cancer Centre Singapore/Duke-NUS Medical School
Choon Kiat Ong, National Cancer Centre Singapore/Duke-NUS Medical School
Andrew L. Feldman, Mayo Clinic College of Medicine
Ming-Qing Du, University of Cambridge
Anamarija M. Perry, University of Michigan
Laurence de Leval, Lausanne University Hospital (CHUV) and University of Lausanne
Timothy C. Greiner, University of Nebraska Medical Center
Kai Fu, Roswell Park Comprehensive Cancer Center
Gunhild Trøen, Oslo University Hospital
Daniel Vodák, Oslo University Hospital
Sigve Nakken, University of Oslo
Jan Delabie, University of Toronto
David Weinstock, Dana Farber Cancer Institute
Stefano Pileri, European Institute of Oncology IRCCS
Antonella Laginestra, European Institute of Oncology IRCCS
KyeongJin Kim, Inha University
Utpal Pajvani, Columbia University
Julie M. Vose, University of Nebraska Medical CenterFollow
Dennis D. Weisenburger, University of Nebraska Medical CenterFollow
Steven M. Horwitz, Memorial Sloan Kettering Cancer Center
Sandeep Dave, Duke University
Joseph Khoury, University of Nebraska Medical CenterFollow
Giorgio Inghirami, Weil Cornell Medical College
Wing C. Chan, City of Hope National Medical Center
Javeed Iqbal, University of Nebraska Medical CenterFollow

Document Type

Article

Journal Title

American Journal of Hematology

Publication Date

2025

Abstract

Nodal follicular helper T-cell (TFH) lymphoma of the angioimmunoblastic (AITL) subtype has a dismal prognosis. Using whole-exome sequencing (n = 124), transcriptomic (n = 78), and methylation (n = 40) analysis, we identified recurrent mutations in known epigenetic drivers (TET2, DNMT3A, IDH2R172) and novel ones (TET3, KMT2D). TET2, IDH2R172, DNMT3A co-mutated AITLs had poor prognosis (p < 0.0001). Genes regulating T-cell receptor (TCR) signaling (CD28, PLCG1, VAV1, FYN) or activation (RHOAG17V) or regulators of the PI3K-pathway (PIK(3)C members, PTEN, PHLPP1, PHLPP2) were mutated. CD28 mutation/fusion was associated with poor prognosis (p = 0.02). WES of purified, neoplastic T-cell (CD3+PD1+) demonstrated high concordance with whole tumor biopsies and validated the presence of TET2 and DNMT3A in tumor and non-lymphoid cells, but other mutations (CD28, RHOAG17V, IDH2R172, PLCG1) in neoplastic cells. Integrated DNA-methylation and mRNA expression analysis revealed epigenetic alterations in genes regulating TCR, cytokines, PI3K-signaling, and apoptosis. RNA-seq analysis identified fusion transcripts regulating TCR-activation (8%), revealed a restricted TCR-repertoire (α = 87%, β = 72%), and showed the presence of Epstein-Barr virus transcriptome (73%). GEP demonstrated the association of B-cells or dendritic cells in the tumor milieu with prognosis (p < 0.01). RNA-seq and WES analysis of 12 AITL-patient-derived-xenografts (PDX) showed that bi-allelic TET2 and DNMT3A mutations or sub-clonal mutations (PLCG1, PHLPP2) propagated in sequential passages, and gene signatures related to TFH and TCM (central-memory) were well-maintained through passages. Gene expression signatures associated with late PDX passages (3rd-5th) were enriched with proliferation and metabolic reprogramming-related genes and predicted prognosis in an independent AITL series. Low PHLPP2 mRNA expression predicted poor prognosis (p = 0.05) and engineered PHLPP2 or TET2 loss in CD4+ T-cells showed enhanced PI(3)K activation, thus uncovering a therapeutic target for clinical trials.

ISSN

1096-8652

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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