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Integrative Genomic and Transcriptomic Analysis Reveals Targetable Vulnerabilities in Angioimmunoblastic T-Cell

Alyssa Bouska¹, Weiwei Zhang¹, Sunandini Sharma¹

¹Department of Pathology, Microbiology, and Immunology, University of Nebraska Medical Center, Omaha, Nebraska, USA.

American Journal of Hematology

|June 13, 2025

Summary

This summary is machine-generated.

Nodal follicular helper T-cell lymphoma (AITL) has poor prognosis. Genetic analysis revealed mutations in epigenetic drivers like TET2 and CD28, impacting T-cell signaling and PI3K pathways, offering potential therapeutic targets.

Keywords:

cancer genetics genomics and transcriptomics lymphomaangioimmunoblastic T‐cell lymphoma

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Area of Science:

Oncology
Immunology
Genetics

Background:

Nodal follicular helper T-cell (T_FH) lymphoma, angioimmunoblastic T-cell lymphoma (AITL) subtype, is associated with a poor prognosis.
Understanding the genetic landscape of AITL is crucial for developing targeted therapies.

Purpose of the Study:

To identify recurrent mutations and epigenetic alterations in AITL.
To correlate genetic findings with clinical prognosis.
To explore potential therapeutic targets for AITL.

Main Methods:

Whole-exome sequencing (WES) of 124 AITL tumors.
Transcriptomic and methylation analysis of 78 and 40 samples, respectively.
Analysis of AITL-patient-derived-xenografts (PDX) and gene expression profiling (GEP).

Main Results:

Recurrent mutations were found in epigenetic drivers (TET2, DNMT3A, IDH2, TET3, KMT2D) and genes regulating T-cell receptor (TCR) signaling and PI3K pathways (CD28, PLCG1, RHOA, PTEN, PHLPP2).
Co-mutation of TET2, IDH2, and DNMT3A, as well as CD28 mutations/fusions, were associated with poor prognosis.
Epigenetic alterations impacted TCR signaling, cytokine regulation, and apoptosis pathways.
Low PHLPP2 mRNA expression predicted poor prognosis, and its loss enhanced PI3K activation in CD4+ T-cells.

Conclusions:

AITL is characterized by mutations in epigenetic regulators and genes involved in T-cell signaling and PI3K pathway.
Specific mutations and epigenetic alterations serve as prognostic markers.
PHLPP2 and TET2 alterations represent potential therapeutic targets for AITL.