Frontier in Medical & Health Research
T-CELL RECEPTOR REPERTOIRE POLYCLONALITY SUPPRESSES MATURE T-CELL LYMPHOMA THROUGH HOMEOSTATIC CLONAL COMPETITION: A SEVEN-MODULE ARTIFICIAL INTELLIGENCE FRAMEWORK FOR RISK PREDICTION AND GENE THERAPY SAFETY SURVEILLANCE
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Keywords

T-cell receptor diversity
clonal competition
mature T-cell lymphoma
NPM-ALK
gene therapy safety
deep learning
reinforcement learning
graph neural network
TCR repertoire
insertional mutagenesis
ALCL; artificial intelligence
; polyclonality index

How to Cite

T-CELL RECEPTOR REPERTOIRE POLYCLONALITY SUPPRESSES MATURE T-CELL LYMPHOMA THROUGH HOMEOSTATIC CLONAL COMPETITION: A SEVEN-MODULE ARTIFICIAL INTELLIGENCE FRAMEWORK FOR RISK PREDICTION AND GENE THERAPY SAFETY SURVEILLANCE. (2026). Frontier in Medical and Health Research, 4(5), 904-921. https://fmhr.net/index.php/fmhr/article/view/2952

Abstract

Background: Mature T-cell lymphomas (MTCLs) are considered rare and comprise a small percentage of all lymphomas, with varying incidence rates globally. T-cell receptor (TCR) repertoire polyclonality may be an innate tumor-suppressive mechanism functioning via homeostatic clonal competition of antigen-presenting cell (APC) niches.  However, the application of computational models to formalize the principle of clonal competition for lymphoma risk prediction or gene therapy safety monitoring has been limited.

Objective: To suggest and analytically benchmark a seven-module AI/ML framework that puts the clonal competition results into perspective and extrapolates them to TCR repertoire-based lymphoma risk prediction, competitive dynamics simulation, integration site oncogenicity scoring, automated ALCL histopathology classification, and a regulatory-grade gene therapy safety index.

Framework: Seven AI/ML modules are suggested: (1) DeepTCR/BERT-based TCR diversity scorer with an AUROC ≥0.93; (2) a reinforcement learning agent-based model (RL-ABM) with an index of tipping-point polyclonality (PI ≈ 0.30); (3) a graph neural network TCR-MHC niche affinity predictor; (4) an XGBoost transformation susceptibility classifier (F1 ≥0.93, MCC ≥0.84); (5) a CNN-based retroviral integration site oncogenicity predictor; (6) a Vision Transformer ALCL histopathology classifier (AUROC ≥0.97); and (7) a multi-modal ensemble Gene Therapy Safety Index (AUROC ≥0.98, F1 ≥0.96) that generates RED/AMBER/GREEN surveillance alerts.

Conclusion: The suggested framework will convert TCR diversity-mediated lymphoma suppression into a quantitative, predictive AI pipeline with direct regulatory implications to safe design of adoptive TCR therapy and CAR-T cell products.

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