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. 2023 Jun 23;13:1202964. doi: 10.3389/fonc.2023.1202964

Table 1.

Molecular characterization of the main non-cutaneous PTCL entities.

Entity Differentiation Molecular features
TFH-lymphomas TFH - DNA methylation: TET2, DNMT3A, IDH2 R172 mutations
- TCR pathway: RHOA G17V, CD28, VAV1, PLCG1 mutations
- Fusion transcripts: ICOS_CD28, CTLA4_CD28, ITK_SYK, ITK_FER, fusion transcripts involving VAV1
ALK-positive ALCL Activated cytotoxic T cell - Fusion transcripts involving ALK
- Mutations in genes of the NOTCH1 pathway
ALK-negative ALCL Activated cytotoxic T cell STAT3 activation:
JAK1 and/or STAT3 mutations
Fusion transcripts involving ROS, TYK2, FRK, CAPRIN2
Absence of STAT3 activation:
DUSP22/IRF4 (locus 6p25.3) rearrangement
MSCE116K mutation
Others: TP63 rearrangements
Breast-implant ALCL Activated cytotoxic T cell - JAK/STAT pathway: STAT3, JAK1, SOCS3, STAT5B, SOCS1, PTPN1 mutations
- Epigenetics: KMT2D, KMT2C, CREBBP, CHD2, TET2, DNMT3A mutations
ATLL Memory regulator T cell - TCR pathway: PLCG1, PRKCB, CARD11, VAV1, IRF4, FYN, CCR4, CCR7, RHOA, CD28 mutations
- Immunosurveillance: CD58, B2M, HLA (class I) mutations
- JAK/STAT pathway: JAK3, STAT3, PTPN1 mutations
- Transcription factor: GATA3, IKZF2, PRDM1 mutations
- Epigenetics: TET2, DNMT3A, IDH2, SETD2, EP300, KDM6A mutations
- Fusion transcripts: ICOS_CD28 and/or CTLA4_CD28
ENKTCL (nasal type) NK>>T (γδ or αβ) - BCOR, DDX3X, TP53, MGA, STAT3, STAT5B, MLL2, ARID1A, MSN mutations
- 3 molecular subgroups :
°TSIM : mutations of genes of the JAK/STAT pathway, TP53, amp9p24.1(JAK2, PDL1/2), amp17q21.2 (STAT3/5A/5B), EBV latency type II => NK cells
°HEA: mutations of HDAC9, EP300, ARID1A, EBV latency type II => T-cells
°MB: mutations of MGA, del1p22.1 (BRDT), MYC overexpression, EBV latency type I => T-cells
HSTL Tgδ> Tαβ - SETD2, STAT5B, INO80, ARID1B, STAT3, PIK3CD mutations
Indolent clonal T-cell lymphoproliferative disorder of the gastro-intestinal tract CD8+ or CD4-/CD8- (TH2) - Structural alterations of the 3’UTR regions of IL2 coding gene
CD4+ or CD4+/CD8+ - JAK/STAT pathway: STAT3, SOCS1 mutations, STAT3_JAK2 fusion
- Epigenetics: TET2, DNMT3A, KMT2D mutations
EATL Intraepithelial lymphocyte (Tαβ) - JAK/STAT pathway: JAK1 (p.G1097 dans 50%), JAK3, STAT3, STAT5B, SOCS1 mutations
- KRAS, NRAS mutations
- NFκB pathway: TNFAIP3, TNIP3 mutations
- Epigenetics: TET2, KMT2D, DDX3X, SETD2 (15%) mutations
MEITL Intraepithelial lymphocyte (Tγδ > Tαβ) - Alterations of SETD2 (mutations, deletions)
- STAT5B, JAK3, TP53, GNAI2 mutations
T-LGLL Tαβ (CD8) >> Tγδ - JAK/STAT pathway: STAT3, less frequently STAT5B mutations
- Epigenetics: TET2, DNMT3A
PTCL-NOS TH1 (αβ >> δγ), common cytotoxic phenotype - Epigenetic: TET2, DNMT3A, KMT2D, SETD2 mutations
- TCR pathway: VAV1, PLCG1, PRKCB, CARD11 mutations; fusion transcripts involving VAV1
- JAK/STAT pathway: STAT3, STAT5B, JAK3, SOCS1 mutations
TH2 (Tαβ) - Deletions of CDKN2A, TP53, PDGFA, STK11, WDR24, CDK4, CCND1, AKT, RPTOR
- Gains/amplifications of STAT3, CMYC

TFH, T follicular helper; ALCL, anaplastic large cell lymphoma; PTCL-NOS, peripheral T-cell lymphoma, not otherwise specified; ATLL, adult T-cell leukemia/lymphoma; ENKTCL: extra-nodal NK/T-cell lymphoma, HSTL, hepatosplenic T-cell lymphoma; EATL, enteropathy associated T-cell lymphoma; MEITL, monomorphic epitheliotropic intestinal T-cell lymphoma; T-LGLL, T-cell large granular lymphocytic leukemia.