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. 2023 Feb 7;14:1088685. doi: 10.3389/fimmu.2023.1088685

Table 4.

Molecular subtyping schemes of ENKTCL published in recent years.

Author Subtype Representative genomic alterations or immune characteristics Prognosis Potentially effective treatment
Xiong et al. (213) HEA Mutations in HDAC9, EP300, and ARID1A Good HDAC inhibitor
TSIM Mutations in JAK-STAT pathway and TP53, ampJAK2 locus; amp17q21.2/STAT3/5B/5A locus, amp9p24.1/PD-L1/2 locus, del6q21 Intermediate PD-1 blockade
MB MGA mutation, 1p22.1/BRDT LOH Poor MYC inhibition
Dong et al. (214) C1 Higher CN complexity including gains and losses of 17q21(STAT3), 8q24(MYC), and del19q Intermediate -
C2 KMT2D mutation and chr2 gain Intermediate -
C3 NOTCH2 mutation and del17p Intermediate -
C4 DDX3X mutation and del1p36 Intermediate -
C5 CN gain of chr19q/q13 and JAK3 gain Good -
C6 Aberrations in RAS/RAF/MAPK pathway, JAK3, BCOR, and TP53 Poor -
C7 TET2 loss and ARID1B mutation Good -
Lim et al. (215) GPM Mutations in BCOR, JAK3, KRAS, MYH11, DCC, ITK, NOTCH1, FAS, RET, BIRC3, MLLT1, LRP1B, NRG1 Poor -
Cho et al. (217) Immune tolerance High-Treg counts (> 500/HPF) Good Good response to PD-1 blockage
Immune evasion-A High cytotoxic T-cell counts, high PD-L1 expression, low Treg counts (PD-L1 > 10%) Intermediate Intermediate response to PD-1 blockage
Immune evasion-B Not otherwise specified Intermediate Intermediate response to PD-1 blockage
Immune silenced Immune response exhausted (Process-type CD68 > 90%) Poor Poor to PD-1 blockage