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Table 1 Molecular alterations and their potential implications on therapeutic targeting

From: How we treat NK/T-cell lymphomas

Functional pathways

Genes involved (references)

Potential targeting*

Tumour suppression

PRDM1, FOXO3, HACE1 (7), CAV1, CAV2, DLC1 (15)

Specific gene targeting

Oncogenesis

NOTCH3, KRAS, BRAF, PRKD1, MAP3K5, PTPRK (16, 20, 21); DDX3X (16, 21)

Specific gene targeting

Multi-function pathway activation

PRKCQ, TNFRSF21, CUL1, FSD1, SGK1 (15, 16)

NF-κB, WNT signalling

 

AKT3, IL6R, CCL2 (15, 16); JAK3, STAT3, STAT5B (16, 20, 21)

JAK/STAT signalling

Derangement of tissue proliferation

CCND3 (15); S100A16, LAMB1, LAMC1, COL1A2, CTSB (15, 16)

Cell cycle

 

MET, S100A13 (15)

Angiogenesis

Epigenetic dysregulation

TP73, RARB, P15, P16, PRDM1, ATG5, AIM1, BCL2L11, DAPK1, TET2, PTPN6, SOCS6, PTPRK, ASNS (25, 26); KMT2D, KMT2C, BCOR, EP300, HDAC9, ARID1A, ASXL3 (16, 20,21); EZH2 (17)

Epigenetic modifiers

Immune escape

PD-L1, PD-L2 (15, 16)

Immune checkpoints

  1. *Potential strategies that may or may not yet be supported by experimental or clinical data