Table 3.

Relevant cytogenetic or molecular findings for the management of PTCL patients.

Entity	Diagnosis	Prognosis	Therapeutic relevance	Potential targeted therapies
TFH-lymphoma	- Mutations RHOA G17V, IDH2 R172, - fusions transcript ITK_SYK	DNMT3A R882X	ITK_SYK CTLA4_CD28 FYN_TRAF3IP2	Demethylating agents PI3K inhibitors SYK inhibitors CTLA4 inhibitors IkB inhibitors
ALK-positive ALCL	ALK expression (IHC), rearrangement (FISH), fusion transcript	MYC expression TRAF1_ALK fusion transcript		Brentuximab-vedotin ALK inhibitors JAK/STAT inhibitors
ALK-negative ALCL		FISH for: -DUSP22 rearrangement - TP63 rearrangement	JAK2 fusion transcripts pSTAT3	Brentuximab vedotin JAK/STAT inhibitors Kinase inhibitor
ENKTCL (nasal type)	EBV (EBER ISH)	MYC expression	PDL1 expression	Immune checkpoint inhibitors (pembrolizumab, nivolumab)
HSTL	Iso7q (FISH)		KIR3DL2 expression	Humanized KIR3DL2 antibodies (lacutamab) JAK/STAT inhibitors
EATL	Mutations JAK1 p.G1097, STAT3			JAK/STAT inhibitors
MEITL	SETD2 mutation/deletion	CD20 expression (favorable) TP53 alterations, MYC expression		JAK/STAT inhibitors Wee1 inhibitor (adavosertib)
Indolent NK-LP of the GI tract	STAT3 K563_C565del			JAK-STAT inhibitors
ATLL	HBZ transcript	Aggressive: mutations of CCR4 (frameshift), TP53, IRF4 Indolent: STAT3 mutations	KIR3DL2 expression	Humanized antibodies against CCR4 (mogamulizumab), KIR3DL2 (lacutamab)
PTCL-NOS		TH2 polarization DNMT3A mutations		Humanized antibodies against CCR4 (mogamulizumab)

FISH, fluorescence in situ hybridization; IHC, immunohistochemistry; ISH, in situ hybridization.