Table 4.

New entities in T-ALL (other than BCL11B-activated, all are provisional)

Subtype	Frequency	Partner genes/other rearrangements	Common colesions*
BCL11B-activated	30% of ETP and T/MPAL, <5% of AML	BETA (14q32 enhancer amplification); ARID1B, CCDC26/MYC; CDK6; STAB1; ETV6; ZEB2; RUNX1;	FLT3-ITD; WT1
TAL1/2-R	30–40% (TAL2 rare); poor prognosis	TCRA/D; TCRB (TAL2); 1p32 deletion (STIL); intergenic SNV (super enhancer)	CDKN2A, NOTCH1, PTEN, USP7
TLX1-R	5–10% children; near 30% adult; good prognosis	TCR	PHF6, DNM2, BCL11B, RB1, CDKN1B
TLX3-R	20–25% children <5% adult; good prognosis	TCR; BCL11B; CDK6	CDKN2A, NOTCH1, FBXW7, PTEN
HOXA	15–25%	HOXA::TCRB/TCRG; KMT2A-R; PICALM::MLLT10; SET::NUP214
LMO1/2-R	LMO1-R -5% LMO2-R 10%	TCR; cryptic deletion; enhancer/promoter mutations LMO complex with bHLH factors; Extremely high LMO expression	CDKN2A, NOTCH1, FBXW7, PTEN, LEF1
NKX2-R	<5% children	NKX2.1/NKX2.2/NKX2.5::TCR; BCL11B; CDK6	CDKN2A, NOTCH1 PHF6, LEF1, RPL10
SPI1-R	<5%, children, very poor prognosis	STMN1; TCF7; BCL11B	NRAS,KRAS
BHLH, other	<2%	TCRB::LYL1 TCR::BHLHB1; high LMO expression

^*NOTCH1 and CDKN2A mutations are common throughout T ALL, except ETP-ALL