IndraLab

Statements

TNFAIP3 activates Receptors, Antigen, B-Cell. 2 / 2
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"The fact that patients with N1 tumors benefitted exceptionally from ibrutinib suggests that the recurrent mutations in PRKCB, BCL10, IKBKB, TNFAIP3 and TNIP1 in these tumors might also potentiate chronic active BCR signaling and reinforce BTK dependency."
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"83 In ABC DLBCL, biallelic inactivation of TNFAIP3 (by mutations, deletions or both) occurs in 30% of cases and can coexist with mutations in both MYD88 and CD79B, suggesting that inactivation of TNFAIP3 can enhance both BCR and TLR signalling pathways."
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