IndraLab
Statements
reach
"Aberrant expression and genetic disorders of CD79b, CARD11, MYD88, TNFAIP3, BCL-10, TRAF3, TRAF2, NFKBIA, and NFKBIE (IkBepsilon), in concordance with the prevalence of chronic-active B cell receptor (BCR) signaling, JAK-STAT3 signaling, and canonical NF-kappaB signaling, were believed to underlie the inferior outcomes of ABC DLBCL [XREF_BIBR]."
reach
"DLBCL development relies on the NF-KB signalling pathway, and the high frequency of mutations leading to NF-KB activation (such as CD79, CARD11 [109], MYD88, or TNFAIP3) in activated B-cell (ABC) DLBCL suggests that the loss or activation of these genes promotes DLBCL development through aberrant activation of NF-KB [110]."