Mutations in 2 upstream components of the nuclear factor κB (NF-κB) pathway, CD79B and MYD88, are important information for new target therapy in malignant lymphoma. In diffuse large B cell lymphoma, the mechanism of constitutive NF-κB activity has been traced to somatic genetic alterations in the upstream pathway components such as CD79A, CD79B, CARD11, A20 and MYD88. It has been reported that immunoreceptor tyrosine-based activation motif (ITAM) mutations of CD79B and, less frequently, of CD79A were present in diffuse large B cell lymphoma (DLBCL) cell lines and biopsy samples, which were largely of the ABC subtype (21% of ABC DLBCL and 3% of GCB DLBCL, for CD79B). CD79 mutations were shown to increase surface B-cell receptor (BCR) expression and nullify the negative regulation of BCR, which were suggested to support the "chronic active" BCR signaling leading to constitutive NF-κB activation in ABC diffuse large B cell lymphoma.
Drug targets for cancer: CD79b research reagents
Other vital drug targets for cancer likeCD79b:
Kim Y, et al. CD79B and MYD88 mutations in diffuse large B-cell lymphoma[J]. Human pathology, 2014, 45(3): 556-564.