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Diffuse large B-cell lymphoma (DLBCL) has a heterogenous biological behavior, and the western literature has reported activating oncogenic mutations in myeloid differentiation primary response gene 88 (MYD88), in conjunction with B-cell receptor signaling pathway genes, CARD11 and CD79B as the driving force for activating the NF-κB pathway implicated in the pathogenesis of DLBCL. The mutation profile of MYD88 genes was evaluated by Sanger sequencing in a cohort of 97 patients [DLBCL (N= 55), non-DLBCL lymphomas (N= 30), reactive lymphadenopathy (N= 10), and 2 cases of lymphoplasmacytic lymphoma (positive control)]. The mutation profile of CARD11 and CD79B were evaluated in 70 patients [DLBCL (N= 30), non-DLBCL lymphomas (N= 30), and reactive lymphadenopathy (N= 10). MYD88 and NF-κB mRNA expression was also evaluated by quantitative reverse transcriptase polymerase …