| Literature DB >> 22808296 |
Fang Liu1, Kennosuke Karube, Harumi Kato, Kotaro Arita, Noriaki Yoshida, Kiyoko Yamamoto, Shinobu Tsuzuki, Wonseog Kim, Young-Hyeh Ko, Masao Seto.
Abstract
Constitutive nuclear factor-kappa B (NF-κB) activation has been reported in ocular adnexal lymphoma (OAL). TNFAIP3/A20 is a "global" inhibitor of NF-κB pathway. We have shown that OAL has preferential loss of the 6q23.3 region where TNFAIP3/A20 exist, which is suggested to involve in lymphomagenesis of OAL. The mechanisms causing NF-κB activity in OAL remain elusive. Recently, NF-κB canonical pathway genes including CARD11, CD79B and MYD88 were shown to be frequently mutated in diffuse large B-cell lymphomas. In this study, we analyzed the mutation status of these genes by direct sequencing in 24 OAL cases including 9 cases with loss of 6q23.3 previously identified by array comparative genomic hybridization. We showed that genetic alterations of these genes were not found in OAL, a finding differing from that of most B-cell lymphomas. Genetic or epigenetic alterations in other genes are likely to be relevant in pathogenesis of OAL case without A20 loss.Entities:
Keywords: NF-κB related gene mutation; Ocular adnexal lymphoma; TNFAIP3 (A20) deletion
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Year: 2012 PMID: 22808296 PMCID: PMC3396059
Source DB: PubMed Journal: Int J Clin Exp Pathol ISSN: 1936-2625