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Diffuse large B‐cell lymphoma ( DLBCL ) is the most common B‐cell lymphoma subtype, and the Epstein–Barr virus ( EBV )‐positive subtype of  DLBCL  is known to show a more aggressive clinical behavior than the  EBV ‐negative one.  BTB  and  CNC  homology 2 ( BACH 2) has been highlighted as a tumor suppressor in hematopoietic malignancies; however, the role of  BACH 2 in  EBV ‐positive  DLBCL  is unclear. In the present study,  BACH 2 expression and its significance were studied in 23  EBV ‐positive and 43  EBV ‐negative patient samples. Immunohistochemistry revealed  BACH 2 downregulation in  EBV ‐positive cases ( P  < 0.0001), although biallelic deletion of   BACH 2  was not detected by  FISH . Next, we analyzed the contribution of  BACH 2 negativity to aggressiveness in  EBV ‐positive B‐cell lymphomas using  FL ‐18 ( EBV ‐negative) and  FL ‐18‐ EB  cells ( FL ‐18 sister cell line,  EBV ‐positive). In   BACH 2 ‐transfected  FL ‐18‐ EB  cells, downregulation of phosphorylated transforming growth factor‐β‐activated kinase 1 ( pTAK 1) and suppression in p65 nuclear fractions were observed by Western blot analysis contrary to non‐transfected  FL ‐18‐ EB  cells. In patient samples,  pTAK 1 expression and significant nuclear p65, p50, and p52 localization were detected immunohistochemically in  BACH 2‐negative  DLBCL  ( P  < 0.0001,  P  = 0.006, and  P  = 0.001, respectively), suggesting that  BACH 2 downregulation contributes to constitutive activation of the nuclear factor‐κB pathway through  TAK 1 phosphorylation in  BACH 2‐negative  DLBCL  (most  EBV ‐positive cases). Although further molecular and pathological studies are warranted to clarify the detailed mechanisms, downregulation of  BACH 2 may contribute to constitutive activation of the nuclear factor‐κB pathway through  TAK 1 activation.

Frequent downregulation of BTB and CNC homology 2 expression in Epstein–Barr virus‐positive diffuse large B‐cell lymphoma