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Blood, 15 November 2002, Vol. 100, No. 10, pp. 3749-3756
NEOPLASIA
Tumor necrosis factor receptor-associated factor 1 gene
overexpression in B-cell chronic lymphocytic leukemia: analysis of
NF- B/Rel-regulated inhibitors of apoptosis
Gerd Munzert,
Dieter Kirchner,
Heike Stobbe,
Lothar Bergmann,
Roland M. Schmid,
Hartmut Döhner, and
Hermann Heimpel
From the Abteilung Innere Medizin III and Abteilung
Innere Medizin I, Universität Ulm, Ulm, Germany.
B-cell chronic lymphocytic leukemia (B-CLL)
is characterized by a resistance toward apoptosis-inducing agents.
Nuclear factor- B (NF-B)/Rel has been shown to regulate the
expression of antiapoptotic genes, such as members of the inhibitor of
apoptosis protein (IAP) and tumor necrosis factor
receptor-associated factor (TRAF) gene families. Expression
and regulation of NF-B/Rel-dependent inhibitors of apoptosis have
not been collectively studied in B-CLL. We examined expression of known
NF-B/Rel-regulated antiapoptotic genes by RNAse protection
assay, real-time polymerase chain reaction, and immunoblotting in
patients with B-CLL. TRAF1 and to a lesser extent TRAF2 were
overexpressed in B-CLL lymphocytes as compared with normal
CD19+ B cells. TRAF1 overexpression did not correlate with
markers of disease progression or overall survival. Furthermore, we
found high constitutive expression of the IAP genes c-IAP-1, c-IAP-2, and XIAP both in normal and B-CLL lymphocytes. Focusing on the regulation of TRAF1, NF-B/Rel activity in B-CLL nuclear extracts was
shown to bind to TRAF1 promoter elements. However, IB kinase (IKK)
activity was not increased in CLL lymphocytes as compared with normal
CD19+ B cells. The known IKK inhibitor
sulfasalazine did not compromise TRAF1 expression. Thus,
although our study revealed a common expression pattern of
NF-B/Rel-regulated inhibitors of apoptosis, our findings indicate an IKK-independent regulation of TRAF1 in B-CLL.
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