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Blood, 15 June 2001, Vol. 97, No. 12, pp. 3896-3901
NEOPLASIA
Coexpression of BMI-1 and EZH2 polycomb-group proteins is
associated with cycling cells and degree of malignancy in B-cell
non-Hodgkin lymphoma
Folkert J. van Kemenade,
Frank M. Raaphorst,
Tjasso Blokzijl,
Elly Fieret,
Karien M. Hamer,
David P. E. Satijn,
Arie P. Otte, and
Chris J. L. M. Meijer
From the Department of Pathology, VU University
Hospital, Amsterdam; and Swammerdam Institute for Life Sciences,
BioCentrum Amsterdam, University of Amsterdam, The Netherlands.
Polycomb-group (PcG) proteins, such as BMI-1 and EZH2, form
multimeric gene-repressing complexes involved in axial patterning, hematopoiesis, and cell cycle regulation. In addition, BMI-1 is involved in experimental lymphomagenesis. Little is known about its
role in human lymphomagenesis. Here, BMI-1 and EZH2 expression patterns are analyzed in a variety of B-cell non-Hodgkin lymphomas (B-NHLs), including small lymphocytic lymphoma, follicular lymphoma, large B-cell lymphoma, mantle-cell lymphoma, and Burkitt lymphoma. In
contrast to the mutually exclusive pattern of BMI-1 and EZH2 in
reactive follicles, the neoplastic cells in B-NHLs of intermediate- and
high-grade malignancy showed strong coexpression of BMI-1 and EZH2.
This pattern overlapped with the expression of Mib-1/Ki-67, a marker
for proliferation. Neoplastic cells in B-NHL of low-grade malignancy
were either BMI-1low/EZH2+ (neoplastic
centroblasts) or BMI-1lowEZH2
(neoplastic centrocytes). These observations show that low-, intermediate-, and high grade B-NHLs are associated with increased coexpression of the BMI-1 and EZH2 PcG proteins, whose normal expression pattern is mutually exclusive. This expression pattern is
probably caused by a failure to down-regulate BMI-1 in dividing neoplastic cells, because BMI-1 expression is absent from normal dividing B cells. These observations are in agreement with findings in
studies of Bmi-1 transgenic mice. The extent of BMI-1/EZH2 coexpression
correlated with clinical grade and the presence of Mib-1/Ki-67
expression, suggesting that the irregular expression of BMI-1 and EZH2
is an early event in the formation of B-NHL. This points to a role for
abnormal PcG expression in human lymphomagenesis.
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