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Heterogeneity of protein kinase C β2 expression in lymphoid malignancies

Aims:  Protein kinase C (PKC) β is an important regulator of lymphoid survival and its expression has been shown to be altered in lymphomas. The aim was to determine the expression of PKC β2 in various subtypes of lymphoproliferative diseases by immunohistochemistry. Methods and results:  One hundre...

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Bibliographic Details
Published in:Histopathology 2007-04, Vol.50 (5), p.561-566
Main Authors: Decouvelaere, A-V, Morschhauser, F, Buob, D, Copin, M C, Dumontet, C
Format: Article
Language:English
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Summary:Aims:  Protein kinase C (PKC) β is an important regulator of lymphoid survival and its expression has been shown to be altered in lymphomas. The aim was to determine the expression of PKC β2 in various subtypes of lymphoproliferative diseases by immunohistochemistry. Methods and results:  One hundred and forty archival samples representing various subtypes of lymphoproliferative diseases were analysed. Certain subtypes, such as mantle cell, lymphocytic or follicular lymphoma, were found to express PKC β2 in > 90% of the samples. In follicular lymphomas, the follicular lymphomatous areas were constantly labelled, whereas residual germinal centres remained negative. In follicular hyperplasia, PKC β2+ cells were found in the mantle and marginal zones. Most angioimmunoblastic T‐cell lymphomas, lymphoblastic T‐cell lymphomas and marginal zone/mucosa‐associated lymphoid tissue (MALT) lymphomas were labelled with anti‐PKC βII antibody, but the pattern of expression was more heterogeneous in these subtypes. A minority of diffuse large B‐cell lymphomas were stained and most plasma cell malignancies were negative. None of the cases of Hodgkin's disease and anaplastic large cell lymphoma expressed PKC β2. Conclusions:  PKC β2 expression varies significantly among lymphoproliferative diseases. In our series, the highest level of expression was found in mantle cell lymphomas and chronic lymphocytic lymphoma.
ISSN:0309-0167
1365-2559
DOI:10.1111/j.1365-2559.2007.02666.x