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BCL2 Overexpression Associated With Chromosomal Amplification in Diffuse Large B-Cell Lymphoma
Outi Monni,
Heikki Joensuu,
Kaarle Franssila,
Juha Klefstrom,
Kari Alitalo, and
Sakari Knuutila
From the Department of Medical Genetics, Haartman Institute, University of Helsinki, Finland; the Department of Oncology, Helsinki University Central Hospital, Helsinki, Finland; the Pathology Laboratory, Department of Oncology, Helsinki University Central Hospital, Helsinki, Finland; and the Molecular/Cancer Biology Laboratory, Haartman Institute, University of Helsinki, Helsinki, Finland.
Gene activation by translocation between an oncogene and an immunoglobulin heavy-chain gene, which leads to increased expression of the oncoprotein, is a well-known mechanism in the genesis of B-cell lymphomas. In contrast, the role of gene amplification in activation of oncogenes in non-Hodgkin's lymphomas is poorly characterized. To study the BCL2 amplification we performed comparative genomic hybridization (CGH), Southern blot hybridization, Western analysis, immunohistochemistry, metaphase fluorescence in situ hybridization, and chromosome analysis on 26 cases of diffuse large B-cell lymphoma (large noncleaved cell lymphoma). The gain or high-level amplification of 18q was found in eight tumors (31%) by CGH, and Southern analysis revealed BCL2 amplification in these cases, but not in the cases with normal chromosome 18 or t(14; 18)(q32; q21). Western immunoblot analysis and immunohistochemistry revealed a high-level expression of BCL2 protein in the cases with BCL2 amplification and t(14; 18)(q32; q21). However, translocation (14; 18)(q32; q21) was not detected in any of the cases with BCL2 amplification. Therefore, our results suggest that amplification of the BCL2 gene is an important mechanism for BCL2 protein overexpression in diffuse large B-cell lymphoma.
Blood, Vol. 90 No. 3 (August 1), 1997:
pp. 1168-1174
© 1997 by The American Society of Hematology.
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