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(American Journal of Pathology. 2005;166:1773-1779.)
© 2005 American Society for Investigative Pathology

Absence of Immunoglobulin Class Switch in Primary Lymphomas of the Central Nervous System

Manuel Montesinos-Rongen^*, Roland Schmitz, Cornelius Courts^*, Werner Stenzel^*, Dörte Bechtel, Gerald Niedobitek, Ingmar Blümcke, Guido Reifenberger^¶, Andreas von Deimling^||, Berit Jungnickel^**, Otmar D. Wiestler, Ralf Küppers and Martina Deckert^*

From the Department of Neuropathology,^* University of Cologne, Köln; the Institute for Cell Biology (Tumor Research), University of Essen, Medical School, Essen; the Institute for Pathology and Department of Neuropathology, Friedrich-Alexander-University, Erlangen; the Department of Neuropathology,^¶ Heinrich-Heine-University, Düsseldorf; the Department of Neuropathology,|| Charité, University Medicine, Berlin; the Institute of Clinical Molecular Biology and Tumor Genetics,^** GSF, München; and the German Cancer Research Center, Heidelberg, Germany

Primary lymphomas of the central nervous system (PCNSLs) were investigated for their capacity to perform further maturation steps. We studied a series of 11 PCNSLs derived from immunocompetent patients for immunoglobulin (Ig) class switch recombination (CSR) by performing reverse transcriptase-polymerase chain reaction (RT-PCR) for transcripts of Ig constant region gene segments (IGHC). This analysis revealed exclusive transcription of IgM and IgD mRNA in the absence of IgG, IgA, or IgE transcription. This finding was corroborated at the protein level by the immunohistochemical demonstration of IgM on the surface of the tumor cells. The unexpected lack of CSR may be due to internal switch µ region deletions, which were detected in 7 of 11 cases. We also found that expression of activation-induced cytidine deaminase (AID), which is required for CSR and somatic hypermutation, was detectable by RT-PCR in 4 of 10 cases and by immunohistochemistry in one of three cases analyzed. This may indicate that ongoing somatic mutation, which is often observed in PCNSL, could be due to sustained AID expression in a fraction of cases and that intraclonal V gene diversity may occur in other cases at an earlier phase of tumor clone expansion, when AID may have been expressed.

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