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NEUROLOGY 2004;63:167-169
© 2004 American Academy of Neurology
Brief Communications

Clonal evolution as pathogenetic mechanism in relapse of primary CNS lymphoma

H. Pels, MD, M. Montesinos-Rongen, PhD, C. Schaller, MD, D. Van Roost, MD, U. Schlegel, MD, O. D. Wiestler, MD and M. Deckert, MD

From the Departments of Neurology (Drs. Pels and Schlegel), Neuropathology (Drs. Montesinos-Rongen and Wiestler), and Neurosurgery (Drs. Schaller and Van Roost), University of Bonn, Germany; and Department of Neuropathology (Drs. Montesinos-Rongen and Deckert), University of Cologne, Germany.

Address correspondence and reprint requests to Dr. Martina Deckert, Department of Neuropathology, University of Cologne, Joseph-Stelzmann-Strasse 9, D-50931 Cologne, Germany; e-mail: neuropatho{at}uni-koeln.de

Comparative investigation of immunoglobulin (Ig) heavy chain gene rearrangements and DNA sequence analyses of a primary lymphoma of the CNS (PCNSL) and its recurrence revealed that both tumors used the same Ig gene segment. In addition to shared somatic mutations, the primary and the recurrent PCNSLs harbored somatic mutations unique to each tumor. Clonal evolution rather than subclone selection appears to underlie the development of tumor recurrence in this case.

Received September 12, 2003. Accepted in final form March 2, 2004.

H. Pels and M. Monesinos-Rongen contributed equally to the study.




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