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Blood, 1 March 2004, Vol. 103, No. 5, pp. 1869-1875. Prepublished online as a Blood First Edition Paper on October 30, 2003; DOI 10.1182/blood-2003-05-1465. This Article Full Text (PDF) All Versions of this Article: 2003-05-1465v1 103/5/1869    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Montesinos-Rongen, M. Articles by Deckert, M. Search for Related Content PubMed PubMed Citation Articles by Montesinos-Rongen, M. Articles by Deckert, M. Social Bookmarking                   What's this? Submitted May 20, 2003 Accepted October 20, 2003 Primary diffuse large B-cell lymphomas of the central nervous system are targeted by aberrant somatic hypermutation Manuel Montesinos-Rongen, Dirk Van Roost, Carlo Schaller, Otmar D Wiestler, and Martina Deckert* Department of Neuropathology, University of Cologne, Cologne, Germany Department of Neuropathology, University of Bonn, Bonn, Germany Department of Neurosurgery, University of Bonn, Bonn, Germany * Corresponding author; email: neuropatho{at}uni-koeln.de. We have addressed the question whether aberrant ongoing hypermutation can be detected in the proto-oncogenes PIM1, c-MYC, RhoH/TTF, PAX5, and the tumor suppressor gene CD95 in PCNSL derived from immunocompetent, HIV-negative patients. Nine of 10 PCNSL analyzed harbored somatic mutations in the PIM1, c- MYC, RhoH/TTF, and PAX5 genes, but not in the CD95 gene, with eight tumors carrying alterations in at least two of these genes. Furthermore, ongoing aberrant mutation was evidenced in a subset of primary CNS lymphomas (PCNSL) (2/3). While the majority of the mutations corresponded to base pair substitutions, deletions were also present. The mean mutation frequency for these genes was approximately 60-fold lower compared to the values obtained for Ig genes in PCNSL. They were increased 2- to 5-fold compared to extracerebral DLBCL. In summary, our data demonstrate aberrant somatic hypermutations at high frequency in the PIM1, PAX5, RhoH/TTF, and c-MYC genes in the majority of PCNSL. These findings may indicate a pathogenic role for aberrant somatic hypermutation in PCNSL development. In contrast, although mutations were detected in exon 9 of the CD95 gene, the lack of mutations in the 5' region provides no evidence for the CD95 gene as a target for aberrant somatic mutation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. 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