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Blood, 15 April 2007, Vol. 109, No. 8, pp. 3500-3504. Prepublished online as a Blood First Edition Paper on December 29, 2006; DOI 10.1182/blood-2006-06-030494. This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: blood-2006-06-030494v1 109/8/3500    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Deutsch, A. J. A. Articles by Neumeister, P. Search for Related Content PubMed PubMed Citation Articles by Deutsch, A. J. A. Articles by Neumeister, P. Related Collections Immunobiology Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief Report MALT lymphoma and extranodal diffuse large B-cell lymphoma are targeted by aberrant somatic hypermutation Alexander J. A. Deutsch1, Ariane Aigelsreiter2, Philipp B. Staber1, Alfred Beham2, Werner Linkesch1, Christian Guelly3, Ruth I. Brezinschek1, Margareta Fruhwirth1, Werner Emberger4, Maike Buettner5, Christine Beham-Schmid2, and Peter Neumeister1 1 Division of Haematology, Medical University Graz, Graz, Austria; 2 Institute of Pathology, Medical University, Graz, Austria; 3 Centre for Medical Research, Medical University Graz, Austria; 4 Institute of Medical Biology and Human Genetics, Medical University, Graz, Austria; 5 Institute of Pathology, Friedrich-Alexander-Universität, Erlangen, Germany Recently, a novel mechanism introducing genetic instability, termed aberrant somatic hypermutation (ASHM), has been described in diffuse large B-cell lymphoma. To further investigate whether ASHM also occurs in mucosa-associated lymphoid tissue type (MALT) lymphoma, we studied the mutation profile of PIM1, PAX5, RhoH/TTF, and c-MYC in 17 MALT lymphomas and 17 extranodal diffuse large B-cell lymphomas (DLBCLs) still exhibiting a low-grade MALT lymphoma component (transformed MALT lymphoma). Mutations in one or more genes were detected in 13 (76.5%) of 17 cases of MALT lymphomas and in all of 17 (100%) cases of extranodal DLBCL. A total of 100 sequence variants were found in 30 of 34 cases, 28 in the MALT lymphomas and 72 in extranodal DLBCL. Further, in PIM1 and c-MYC some of the mutations were found to affect coding exons, leading to amino acid exchanges, thus potentially altering gene function. Expression levels of activation-induced cytidine deaminase (AID), an enzyme essential for somatic hypermutation (SHM), was associated with the mutational load. These data indicate that aberrant SHM is associated with extranodal DLBCL and MALT lymphoma, likewise. By mutating regulatory and coding sequences of the targeted genes, ASHM may represent a major contributor to their pathogenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. Barone, M. Bombardieri, M. M. Rosado, P. R. Morgan, S. J. Challacombe, S. De Vita, R. Carsetti, J. Spencer, G. Valesini, and C. Pitzalis CXCL13, CCL21, and CXCL12 Expression in Salivary Glands of Patients with Sjogren's Syndrome and MALT Lymphoma: Association with Reactive and Malignant Areas of Lymphoid Organization J. Immunol., April 1, 2008; 180(7): 5130 - 5140. [Abstract] [Full Text] [PDF] J.-L. Chen, A. Limnander, and P. B. Rothman Pim-1 and Pim-2 kinases are required for efficient pre-B-cell transformation by v-Abl oncogene Blood, February 1, 2008; 111(3): 1677 - 1685. [Abstract] [Full Text] [PDF]

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