|
|
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.
 Previous Article | Next Article 
Submitted June 21, 2006
Accepted December 6, 2006
MALT lymphoma and extranodal diffuse large B-cell lymphoma are targeted by aberrant somatic hypermutation
Alexander JA Deutsch, Ariane Aigelsreiter, Philipp B Staber, Alfred Beham, Werner Linkesch, Christian Guelly, Ruth I Brezinschek, Margareta Fruhwirth, Werner Emberger, Maike Buettner, Christine Beham-Schmid, and Peter Neumeister*
Division of Hematology, Institute of Pathology, & Centre for Medical Research, Institute Medical Biology & Human Genetics, Medical University Graz, Graz, Austria
Friedrich-Alexander Unversitat, Erlangen, Germany
* Corresponding author; email: peter.neumeister{at}meduni-graz.at.
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 MALT lymphoma, we studied the mutation profile of PIM-1, PAX-5, RhoH/TTF and c-MYC in 17 MALT lymphomas and 17 extranodal DLBCL still exhibiting a low grade MALT lymphoma component (transformed MALT lymphoma). Mutations in one or more genes were detected in 13/17 (76.5%) 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 PIM-1 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:
|
|
|
|
 
A. Mottok, C. Renne, M. Seifert, E. Oppermann, W. Bechstein, M.-L. Hansmann, R. Kuppers, and A. Brauninger
Inactivating SOCS1 mutations are caused by aberrant somatic hypermutation and restricted to a subset of B-cell lymphoma entities
Blood,
November 12, 2009;
114(20):
4503 - 4506.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. J. Bende, F. van Maldegem, and C. J.M. van Noesel
Chronic inflammatory disease, lymphoid tissue neogenesis and extranodal marginal zone B-cell lymphomas
Haematologica,
August 1, 2009;
94(8):
1109 - 1123.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Adamia, A. A. Reichert, H. Kuppusamy, J. Kriangkum, A. Ghosh, J. J. Hodges, P. M. Pilarski, S. P. Treon, M. J. Mant, T. Reiman, et al.
Inherited and acquired variations in the hyaluronan synthase 1 (HAS1) gene may contribute to disease progression in multiple myeloma and Waldenstrom macroglobulinemia
Blood,
December 15, 2008;
112(13):
5111 - 5121.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
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]
|
|
|
|
|
