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Annals of Oncology 11:S127-S130, 2000
© 2000 European Society for Medical Oncology

Symposium Articles

The ATM gene in the pathogenesis of mantle-cell lymphoma

S. Stilgenbauer1, C. Schaffner2, D. Winkler1, G. Ott3, E. Leupolt1, M. Bentz1, P. Möller4, H. K. Müller-Hermelink3, M. R. James5, P. Lichter2 and H. Döhner1

1 Abteilung Innere Medizin III, University of Ulm Heidelberg, Germany
2 Deutsches Krebsforschungszentrum Heidelberg; Germany
3 Department of Pathology, University of Würzburg Germany
4 Department of Pathology, University of Ulm Germany
5 Wellcome Trust Centre for Human Genetics Oxford, UK

Correspondence to: Prof. Dr H. Döhner, Abteilung Innere Medizin III, Universität Ulm, Robert-Koch Str. 8, D-89081 Ulm, Germany

Background: Mantle-cell lymphoma (MCL) is genetically characterized by the translocation t(11;14)(q13;q32) leading to an overexpression of cyclin-D1, but additional chromosomal abnormalities appear to be required for MCL pathogenesis.

Patients and methods: Deletions involving chromosome 11q, which were recently found as recurrent aberrations in MCL, were analyzed at the molecular level in a series of 81 MCL by fluorescence in situ hybridization (FISH) with probes from a contiguous set of yeast artificial chromosomes (YACs) spanning bands 11q14–q24.

Results and conclusions: Loss of chromosome 11 material was observed in 37 of the 81 MCL cases (46%). The consensus deletion comprised YAC 801e11 containing the ATM gene. The minimal region of loss was further narrowed with P1-derived artificial chromosome (PAC) probes. This allowed the identification of a deletion confined to the genomic region of ATM, which, together with intragenic mutations found in the coding sequence, suggests a role of ATM as a tumor suppressor gene in MCL.

11q22-q23 deletion, ataxia-telangiectasia, ATM, mantle-cell lymphoma, tumor suppressor gene


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