Molecular Characterization of 11q Deletions Points to a Pathogenic Role of the ATM Gene in Mantle Cell Lymphoma

Deletions involving the long arm of chromosome 11 (11q) have been recently found as recurrent chromosome aberrations in mantle cell lymphoma (MCL). In the current study, the incidence and molecular extent of 11q deletions were analyzed in a series of 81 MCL by fluorescence in situ hybridization with...

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Published in:Blood 1999-11, Vol.94 (9), p.3262-3264
Main Authors: Stilgenbauer, Stephan, Winkler, Dirk, Ott, German, Schaffner, Claudia, Leupolt, Elke, Bentz, Martin, Mo¨ller, Peter, Mu¨ller-Hermelink, Hans K., James, Michael R., Lichter, Peter, Do¨hner, Hartmut
Format: Article
Language:English
Subjects:
Ataxia Telangiectasia Mutated Proteins
Biological and medical sciences
Cell Cycle Proteins
Chromosomes, Artificial, Yeast
Chromosomes, Human, Pair 11
DNA-Binding Proteins
Hematologic and hematopoietic diseases
Humans
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Lymphoma, Mantle-Cell - etiology
Lymphoma, Mantle-Cell - genetics
Medical sciences
Protein-Serine-Threonine Kinases
Proteins - genetics
Sequence Deletion
Tumor Suppressor Proteins
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Summary:Deletions involving the long arm of chromosome 11 (11q) have been recently found as recurrent chromosome aberrations in mantle cell lymphoma (MCL). In the current study, the incidence and molecular extent of 11q deletions were analyzed in a series of 81 MCL by fluorescence in situ hybridization with probes from a contiguous set of yeast artificial chromosomes (YACs). Loss of chromosome 11 material was observed in 37 of 81 cases (46%). The minimally deleted segment comprised YAC 801e11 containing the ATM gene. To further narrow the minimal region of loss, P1-derived artificial chromosomes mapping to the critical region were isolated and used as probes in cases without aberrations detectable with YACs. This allowed the identification of an ATM deletion that was beyond the resolution of YAC probes. The identification of a minimally deleted segment affecting ATM suggests a pathogenic role of ATMas a tumor suppressor gene in MCL.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V94.9.3262