Patients with Nijmegen breakage syndrome (NBS) have a high risk to develop malignant diseases, most frequently B-cell lymphomas. The NBS gene product, nibrin, is involved in DNA recombination repair, a function shared with known tumor suppressor genes like BRCA1 and BRCA2. This led us to investigate whether NBS acts as tumor suppressor gene in the development of non-Hodgkin lymphomas. Therefore, we performed fluorescence in situ hybridization analysis using a BAC clone containing the entire NBS1 region on eight B-cell and eight T-cell lymphomas, including one B-cell and two T-cell lymphomas with structural abnormalities of 8q. None of the tumors showed a deletion of the NBS1 gene, demonstrating that deletion of the NBS1 gene is not a major cause or a primary event in tumorigenesis of human B- and T-cell lymphomas.