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Nijmegen breakage syndrome (NBS) is an autosomal recessive DNA repair disorder characterized by microcephaly, immunodeficiency, and chromosomal instability. It is caused by a mutation in the NBS1 gene which encodes for a protein called NBS1 that participates in the repair of DNA single-strand breaks. Recently, a novel NBS1 mutation was reported, that is responsible for some atypical clinical features, such as severe immunodeficiency, onset of diabetes mellitus and high predisposition to develop leukemia. In this study we report the identification of a novel mutation in a patient displaying the full spectrum of clinical features associated with NBS. We used deoxyribonucleic acid sequence analysis (DNASCAP) of a PCR-amplified sequence covering the entire NBS1 coding region to identify the mutation. The sequence analysis of the patient’s lymphocytes identified a previously undescribed mutation in the coding region of the NBS1 gene (c.3754G>T) predicting the substitution of histidine (p.G1218C) by tyrosine. Comparison of the crystal structure of NBS1 protein suggests that this mutation could be responsible for the atypical clinical features. Our results confirm the importance of mutation screening in NBS patients and suggest that the c.3754G>T mutation could predispose to developing cancer.PROVIDENCE, R.I. (AP) – Police are looking for the individual who shot a homeowner in the leg while trying to break in his house.
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