Leybrand Sabine, Rossier Eva, Barbi Gotthold, Cooper David N, Kehrer-Sawatzki Hildegard
Department of Human Genetics, Institute of Human Genetics, University of Ulm, Albert-Einstein-Allee 11, 89081, Ulm, Germany.
Genomic Med. 2007;1(1-2):65-73. doi: 10.1007/s11568-007-9008-3. Epub 2007 Jul 11.
We report on a patient with severe mental retardation, dysmorphic features as well as juvenile idiopathic arthritis. G-banding indicated two independent karyotypic anomalies in this patient: an interstitial deletion del(X)(p21p22.3) and a rearrangement involving chromosomes 1 and 7, which represents a direct insertion, ins(7;1)(q36;p13.2p31.2). Non-random inactivation of the paternally derived del(X) chromosome was observed in blood lymphocytes and fibroblasts. High resolution analysis of the rearrangement involving chromosomes 1 and 7 subsequently revealed the additional submicroscopic deletion of at least 5 Mb at the 1p13.2 breakpoint. The deletion occurred on the paternal chromosome and encompasses the PTPN22 gene, already known to be associated with juvenile idiopathic arthritis. Our findings underline the importance of closely investigating the breakpoint regions of apparently balanced rearrangements in patients with abnormal phenotypes since complex chromosomal rearrangements (CCRs) may turn out to be unbalanced.
我们报告了一名患有严重智力障碍、畸形特征以及幼年特发性关节炎的患者。G显带显示该患者存在两种独立的核型异常:一种是中间缺失del(X)(p21p22.3),另一种是涉及染色体1和7的重排,表现为直接插入,即ins(7;1)(q36;p13.2p31.2)。在血液淋巴细胞和成纤维细胞中观察到父源del(X)染色体的非随机失活。随后对涉及染色体1和7的重排进行高分辨率分析,发现1p13.2断点处至少有5 Mb的额外亚显微缺失。该缺失发生在父源染色体上,包含已知与幼年特发性关节炎相关的PTPN22基因。我们的研究结果强调了对于具有异常表型的患者,密切研究明显平衡重排的断点区域的重要性,因为复杂染色体重排(CCR)可能最终被证明是不平衡的。