Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Kita-ku, Okayama, Japan.
Matrix Biol. 2011 Jan;30(1):3-8. doi: 10.1016/j.matbio.2010.09.003. Epub 2010 Oct 14.
This is a study of a patient who manifests all of the features of a diffuse leiomyomatosis-Alport syndrome (DL-ATS), and her two-year-old son who has already been diagnosed with Alport syndrome. Fourteen years ago, the patient underwent a partial esophageal resection followed by a replacement with jejunum. Recently, she underwent a surgical resection of the esophagus due to esophageal dysfunction. Genetic analyses of COL4A5 and COL4A6 on the X-chromosome were efficiently performed using the genomic DNA of her son. We have identified a novel deletion of 194-kb in length, encompassing COL4A5-COL4A6 promoters as well as nearly the entire large intron 1 of COL4A5 and intron 2 of COL4A6. To uncover the relationship of the esophagus-specific occurrence of the tumor and the expression of those genes, immunohistochemical analyses of type IV collagen α chains were conducted in the non-affected individuals. The esophageal smooth muscle-specific expression of α5(IV) and α6(IV) chains in the gastrointestinal tract was observed. Moreover, CAG repeat analysis of the androgen receptor gene and an immunohistochemical analysis in the leiomyoma revealed clonal overgrowth of the cells which received X-inactivation on the non-affected allele. These results may suggest that the dominant effect was caused by the partial deletion of the esophageal smooth muscle-specific genes, COL4A5 and COL4A6.
这是一项关于一名患者的研究,该患者表现出弥漫性平滑肌瘤病- Alport 综合征(DL-ATS)的所有特征,她两岁的儿子已被诊断为 Alport 综合征。十四年前,该患者接受了部分食管切除术,随后用空肠进行了替代。最近,由于食管功能障碍,她接受了食管切除术。使用其子的基因组 DNA,对 X 染色体上的 COL4A5 和 COL4A6 进行了有效的基因分析。我们已经确定了一个新的 194-kb 缺失,包含 COL4A5-COL4A6 启动子以及 COL4A5 的几乎整个大内含子 1 和 COL4A6 的内含子 2。为了揭示肿瘤在食管中特异性发生与这些基因表达之间的关系,对非受累个体的 IV 型胶原α链进行了免疫组织化学分析。观察到胃肠道中平滑肌特异性表达的α5(IV)和α6(IV)链。此外,对雄激素受体基因的 CAG 重复分析和 leiomyoma 的免疫组织化学分析显示,在非受累等位基因上接受 X 失活的细胞发生了克隆性过度生长。这些结果可能表明,显性效应是由食管平滑肌特异性基因 COL4A5 和 COL4A6 的部分缺失引起的。