Department of Surgery, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
Clin Genet. 2012 Feb;81(2):110-6. doi: 10.1111/j.1399-0004.2011.01763.x. Epub 2011 Sep 6.
Juvenile polyposis (JP) is an autosomal dominant hamartomatous polyposis syndrome that carries a significant risk for the development of colorectal cancer. Microdeletions of one of the two predisposing genes to JP, BMPR1A, have been associated with a severe form of JP called juvenile polyposis of infancy. Many of these deletions have also been found to contiguously include PTEN, which is the gene responsible for the development of Cowden syndrome. The advent of molecular techniques that localize genomic copy number variations and others that target specific genes such as multiplex-ligation probe analysis has allowed researchers to explore this area further for deletions. Here, we review the literature for microdeletions described on chromosome 10q22-23 in patients with JP and other intestinal polyposis syndromes.
少年性息肉病(JP)是一种常染色体显性错构瘤性息肉病综合征,其结直肠癌发病风险显著增加。JP 的两个易患基因之一 BMPR1A 的微缺失与一种称为婴儿期少年性息肉病的严重形式有关。许多这些缺失也被发现连续包含 PTEN,后者是导致 Cowden 综合征的基因。用于定位基因组拷贝数变异的分子技术以及针对特定基因(如多重连接探针分析)的技术的出现,使得研究人员能够进一步探索该领域的缺失。在这里,我们回顾了描述在 JP 和其他肠息肉病综合征患者中 10q22-23 染色体上的微缺失的文献。