Solomon S D, Jarcho J A, McKenna W, Geisterfer-Lowrance A, Germain R, Salerni R, Seidman J G, Seidman C E
Cardiovascular Division, Brigham & Women's Hospital, Boston, Massachusetts 02115.
J Clin Invest. 1990 Sep;86(3):993-9. doi: 10.1172/JCI114802.
We demonstrate that familial hypertrophic cardiomyopathy (FHC), an autosomal dominant disorder of heart muscle, is a genetically heterogeneous disease. The locus responsible for FHC in members of one large kindred was recently mapped to chromosome 14q11-12 (FHC-1). We have characterized three additional unrelated families in which the gene for FHC segregates as an autosomal dominant trait to determine if these disease loci also map to FHC-1. All family members were clinically studied by physical examination, electrocardiogram, and two-dimensional echocardiography. Genetic studies were performed using DNA probes which are derived from loci that are closely linked to FHC-1. In one family the genetic defect maps to the previously identified FHC-1 locus. However, the loci responsible for FHC in two other families were not linked to FHC-1. We conclude that FHC can be caused by defects in at least two loci and is a genetically heterogeneous disorder.
我们证明,家族性肥厚型心肌病(FHC)是一种常染色体显性遗传的心肌疾病,是一种基因异质性疾病。一个大家族成员中导致FHC的基因座最近被定位到14号染色体的q11 - 12区域(FHC - 1)。我们对另外三个无血缘关系的家族进行了特征分析,在这些家族中FHC基因作为常染色体显性性状进行分离,以确定这些疾病基因座是否也定位于FHC - 1。所有家族成员都通过体格检查、心电图和二维超声心动图进行了临床研究。使用源自与FHC - 1紧密连锁的基因座的DNA探针进行了基因研究。在一个家族中,遗传缺陷定位于先前确定的FHC - 1基因座。然而,另外两个家族中导致FHC的基因座与FHC - 1不连锁。我们得出结论,FHC至少可由两个基因座的缺陷引起,是一种基因异质性疾病。