Andrew S E, Goldberg Y P, Kremer B, Squitieri F, Theilmann J, Zeisler J, Telenius H, Adam S, Almquist E, Anvret M
Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
Am J Hum Genet. 1994 May;54(5):852-63.
Huntington disease (HD) has been shown to be associated with an expanded CAG repeat within a novel gene on 4p16.3 (IT15). A total of 30 of 1,022 affected persons (2.9% of our cohort) did not have an expanded CAG in the disease range. The reasons for not observing expansion in affected individuals are important for determining the sensitivity of using repeat length both for diagnosis of affected patients and for predictive testing programs and may have biological relevance for the understanding of the molecular mechanism underlying HD. Here we show that the majority (18) of the individuals with normal sized alleles represent misdiagnosis, sample mix-up, or clerical error. The remaining 12 patients represent possible phenocopies for HD. In at least four cases, family studies of these phenocopies excluded 4p16.3 as the region responsible for the phenotype. Mutations in the HD gene that are other than CAG expansion have not been excluded for the remaining eight cases; however, in as many as seven of these persons, retrospective review of these patients' clinical features identified characteristics not typical for HD. This study shows that on rare occasions mutations in other, as-yet-undefined genes can present with a clinical phenotype very similar to that of HD.
亨廷顿舞蹈症(HD)已被证明与4p16.3(IT15)上一个新基因内的CAG重复序列扩增有关。在1022名患者中,共有30人(占我们队列的2.9%)在疾病范围内没有CAG重复序列扩增。在受影响个体中未观察到扩增的原因,对于确定使用重复长度进行受影响患者诊断和预测性检测项目的敏感性很重要,并且可能与理解HD潜在分子机制具有生物学相关性。在这里,我们表明,大多数(18名)等位基因大小正常的个体存在误诊、样本混淆或文书错误。其余12名患者可能是HD的表型模拟。在至少4个病例中,对这些表型模拟的家系研究排除了4p16.3作为导致该表型的区域。对于其余8个病例,尚未排除HD基因中除CAG扩增以外的突变;然而,在其中多达7名患者中,对这些患者临床特征的回顾性分析发现了不符合HD典型特征的表现。这项研究表明,在极少数情况下,其他尚未明确的基因中的突变可表现出与HD非常相似的临床表型。