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评估新突变/序列变异的致病性:健康老年人的价值。

Assessing pathogenicity for novel mutation/sequence variants: the value of healthy older individuals.

机构信息

Departamento de Genética e Biologia Evolutiva, Centro de Estudos do Genoma Humano, Universidade de São Paulo, Rua do Matão, 106, Cidade Universitária, São Paulo, SP, 05508-090, Brazil.

出版信息

Neuromolecular Med. 2012 Dec;14(4):281-4. doi: 10.1007/s12017-012-8186-x. Epub 2012 Jun 16.

DOI:10.1007/s12017-012-8186-x
PMID:22707356
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3505535/
Abstract

Improvement in DNA technology is increasingly revealing unexpected/unknown mutations in healthy persons and generating anxiety due to their still unknown health consequences. We report a 44-year-old healthy father of a 10-year-old daughter with bilateral coloboma and hearing loss, but without muscle weakness, in whom a whole-genome CGH revealed a deletion of exons 38-44 in the dystrophin gene. This mutation was inherited from her asymptomatic father, who was further clinically and molecularly evaluated for prognosis and genetic counseling (GC). This deletion was never identified by us in 982 Duchenne/Becker patients. To assess whether the present case represents a rare case of non-penetrance, and aiming to obtain more information for prognosis and GC, we suggested that healthy older relatives submit their DNA for analysis, to which several complied. Mutation analysis revealed that his mother, brother, and 56-year-old maternal uncle also carry the 38-44 deletion, suggesting it an unlikely cause of muscle weakness. Genome sequencing will disclose mutations and variants whose health impact are still unknown, raising important problems in interpreting results, defining prognosis, and discussing GC. We suggest that, in addition to family history, keeping the DNA of older relatives could be very informative, in particular for those interested in having their genome sequenced.

摘要

DNA 技术的进步越来越多地揭示出健康人群中意想不到/未知的突变,并因其未知的健康后果而引发焦虑。我们报告了一例 44 岁的健康男性,他是一名 10 岁女儿的父亲,患有双侧视网膜色素上皮层脱离和听力损失,但没有肌肉无力。全基因组 CGH 显示其肌营养不良蛋白基因外显子 38-44 缺失。该突变是从无症状的父亲那里遗传而来的,进一步对其进行了临床和分子评估,以预测预后和提供遗传咨询 (GC)。我们在 982 例杜氏/贝克肌营养不良症患者中从未发现过这种突变。为了评估该病例是否代表一种罕见的不完全外显率,以及为了获得更多关于预后和 GC 的信息,我们建议健康的年长亲属提交 DNA 进行分析,其中一些人同意了。突变分析显示,他的母亲、兄弟和 56 岁的舅舅也携带 38-44 缺失,表明其不太可能导致肌肉无力。基因组测序将揭示其健康影响仍未知的突变和变异,这在解释结果、定义预后和讨论 GC 方面带来了重要问题。我们建议,除了家族史外,保留年长亲属的 DNA 可能非常有帮助,特别是对于那些有兴趣对其基因组进行测序的人。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af8/3505535/350dcff1afee/12017_2012_8186_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af8/3505535/c124eb7862be/12017_2012_8186_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af8/3505535/350dcff1afee/12017_2012_8186_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af8/3505535/c124eb7862be/12017_2012_8186_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af8/3505535/350dcff1afee/12017_2012_8186_Fig2_HTML.jpg

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Genetics. Gene losses in the human genome.遗传学。人类基因组中的基因缺失。
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