INGEMM (Instituto de Genética Médica y Molecular), IdiPAZ Hospital Universitario La Paz, Paseo de la Castellana 261, 28046 Madrid, Spain.
J Med Genet. 2011 Mar;48(3):212-6. doi: 10.1136/jmg.2010.081919. Epub 2010 Nov 19.
Molecular studies in a patient with Beckwith-Wiedemann syndrome phenotype who developed two different tumours revealed an unexpected observation of almost complete loss of heterozygosity of all chromosomes. It is shown, by means of numerous molecular methods, that the absence of maternal contribution in somatic cells is due to high-degree (∼ 85%) genome-wide paternal uniparental disomy (UPD). The observations indicate that the genome-wide UPD results from diploidisation, and have important implications for genetic counselling and tumour surveillance for the growing number of UPD associated imprinting disorders.
对一位表现出 Beckwith-Wiedemann 综合征表型并发展出两种不同肿瘤的患者进行分子研究,结果发现了一个出乎意料的观察结果,即所有染色体的杂合性几乎完全丧失。通过多种分子方法证明,体细胞中不存在母本贡献是由于高度(约 85%)全基因组父源单亲二倍体(UPD)所致。这些观察结果表明,全基因组 UPD 是由二倍体化引起的,这对遗传咨询和肿瘤监测具有重要意义,因为与 UPD 相关的印迹疾病的数量正在不断增加。