Chouery Eliane, Mehawej Cybel, Saade Rami, Barake Rana, Zarecki Patryk, Gennery Catherine, Corbani Sandra, Korban Rima, Hamam Ali, Nasser Eldin Jade, Yamout Mohamad, Banna Mazen, Yamout Abdul Kader Afif, Adhami Fawaz, Megarbane Andre, Mustapha Mirna
Department of Human Genetics, Gilbert and Rose-Marie Chagoury School of Medicine, Lebanese American University, Byblos, Lebanon.
Department of Otolaryngology-Head and Neck Surgery, Lebanese American University, Byblos, Lebanon.
Eur J Hum Genet. 2025 Jan;33(1):121-130. doi: 10.1038/s41431-024-01715-7. Epub 2024 Oct 16.
Hearing impairment (HI) is a significant health concern globally, influenced by genetic and environmental factors. We had identified a homozygous pathogenic variant in POLD3 in a Lebanese patient with an autosomal congenital recessive syndromic hearing loss (MIM#620869). This variant was found at heterozygous state in the parents, who developed progressive hearing impairment around age 40. We conducted a thorough clinical and genetic assessment of sixteen family members, including physical exams, audiometry and vestibular function evaluations. Additionally, gene expression analysis of the Pold3 gene was performed in mice using RNAscope. Twelve individuals were heterozygous for the variant in POLD3, of whom eight showed bilateral adult-onset HI, typically starting around ages 40-50, and two older patients displaying unilateral vestibular weakness. Additionally, two carriers of the variant developed cancer at an early age. RNAscope confirmed Pold3 expression in auditory and vestibular neurons. Exome sequencing analysis excluded the presence of pathogenic variants in any known hearing impairment or cancer predisposition genes. We present herein, for the first time, evidence of a heterozygous pathogenic POLD3 variant associated with a novel form of autosomal dominant progressive adult-onset hearing and vestibular impairments. We also highlight the necessity for further exploration of the role of POLD3 in cancer predisposition.
听力障碍(HI)是全球范围内一个重要的健康问题,受遗传和环境因素影响。我们在一名患有常染色体先天性隐性综合征性听力损失(MIM#620869)的黎巴嫩患者中,在POLD3基因中鉴定出一个纯合致病变异。在其父母中发现该变异处于杂合状态,他们在40岁左右开始出现进行性听力障碍。我们对16名家庭成员进行了全面的临床和基因评估,包括体格检查、听力测定和前庭功能评估。此外,使用RNAscope在小鼠中对Pold3基因进行了基因表达分析。12个人为POLD3基因变异的杂合子,其中8人表现为双侧成人起病的听力障碍,通常在40 - 50岁左右开始,还有2名老年患者表现为单侧前庭功能减弱。此外,该变异的两名携带者在早年患了癌症。RNAscope证实Pold3在听觉和前庭神经元中表达。外显子组测序分析排除了任何已知听力障碍或癌症易感基因中存在致病变异的情况。我们在此首次展示了与一种新型常染色体显性进行性成人起病听力和前庭障碍相关的杂合致病POLD3变异的证据。我们还强调了进一步探索POLD3在癌症易感性中作用的必要性。