生殖系
PALB2
种系突变
癌变
遗传学
癌症研究
医学
胶质瘤
外显子组测序
生物
癌症
肿瘤科
基因
突变
作者
Marion K. Mateos,Pamela Ajuyah,Noemi Fuentes-Bolanos,Sam El-Kamand,Paulette Barahona,Ann-Kristin Alteköester,Chelsea Mayoh,Holly Holliday,Jie Liu,Lujing Cui,Elke Pfaff,Alan Mackay,Adam C Resnick,Mark Pinese,Loretta M. S. Lau,Dong-Anh Khuong-Quang,Kimberly Dias,Catherine Goudie,Alison Salkeld,Jo Lynne Rokita
标识
DOI:10.1093/neuonc/noaf061
摘要
Abstract Background Factors that drive the development of diffuse midline gliomas (DMG) are unknown. Our study aimed to determine the prevalence of pathogenic/likely pathogenic (P/LP) germline variants in pediatric patients with DMG. Methods We assembled an international cohort of 252 pediatric patients with DMG, including diffuse intrinsic pontine glioma (n=153), with germline whole genome or whole exome sequencing. Results We identified P/LP germline variants in cancer predisposition genes in 7.5% (19/252) of patients. Tumor profiles differed, with absence of somatic drivers in the PI3K/mTOR pathway in patients with germline P/LP variants versus those without (P = 0.023). P/LP germline variants were recurrent in homologous recombination (n=9; BRCA1, BRCA2, PALB2) and Fanconi anemia genes (n=4). Somatic findings established that the germline variants definitively contributed to tumorigenesis in at least 1% of cases. One patient with recurrent DMG and pathogenic germline variants (BRCA2, FANCE) showed near-complete radiological response to PARP and immune checkpoint inhibition. Conclusions Our study determined the prevalence of pathogenic germline variants in pediatric DMG, and suggests a role in tumorigenesis for a subset of patients.
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