TY - JOUR
T1 - Characterizing somatic mutations in ovarian cancer germline risk regions
AU - Lai, Ping Hung
AU - Tyrer, Jonathan P.
AU - Pharoah, Paul
AU - Gayther, Simon A.
AU - Jones, Michelle R.
AU - Peng, Pei Chen
N1 - Publisher Copyright:
© The Author(s) 2025.
PY - 2025/12
Y1 - 2025/12
N2 - Epithelial ovarian cancer (EOC) genetics research has been focused on germline or somatic mutations independently. Emerging evidence suggests that the somatic mutational landscape can be shaped by the germline genetic background. In this study, we aim to unravel the role of somatic alterations within EOC germline susceptibility regions by incorporating functional annotations. We investigate somatic events, including mutational signatures, point mutations, copy number alterations, and transcription factor binding disruptions, within 33 EOC germline susceptibility regions. Our analysis identifies significant associations between candidate germline susceptibility genes and somatic mutational signatures known to be key risk factors for EOC, such as mismatch repair deficiency, age-related mutagenesis, and homologous recombination deficiency. In addition, we find somatic point mutations and copy number alterations are significantly enriched in histotype-specific active enhancers and promoters within EOC risk loci. Furthermore, we examine the impact of germline variants and somatic mutations on transcription factor binding sites, identifying cancer developmental transcription factor motifs frequently affected by both types of mutations. Overall, our study highlights the importance of integrating germline and somatic mutations with regulatory and epigenomic data to gain insights into the genetic basis of EOC.
AB - Epithelial ovarian cancer (EOC) genetics research has been focused on germline or somatic mutations independently. Emerging evidence suggests that the somatic mutational landscape can be shaped by the germline genetic background. In this study, we aim to unravel the role of somatic alterations within EOC germline susceptibility regions by incorporating functional annotations. We investigate somatic events, including mutational signatures, point mutations, copy number alterations, and transcription factor binding disruptions, within 33 EOC germline susceptibility regions. Our analysis identifies significant associations between candidate germline susceptibility genes and somatic mutational signatures known to be key risk factors for EOC, such as mismatch repair deficiency, age-related mutagenesis, and homologous recombination deficiency. In addition, we find somatic point mutations and copy number alterations are significantly enriched in histotype-specific active enhancers and promoters within EOC risk loci. Furthermore, we examine the impact of germline variants and somatic mutations on transcription factor binding sites, identifying cancer developmental transcription factor motifs frequently affected by both types of mutations. Overall, our study highlights the importance of integrating germline and somatic mutations with regulatory and epigenomic data to gain insights into the genetic basis of EOC.
UR - https://www.scopus.com/pages/publications/105003874130
UR - https://www.scopus.com/inward/citedby.url?scp=105003874130&partnerID=8YFLogxK
U2 - 10.1038/s42003-025-08072-1
DO - 10.1038/s42003-025-08072-1
M3 - Article
C2 - 40301634
AN - SCOPUS:105003874130
SN - 2399-3642
VL - 8
JO - Communications Biology
JF - Communications Biology
IS - 1
M1 - 676
ER -