Sensitive detection of somatic mutations in GC-rich cancer gene promoters

NAR Cancer. 2026 May 4;8(2):zcag011. doi: 10.1093/narcan/zcag011. eCollection 2026 Jun.

Abstract

Somatic mutations in protein-coding genes and noncoding regulatory regions are the major drivers of cancer. Only a relatively small number of somatic noncoding mutations that are likely drivers have been described to date, including those in the promoters of the TERT, FOXA1, and TP53 genes. The impact of these alterations can be profound by initiating, increasing, or abolishing gene expression. Promoter mutations in particular have been difficult to identify even from whole tumor genomes due to their high content of G and C nucleotides, which leads to loss of sequencing coverage in these regions. Therefore, the landscape of somatic drivers in gene promoters remains incomplete. Here, we present a hybrid capture assay optimized for >3000 promoters of cancer genes. We show that this assay allows for deep sequencing of challenging GC-rich promoter regions, enabling discovery of reliable point mutations, short insertions and deletions, copy number variants, and mutational signatures in cell line models as well as formalin-fixed, paraffin-embedded archival tissue samples. Our assay nominated candidate noncoding driver mutations in CDK4, SMAD3, and GATA3 in breast cancer for future functional follow-up.

MeSH terms

  • Base Composition
  • Breast Neoplasms* / genetics
  • Cell Line, Tumor
  • Cyclin-Dependent Kinase 4 / genetics
  • DNA Mutational Analysis / methods
  • Female
  • GATA3 Transcription Factor / genetics
  • High-Throughput Nucleotide Sequencing / methods
  • Humans
  • Mutation*
  • Neoplasms* / genetics
  • Promoter Regions, Genetic* / genetics

Substances

  • Cyclin-Dependent Kinase 4
  • GATA3 Transcription Factor
  • GATA3 protein, human
  • CDK4 protein, human