ArticleGut2025
Large-scale multiomic analysis identifies non-coding somatic driver mutations and nominates
Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Article
- The ZFP36 Family as Post-Transcriptional Regulators in Physiology and Disease.International journal of molecular sciences · 2026Review
- Characterization of a pancreatic cancer GWAS signal suggests PDX1 buffers stress in the exocrine pancreas.medRxiv : the preprint server for health sciences · 2026Article
- Integrative screening identifies functional variants and VNTRs underlying GWAS signals at the 5p15.33 multi-cancer susceptibility locus.medRxiv : the preprint server for health sciences · 2026Article
- Allelic effects on KLHL17 expression underlie a pancreatic cancer genome-wide association signal at chr1p36.33.Nature communications · 2025Article
- Allelic effects onmedRxiv : the preprint server for health sciences · 2024Article
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Authors and funding
24 authors.
Funding
Abstract
backgroundThe identification and characterisation of somatic cancer driver mutations in the non-coding genome remains challenging.
objectiveTo broadly characterise non-coding driver mutations for pancreatic ductal adenocarcinoma (PDAC).
designUsing mutation calls from whole-genome sequence data in PDACs and genome-scale maps of accessible gene regulatory regions in normal-derived and tumour-derived pancreatic samples, we analysed enrichment of non-coding mutations in gene regulatory regions relevant to normal-derived and tumour-derived pancreatic contexts. Functional follow-up of potential driver mutations was performed using chromatin interaction analyses, massively parallel reporter assays (MPRA) and targeted analysis of selected non-coding somatic mutations (NCSMs).
resultsWe first created genome-scale maps of accessible chromatin regions (ACRs) and histone modification marks (HMMs) in pancreatic cell lines and purified pancreatic acinar and duct cells. Integration with whole-genome mutation calls from 506 PDACs revealed 314 ACRs/HMMs significantly enriched with 3614 NCSMs. Chromatin interaction analysis identified 416 potential target genes and MPRA revealed 178 NCSMs impacting reporter activity (19.45% of those tested). Targeted luciferase validation confirmed negative effects on gene regulatory activity for NCSMs near
conclusionOur integrative approach provides a catalogue of potential non-coding driver mutations and nominates
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.