ArticleInternational journal of cancer2025
Comprehensive genetic and epigenetic characterization of Lynch-like syndrome patients.
Article in International journal of cancer, 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.
- The New Tumor Predisposition Syndromes with Neuro-Oncological Relevance-A Comprehensive Review for Neuroradiologists.Clinical neuroradiology · 2026Review
- Germline pathogenic variant spectrum and prevalence among colorectal cancer patients undergoing multigene panel testing in Kazakhstan.Scientific reports · 2026Article
- Epimutations in migraine and in medication overuse headache: a longitudinal study after acute medication withdrawal.The journal of headache and pain · 2026Article
- Case Report: Synchronous colorectal adenocarcinomas with discordant mismatch repair status: a case of lynch-like syndrome and serrated pathway association.Frontiers in oncology · 2026Article
- Comprehensive genetic and epigenetic characterization of Lynch-like syndrome patients.International journal of cancer · 2025Article
- Pathological diagnosis experience and literature review of four cases suspected Lynch-like syndrome.Frontiers in oncology · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
Lynch-like syndrome (LLS) presents very similar clinicopathological characteristics to Lynch syndrome (LS) but the mechanism for cancer predisposition remains unknown. The present study aims to investigate the causal mechanism of LLS by a comprehensive genetic and epigenetic approach. Thirty-two LLS and 34 LS patients with colorectal cancer (CRC) fitting the Amsterdam and Bethesda criteria were included, along with 29 CRC sporadic patients, and analyzed for the presence of pathogenic variants in 94 genes associated with hereditary tumors. The cohorts were also characterized for the methylation profile and examined through a sample group analysis and a Stochastic Epigenetic Mutations (SEMs) analysis in comparison with 29 age-matched healthy controls. The multigene panel analysis revealed the presence of pathogenic variants in non-mismatch repair (MMR) genes and three variants classified as pathogenic/likely pathogenic possibly predisposing to LLS. The epigenetic analysis showed epivariations targeting genes associated with LS or DNA repair, most of them associated with the Fanconi Anemia pathway, which could explain the susceptibility to cancer. Our results highlight the need for using extended genetic and epigenetic analyses to understand the causal mechanism of LLS.
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