ArticleNAR genomics and bioinformatics2024
A single-cell strategy for the identification of intronic variants related to mis-splicing in pancreatic cancer.
Article in NAR genomics and bioinformatics, 2024. 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.
- Real-time monitoring of CAR T cell dynamics in tumor patient-derived organoids using the OrganoIDNet algorithm.Journal of translational medicine · 2026Article
- Advanced Human Immune Cell-Organoid Co-Cultures for Functional Testing of Cancer Nanovaccines.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- OrganoIDNet: a deep learning tool for identification of therapeutic effects in PDAC organoid-PBMC co-cultures from time-resolved imaging data.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- PRDM16-DT is a novel lncRNA that regulates astrocyte function in Alzheimer's disease.Acta neuropathologica · 2024Article
- A Curated Cell Life Imaging Dataset of Immune-enriched Pancreatic Cancer Organoids with Pre-trained AI Models.Scientific data · 2024Article
- PRDM16-DT: A Brain and Astrocyte-Specific lncRNA Implicated in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
10 authors.
Funding
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Abstract
Most clinical diagnostic and genomic research setups focus almost exclusively on coding regions and essential splice sites, thereby overlooking other non-coding variants. As a result, intronic variants that can promote mis-splicing events across a range of diseases, including cancer, are yet to be systematically investigated. Such investigations would require both genomic and transcriptomic data, but there currently exist very few datasets that satisfy these requirements. We address this by developing a single-nucleus full-length RNA-sequencing approach that allows for the detection of potentially pathogenic intronic variants. We exemplify the potency of our approach by applying pancreatic cancer tumor and tumor-derived specimens and linking intronic variants to splicing dysregulation. We specifically find that prominent intron retention and pseudo-exon activation events are shared by the tumors and affect genes encoding key transcriptional regulators. Our work paves the way for the assessment and exploitation of intronic mutations as powerful prognostic markers and potential therapeutic targets in cancer.
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Registered trials
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