ArticleNature communications2024
Reconstitution of human PDAC using primary cells reveals oncogenic transcriptomic features at tumor onset.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Patient-derived organoids reveal ductal dysfunction and CFTR-modulator responses in chronic pancreatitis.Cell stem cell · 2026Article
- metileneNature communications · 2026Article
- NF2 loss malignantly transforms human pancreatic acinar cells and enhances cell fitness under environmental stress.The Journal of clinical investigation · 2026Article
- Transcriptomic Analyses of Normal Human Pancreata Reveal the Presence of Cancer Subtypes that Correlate with Acinar Ductal Metaplasia and Donor Ancestry.Cancer research communications · 2026Article
- Chronic pancreatitis patient-derived organoids reveal new paths to precision therapeutics.bioRxiv : the preprint server for biology · 2025Article
- Article
- Bioinformatics-based Investigation to Unveiling The miRNA-Immunity Axis in The Tumor Microenvironment of Pancreatic Cancer.F1000Research · 2025Article
- Small molecules enhance the high-efficiency generation of pancreatic ductal organoids.Acta biochimica et biophysica Sinica · 2024Article
- Emerging strategies to investigate the biology of early cancer.Nature reviews. Cancer · 2024Review
- TGFβ and Hippo Signaling Pathways Coordinate to Promote Acinar to Ductal Metaplasia in Human Pancreas.Cells · 2024Article
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
Abstract
Animal studies have demonstrated the ability of pancreatic acinar cells to transform into pancreatic ductal adenocarcinoma (PDAC). However, the tumorigenic potential of human pancreatic acinar cells remains under debate. To address this gap in knowledge, we expand sorted human acinar cells as 3D organoids and genetically modify them through introduction of common PDAC mutations. The acinar organoids undergo dramatic transcriptional alterations but maintain a recognizable DNA methylation signature. The transcriptomes of acinar organoids are similar to those of disease-specific cell populations. Oncogenic KRAS alone do not transform acinar organoids. However, acinar organoids can form PDAC in vivo after acquiring the four most common driver mutations of this disease. Similarly, sorted ductal cells carrying these genetic mutations can also form PDAC, thus experimentally proving that PDACs can originate from both human acinar and ductal cells. RNA-seq analysis reveal the transcriptional shift from normal acinar cells towards PDACs with enhanced proliferation, metabolic rewiring, down-regulation of MHC molecules, and alterations in the coagulation and complement cascade. By comparing PDAC-like cells with normal pancreas and PDAC samples, we identify a group of genes with elevated expression during early transformation which represent potential early diagnostic biomarkers.
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Registered trials
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