{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xu Y"],"funding":["William and Ella Owens Medical Research Foundation","NIDDK NIH HHS","U.S. Department of Health & Human Services | NIH | National Cancer Institute","NCI NIH HHS","NIGMS NIH HHS","NIH HHS","Cancer Prevention and Research Institute of Texas","U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["818"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10821902"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_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"],"journal":["Nature communications"],"pubmed_title":["Reconstitution of human PDAC using primary cells reveals oncogenic transcriptomic features at tumor onset."],"pmcid":["PMC10821902"],"funding_grant_id":["R01DK110361","R1219","T32 GM148752","P30 CA054174","R21 CA245437","R01 CA237159","R01 DK110361","P01 CA117969","S10 OD030311","S10 OD030432","R21 CA218968"],"pubmed_authors":["Nipper MH","Liu J","Sun LZ","Zheng S","Wang H","Ye Z","Fernandez-Zapico ME","Lopez K","Akanuma N","Sanchez A","Wang P","Sharkey FE","Singhi AD","Dominguez AA","Deng JJ","Arenas D","Court CM","Chen Y","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"Reconstitution of human PDAC using primary cells reveals oncogenic transcriptomic features at tumor onset.","description":"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","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jan","modification":"2026-07-15T10:29:29.82Z","creation":"2025-05-29T21:30:31.801Z"},"accession":"S-EPMC10821902","cross_references":{"pubmed":["38280869"],"doi":["10.1038/s41467-024-45097-2"]}}