ArticleCell reports2017
Duct- and Acinar-Derived Pancreatic Ductal Adenocarcinomas Show Distinct Tumor Progression and Marker Expression.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
71 citing papers in PubMed, 120 citations in OpenAlex.
- Clinical Significance of a Cell-Of-Origin-Based Classification in Pancreatic Ductal Adenocarcinoma.Cancer science · 2026Article
- Transcriptomic regulation of pancreatic acinar cell homeostasis and plasticity.Biochemical Society transactions · 2026Review
- GATA4 loss promotes mutantbioRxiv : the preprint server for biology · 2026Article
- Pancreatic cancer.Nature reviews. Disease primers · 2026Review
- Integrated epidemiological and molecular data inform the relationship between precancer and cancer states of esophageal adenocarcinoma.Nature medicine · 2026Article
- DNA hypermethylation of nonspecific cytotoxic cell receptor protein 1 and poor prognosis of pancreatic cancer.Oncology letters · 2026Article
- Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development.Nature communications · 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
- Article
- An injury-associated lobular microniche is associated with the classical tumor cell phenotype in pancreatic cancer.Nature communications · 2025Article
- Comparative spatial transcriptomics of pancreatic cancer with ductal and acinar origins in mouse models.Clinical and translational medicine · 2025Article
- Early neoplastic lesions of the pancreas: initiation, progression, and opportunities for precancer interception.The Journal of clinical investigation · 2025Review
- Lfng-expressing centroacinar cell is a unique cell-of-origin for p53 deficient pancreatic cancer.Oncogene · 2025Article
- Inhibition of Ribosome Biogenesis In Vivo Causes p53-Dependent Death and p53-Independent Dysfunction.Cellular and molecular gastroenterology and hepatology · 2025Article
- Small molecules enhance the high-efficiency generation of pancreatic ductal organoids.Acta biochimica et biophysica Sinica · 2024Article
- The Integrated Stress Response in Pancreatic Development, Tissue Homeostasis, and Cancer.Gastroenterology · 2024Review
- Exploring human pancreatic organoid modelling through single-cell RNA sequencing analysis.Communications biology · 2024Article
- NFAT5 governs cellular plasticity-driven resistance to KRAS-targeted therapy in pancreatic cancer.The Journal of experimental medicine · 2024Article
- AGR2: The Covert Driver and New Dawn of Hepatobiliary and Pancreatic Cancer Treatment.Biomolecules · 2024Review
- Reconstitution of human PDAC using primary cells reveals oncogenic transcriptomic features at tumor onset.Nature communications · 2024Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The cell of origin of pancreatic ductal adenocarcinoma (PDAC) has been controversial. Here, we show that identical oncogenic drivers trigger PDAC originating from both ductal and acinar cells with similar histology but with distinct pathophysiology and marker expression dependent on cell of origin. Whereas acinar-derived tumors exhibited low AGR2 expression and were preceded by pancreatic intraepithelial neoplasias (PanINs), duct-derived tumors displayed high AGR2 and developed independently of a PanIN stage via non-mucinous lesions. Using orthotopic transplantation and chimera experiments, we demonstrate that PanIN-like lesions can be induced by PDAC as bystanders in adjacent healthy tissues, explaining the co-existence of mucinous and non-mucinous lesions and highlighting the need to distinguish between true precursor PanINs and PanIN-like bystander lesions. Our results suggest AGR2 as a tool to stratify PDAC according to cell of origin, highlight that not all PanIN-like lesions are precursors of PDAC, and add an alternative progression route to the current model of PDAC development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.