ReviewCellular and molecular gastroenterology and hepatology2022
Uncertain Beginnings: Acinar and Ductal Cell Plasticity in the Development of Pancreatic Cancer.
Review in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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
33 citing papers in PubMed, 56 citations in OpenAlex.
- Molecular dynamics driving phenotypic divergence among KRAS mutants in pancreatic tumorigenesis.Developmental cell · 2026Article
- Pancreatic cancer.Nature reviews. Disease primers · 2026Review
- Opportunities to Avoid Invasive Cancer by Diagnosis and Interception of Preneoplastic Lesions and Cancer Risk Conditions.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026Article
- Merlin's disappearing act: NF2 loss conjures pancreatic cancer survival in the hostile tumor microenvironment.The Journal of clinical investigation · 2026Article
- DNA methylation profile to aid in the diagnosis of pancreatic ductal adenocarcinoma and its role in disease progression.Epigenomics · 2025Review
- Latent plasticity of the human pancreas across development, health, and disease.bioRxiv : the preprint server for biology · 2025Article
- RalGAP complexes control secretion and primary cilia in pancreatic disease.Life science alliance · 2025Article
- Early neoplastic lesions of the pancreas: initiation, progression, and opportunities for precancer interception.The Journal of clinical investigation · 2025Review
- In Vivo Regenerative Potential ofMolecules (Basel, Switzerland) · 2025Article
- Allelic effects on KLHL17 expression underlie a pancreatic cancer genome-wide association signal at chr1p36.33.Nature communications · 2025Article
- Protective role of oleic acid against palmitic acid-induced pancreatic fibrosis.Journal of translational medicine · 2025Article
- Therapeutical potential of natural products in treatment of pancreatic cancer: a review.Molecular biology reports · 2025Review
- Integrative multi-omics analysis reveals the role of toll-like receptor signaling in pancreatic cancer.Scientific reports · 2025Article
- Inhibition of Ribosome Biogenesis In Vivo Causes p53-Dependent Death and p53-Independent Dysfunction.Cellular and molecular gastroenterology and hepatology · 2025Article
- Allelic effects onmedRxiv : the preprint server for health sciences · 2024Article
- Biomarkers in Cancer Screening: Promises and Challenges in Cancer Early Detection.Hematology/oncology clinics of North America · 2024Review
- New avenues for the treatment of immunotherapy-resistant pancreatic cancer.World journal of gastrointestinal oncology · 2024Review
- A neuroligin-2-YAP axis regulates progression of pancreatic intraepithelial neoplasia.EMBO reports · 2024Article
- Diagnostic Challenges during Inflammation and Cancer: Current Biomarkers and Future Perspectives in Navigating through the Minefield of Reactive versus Dysplastic and Cancerous Lesions in the Digestive System.International journal of molecular sciences · 2024Review
- Hallmarks of stemness in mammalian tissues.Cell stem cell · 2024Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The pancreas consists of several specialized cell types that display a remarkable ability to alter cellular identity in injury, regeneration, and repair. The abundant cellular plasticity within the pancreas appears to be exploited in tumorigenesis, with metaplastic, dedifferentiation, and transdifferentiation processes central to the development of pancreatic intraepithelial neoplasia and intraductal papillary neoplasms, precursor lesions to pancreatic ductal adenocarcinoma. In the face of shifting cellular identity, the cell of origin of pancreatic cancer has been difficult to elucidate. However, with the extensive utilization of in vivo lineage-traced mouse models coupled with insights from human samples, it has emerged that the acinar cell is most efficiently able to give rise to both intraductal papillary neoplasms and pancreatic intraepithelial neoplasia but that acinar and ductal cells can undergo malignant transformation to pancreatic ductal adenocarcinoma. In this review, we discuss the cellular reprogramming that takes place in both the normal and malignant pancreas and evaluate the current state of evidence that implicate both the acinar and ductal cell as context-dependent origins of this deadly disease.
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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.