ArticleCancer cell2009
Context-dependent transformation of adult pancreatic cells by oncogenic K-Ras.
Article in Cancer cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 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
204 citing papers in PubMed, 22 citations in OpenAlex.
- Unravelling the genetics and epigenetics of the ageing tumour microenvironment in cancer.Nature reviews. Cancer · 2025Review
- Kras and ciliary gene mutations cooperatively lead to pancreatic tumorigenesis only when induced during embryogenesis.Scientific reports · 2025Article
- Cell reprogramming in cancer: Interplay of genetic, epigenetic mechanisms, and the tumor microenvironment in carcinogenesis and metastasis.World journal of clinical oncology · 2025Review
- Progress in Intestinal Homeostasis and Mechanisms of Pancreatic Cancer.Phenomics (Cham, Switzerland) · 2025Review
- Regulatory network analysis of Dclk1 gene expression reveals a tuft cell-ILC2 axis that inhibits pancreatic tumor progression.Cell reports · 2025Article
- An Analysis of the mRNA Expression of Peripheral-Blood Stem and Progenitor Cell Markers in Pancreatic Neoplastic Disorders.Current issues in molecular biology · 2025Article
- Regulatory network analysis ofbioRxiv : the preprint server for biology · 2024Article
- Article
- A mathematical model for pancreatic cancer during intraepithelial neoplasia.Royal Society open science · 2024Article
- Emerging mechanisms and promising approaches in pancreatic cancer metabolism.Cell death & disease · 2024Review
- Gut-Liver-Pancreas Axis Crosstalk in Health and Disease: From the Role of Microbial Metabolites to Innovative Microbiota Manipulating Strategies.Biomedicines · 2024Review
- Cellular Origins and Lineage Plasticity in Cancer.Cold Spring Harbor perspectives in medicine · 2024Review
- Challenges of Managing Type 3c Diabetes in the Context of Pancreatic Resection, Cancer and Trauma.Journal of clinical medicine · 2024Review
- Early elevations of RAS protein level and activity are critical for the development of PDAC in the context of inflammation.Cancer letters · 2024Article
- Deciphering cellular plasticity in pancreatic cancer for effective treatments.Cancer metastasis reviews · 2024Review
- Tff2 defines transit-amplifying pancreatic acinar progenitors that lack regenerative potential and are protective against Kras-driven carcinogenesis.Cell stem cell · 2023Article
- Intrapancreatic fat, pancreatitis, and pancreatic cancer.Cellular and molecular life sciences : CMLS · 2023Review
- Splicing Factor SRSF1 Promotes Pancreatitis and KRASG12D-Mediated Pancreatic Cancer.Cancer discovery · 2023Article
- Hematopoietic progenitor kinase 1 inhibits the development and progression of pancreatic intraepithelial neoplasia.The Journal of clinical investigation · 2023Article
- Review
144 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies. To investigate the cellular origin(s) of this cancer, we determined the effect of PDAC-relevant gene mutations in distinct cell types of the adult pancreas. We show that a subpopulation of Pdx1-expressing cells is susceptible to oncogenic K-Ras-induced transformation without tissue injury, whereas insulin-expressing endocrine cells are completely refractory to transformation under these conditions. However, chronic pancreatic injury can alter their endocrine fate and allow them to serve as the cell of origin for exocrine neoplasia. These results suggest that one mechanism by which inflammation and/or tissue damage can promote neoplasia is by altering the fate of differentiated cells that are normally refractory to oncogenic stimulation.
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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.