ArticleInternational journal of cancer2018
KRAS mutation and epithelial-macrophage interplay in pancreatic neoplastic transformation.
Article in International journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review.Signal transduction and targeted therapy · 2023Pooled it
- Patient-derived tumor organoids for new drug development: promises and challenges.Investigational new drugs · 2026Review
- Functional Precision in Pancreatic Cancer: Redefining Biomarkers with Patient-Derived Organoids.International journal of molecular sciences · 2025Review
- Mechanistic Foundations of KRAS-Driven Tumor Ecosystems: Integrating Crosstalk among Immune, Metabolic, Microbial, and Stromal Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Precision immune regulation in KRAS-mutated cancers: the final piece of the puzzle?Journal of experimental & clinical cancer research : CR · 2025Review
- Shaping the battlefield: EGFR and KRAS tumor mutations' role on the immune microenvironment and immunotherapy responses in lung cancer.Cancer metastasis reviews · 2025Review
- Tumor-associated macrophages (TAMs): Constructing an immunosuppressive microenvironment bridge for pancreatic ductal adenocarcinoma (PDAC).Cancer pathogenesis and therapy · 2025Review
- Advancing pancreatic cancer research and therapeutics: the transformative role of organoid technology.Experimental & molecular medicine · 2025Review
- Pigment Epithelial-Derived Factor in Pancreatic and Liver Cancers-From Inflammation to Cancer.Biomedicines · 2024Review
- The cross-talk between the macro and micro-environment in precursor lesions of pancreatic cancer leads to new and promising circulating biomarkers.Journal of experimental & clinical cancer research : CR · 2024Review
- Pancreatic Organoids: A Frontier Method for Investigating Pancreatic-Related Diseases.International journal of molecular sciences · 2023Review
- Tumor organoids: applications in cancer modeling and potentials in precision medicine.Journal of hematology & oncology · 2022Review
- Novel role of the Mu-opioid receptor in pancreatic cancer: potential link between opioid use and cancer progression.Molecular and cellular biochemistry · 2022Article
- The Intricate Crosstalk Between Insulin and Pancreatic Ductal Adenocarcinoma: A Review From Clinical to Molecular.Frontiers in cell and developmental biology · 2022Review
- Patient-derived pancreatic cancer-on-a-chip recapitulates the tumor microenvironment.Microsystems & nanoengineering · 2022Article
- Review
- The tumor microenvironment in pancreatic ductal adenocarcinoma: current perspectives and future directions.Cancer metastasis reviews · 2021Review
- A pancreas tumor derived organoid study: from drug screen to precision medicine.Cancer cell international · 2021Review
- Article
- Establishment of a Macrophage Phenotypic Switch Related Prognostic Signature in Patients With Pancreatic Cancer.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDA) is characterized by epithelial mutations in KRAS and prominent tumor-associated inflammation, including macrophage infiltration. But knowledge of early interactions between neoplastic epithelium and macrophages in PDA carcinogenesis is limited. Using a pancreatic organoid model, we found that the expression of mutant KRAS in organoids increased (i) ductal to acinar gene expression ratios, (ii) epithelial cells proliferation and (iii) colony formation capacity in vitro, and endowed pancreatic cells with the ability to generate neoplastic tumors in vivo. KRAS mutations induced a protumorigenic phenotype in macrophages. Altered macrophages decreased epithelial pigment epithelial derived factor (PEDF) expression and induced a cancerous phenotype. We validated our findings using annotated patient samples from The Cancer Genome Atlas (TCGA) and in our human PDA specimens. Epithelium-macrophage cross-talk occurs early in pancreatic carcinogenesis where KRAS directly induces cancer-related phenotypes in epithelium, and also promotes a protumorigenic phenotype in macrophages, in turn augmenting neoplastic growth.
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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.