ArticleTranslational oncology2017
The Role of Fibroblasts in Pancreatic Cancer: Extracellular Matrix Versus Paracrine Factors.
Article in Translational oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Tumor slice cultures enable rapid ex vivo profiling of patient-specific drug sensitivity in pancreatic ductal adenocarcinoma.NPJ precision oncology · 2026Article
- Glutamine-dependent changes in fibroblast-derived extracellular matrix dictate cancer cell behavior.Matrix biology : journal of the International Society for Matrix Biology · 2026Article
- Article
- Macrophage-linked lipid metabolic signatures for HCC prognosis identified through integrated bulk and single-cell transcriptomics.Frontiers in immunology · 2026Article
- Downregulation of the CCK-B Receptor in Pancreatic Stellate Cells Blocks Molecular Proliferative Pathways and Increases Apoptosis to Decrease Pancreatic Cancer Growth In Vitro.International journal of molecular sciences · 2025Article
- Tumour tissue: heterogeneous, but not disordered.Nature reviews. Cancer · 2025Article
- A bioprinted sea-and-island multicellular model for dissecting human pancreatic tumor-stroma reciprocity and adaptive metabolism.Biomaterials · 2024Article
- Extracellular matrix stiffness and tumor-associated macrophage polarization: new fields affecting immune exclusion.Cancer immunology, immunotherapy : CII · 2024Review
- Optical coherence tomography for multicellular tumor spheroid category recognition and drug screening classification via multi-spatial-superficial-parameter and machine learning.Biomedical optics express · 2024Article
- A comprehensive review of 3D cancer models for drug screening and translational research.Cancer innovation · 2024Review
- Review
- Forces exerted and transduced by cancer-associated fibroblasts during cancer progression.Biology of the cell · 2023Review
- The tumor-stroma ratio and the immune microenvironment improve the prognostic prediction of pancreatic ductal adenocarcinoma.Discover oncology · 2023Article
- Cancer-Associated Fibroblasts and Extracellular Matrix: Therapeutical Strategies for Modulating the Cholangiocarcinoma Microenvironment.Current oncology (Toronto, Ont.) · 2023Review
- Organoids for Modeling (Colorectal) Cancer in a Dish.Cancers · 2022Review
- Immune checkpoint blockade enhances chemophototherapy in a syngeneic pancreatic tumor model.APL bioengineering · 2022Article
- Cancer Associated Fibroblast (CAF) Regulation of PDAC Parenchymal (CPC) and CSC Phenotypes Is Modulated by ECM Composition.Cancers · 2022Article
- Modeling the mechanical stiffness of pancreatic ductal adenocarcinoma.Matrix biology plus · 2022Article
- Self-Assembled Peptide Habitats to Model Tumor Metastasis.Gels (Basel, Switzerland) · 2022Article
- Nanocarriers for pancreatic cancer imaging, treatments, and immunotherapies.Theranostics · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimDesmoplasia is a characteristic feature and a suspected mechanism of tumor progression in pancreatic ductal adenocarcinoma (PDAC). Main constituents of the stroma involve cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM). The aim of this study was to dissect the interaction of CAFs, ECM, and PDAC cells in both an in vitro setting and a large-scale clinical cohort study. METHODS AND MATERIAL: Patients operated for PDAC were identified from our prospectively maintained clinical database. A standard pathology protocol was applied for pancreatoduodenectomy specimens also assessing CAF activation as either CAF grade 0 or CAF grade +. Interaction between a spectrum of pancreatic cancer cell lines (PCCs) and mouse embryonic fibroblasts (NIH 3T3) was assessed in a conditioned medium experimental setup.
resultsOne hundred eleven patients operated for PDAC from 2001 to 2011 were identified. Univariate analysis disclosed CAF grade + (P = .030), positive M status (P < .001), and lymph node ratio (LNR) > 0.1 (P = .045) to impair overall survival. Independent prognostic factors were CAF grade (P = .050) and positive M status (P = .002). CAF grade correlated with N status (CC = 0.206, P = .030), LNR (CC = 0.187, P = .049), tumor size (CC = -0.275, P = .003), and M status (CC = 0.190, P = .045). In the in vitro setting, paracrine effects of pancreatic cancer cell resulted in morphological activation of fibroblasts and tumor cell differentiation-dependent increase of fibroblast growth. Paracrine effects of poorly differentiated PCCs led to an upregulation of Vimentin in NIH 3T3 fibroblasts. Paracrine effects of fibroblasts on their part promoted cancer cell motility in all PCCs. As the second stromal component, fibroblast-derived ECM resulted in significantly decreased proliferation depending on density and led to upregulation of ZEB1 in poorly differentiated PCCs.
conclusionIn PDAC patients, positive CAF grading was identified as a negative prognostic parameter correlating with positive N status, high LNR, positive M status, and smaller tumor size. Whereas bilateral interaction of PCCs and CAFs promotes tumor progression, ECM poses PCC growth restrictions. In summary, our study discloses differential effects of stromal components and may help to interpret heterogeneous results of former studies.
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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.