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Updated: May 6, 2026
06:35
A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
Published on: December 22, 2020
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Cancer-Associated Fibroblasts Promote Epithelial-Mesenchymal Transition and Classical to Basal Subtype Shift in
Kylie Belanger1,2,3, Samantha Guinn1,2,3, Brayan Perez1,2,3
1Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Cancer Research
|May 5, 2026
Summary
Cancer-associated fibroblasts (CAFs) drive cellular heterogeneity in pancreatic ductal adenocarcinoma (PDAC). CAF signaling, particularly IL-8, influences tumor cell subtypes and spatial organization, impacting PDAC progression and treatment strategies.
Area of Science:
- Oncology
- Cancer Biology
- Tumor Microenvironment Research
Background:
- Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis due to cellular heterogeneity.
- Cancer-associated fibroblasts (CAFs) significantly influence PDAC biology and treatment response.
- Understanding patient-specific CAF heterogeneity is crucial for characterizing their role in PDAC.
Purpose of the Study:
- To characterize the tumor microenvironment (TME) in PDAC patients undergoing surgery.
- To functionally validate the impact of patient-derived CAFs on tumor cells.
- To investigate CAF signaling as a regulator of PDAC cellular heterogeneity.
Main Methods:
- Multi-omic analyses of PDAC tumors.
- Establishment of matched tumor organoid and CAF lines.
- Functional validation of CAF-tumor cell interactions.
Main Results:
- CAFs promote epithelial-mesenchymal transition (EMT) and a shift from classical to basal tumor cell subtypes.
- CAF-derived interleukin 8 (IL-8) modulates tumor cell subtype.
- Distinct spatial coordination exists between CAF and tumor cell subtypes, including T cell subsets.
Conclusions:
- CAF signaling is a key regulator of cellular and behavioral heterogeneity within the PDAC TME.
- These findings offer insights into rational therapeutic approaches for PDAC.
- Targeting CAF-tumor cell interactions may improve treatment outcomes for this challenging disease.
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