ArticleBJC reports2025
The influence of clinical risk factors on the classification of human cancer-associated fibroblasts in PDAC and pancreatitis patients.
Article in BJC reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- IL-6 as a central driver of immune evasion in PDAC: from IDO-mediated tolerance to multi-pathway immunosuppression.Frontiers in immunology · 2026Review
- Fibroblasts as a ruler of the immune microenvironment: measurement and modulation in tissue homeostasis and disease.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-associated fibroblasts (CAFs) constitute an important cell population in the microenvironment of pancreatic cancer. They can arise from disease-associated fibroblasts (DAFs) to support or restrain tumor growth. How many CAF subtypes exist and what signals drive their development is unclear. Currently, there are three commonly accepted subtypes, namely myofibroblast-like (myCAF), immunomodulatory (iCAF), and antigen-presenting (apCAF). Here, we analyzed the correlation between clinical risk factors with the proportion of each CAF subtype. In our patient cohort (n = 21), we investigated DAFs from patients with chronic pancreatitis (CP) and CAFs from pancreatic ductal adenocarcinoma (PDAC) patients after surgical resection via flow cytometry and RNA expression analysis. The expression of iCAF marker Interleukin-6 displayed significant differences depending on lifestyle factors, such as smoking status, age, and Body Mass Index (BMI). The apCAF marker HLA-DQA1 correlated with age. The largest difference showed the quantitative difference of apCAF markers in ~40% of PDAC- and ~20% of CP patients. In conclusion, clinical risk factors may influence the prevelance of specific CAF subsets. Unraveling the complex interplay between CAFs and tumor cells is crucial for novel therapies to improve long-term survival for pancreatic cancer patients.
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Registered trials
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