ReviewJournal of translational medicine2025
The type I collagen paradox in PDAC progression: microenvironmental protector turned tumor accomplice.
Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Collagenase-mediated extracellular matrix targeting for enhanced drug penetration and therapeutic efficacy in nanoscale delivery systems for cancer therapy.Journal of nanobiotechnology · 2025Pooled it
- High-Density Type I Collagen Promotes IFN-γAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The tumor microenvironment in pancreatic cancer: from composition to therapeutic targeting.Biochemical Society transactions · 2026Review
- A multi-omics integration of bulk and single-cell transcriptomics identifies and validates a 16-gene epithelial-mesenchymal transition prognostic signature in tongue squamous cell carcinoma.Translational cancer research · 2026Article
- Extracellular pH and NHE1 Regulate Ductal Branching Morphogenesis in Organotypic Cultures of Human Pancreatic Duct Epithelial Cells.Journal of cellular physiology · 2026Article
- Integrated single-cell and bulk RNA sequencing analyses identify a myeloid state-related gene signature for molecular subtyping in stomach adenocarcinoma.Frontiers in immunology · 2026Article
- Nanomedicines Reshape the Tumor Microenvironment: Multidimensional Strategies from Modulating "Barriers" to Metabolic Intervention.International journal of nanomedicine · 2026Review
- Bidirectional Endothelial Feedback Drives Turing-Vascular Patterning and Drug-Resistance Niches: A Hybrid PDE-Agent-Based Study.Bioengineering (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Type I collagen (Collagen I, Col I), a principal component of the tumor extracellular matrix (ECM) that accounts for 80% of total ECM collagen, has emerged as a crucial factor in tumor biology. Recent research has found that Col I has influenced tumor growth, invasion, migration, and prognosis by forming a physical barrier and interacting with components in the tumor microenvironment (TME). Pancreatic ductal adenocarcinoma (PDAC) is characterized by a prominent stromal microenvironment with remarkable cellular and spatial heterogeneity, which significantly impacts the biology of the disease and its resistance to treatment. As research on the influence of ECM on tumor behavior progresses, the role of Col I in tumor occurrence and development has also been gradually expounded. Unlike the pro-tumorigenic role caused by excessive deposition in other cancers, PDAC features a dense stroma with spatial heterogeneity, where Col I deposition exhibits paradoxical pro- and anti-tumor effects: Cancer-associated fibroblasts secrete heterotrimeric Col I (α1/α1/α2), which initially suppresses tumor growth by recruiting M1 macrophages, while tumor cells produce homotrimeric Col I (α1/α1/α1, 2-3% of total Col I) to promote immune evasion via CXCL5 secretion and CD8
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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.