ReviewDrug design, development and therapy2026
Cancer-Associated Fibroblasts in Gastrointestinal Cancer Metastasis: Mechanisms and Emerging Therapeutic Strategies.
Review in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis is the primary cause of mortality across gastrointestinal (GI) cancers, including colorectal, gastric, pancreatic, biliary and esophageal cancers. Cancer-associated fibroblasts (CAFs) constitute the dominant stromal component of the desmoplastic GI tumor microenvironment (TME) and regulate every stage of metastatic progression. This review systematically summarizes CAF-mediated pro-metastatic mechanisms in GI tumors, including extracellular matrix (ECM) remodeling, paracrine oncogenic signaling, immune exclusion, angiogenesis, lymphangiogenesis, pre-metastatic niches (PMNs) construction and therapeutic resistance. Notably, CAFs are heterogeneous populations with context-dependent dual functions: certain myofibroblastic CAF (myCAF) subsets restrain tumor progression in pancreatic ductal adenocarcinoma (PDAC), while inflammatory CAFs (iCAFs) drive metastasis and immune suppression. Antigen-presenting CAFs (apCAFs) exert divergent immunomodulatory effects depending on tumor context. Rather than acting as uniformly tumor-promoting stromal cells, CAFs represent heterogeneous and plastic populations whose functions vary by tumor type, spatial niche, and metastatic stage. We further discuss why broad CAF depletion has shown limited clinical success and emphasize the need for subtype-specific, context- aware CAF-targeted strategies.
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