ReviewNeoplasia (New York, N.Y.)2026
From inflammation to malignancy: the dynamic evolution of cancer-associated fibroblasts in IBD-CRC.
Review in Neoplasia (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
6 authors.
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Abstract
Inflammatory bowel disease-associated colorectal cancer (IBD-CRC) represents a distinct clinical and molecular entity characterized by long-standing inflammation and a unique "dysplasia-carcinoma" sequence. While epithelial genetic alterations are well-documented, the role of the mesenchymal stroma as a dynamic driver of malignant transformation remains underappreciated. In this review, we propose a conceptual framework where intestinal fibroblasts contribute significantly to niche construction as key components of the Tumor Microenvironment (TME) architecture. These cells are not merely passive scaffolds but dynamically co-evolve with the epithelium and immune compartment, transitioning into active orchestrators of the pre-malignant niche. We highlight the emerging concept of "stromal inflammatory memory," which is hypothesized to be encoded through stable epigenetic imprinting and persistent metabolic reprogramming, characterized by a PFKFB3-mediated glycolytic shift. This metabolic priming sustains a pro-tumorigenic environment even during clinical remission. We further delineate how the loss of apical polarity regulators, such as aPKC, triggers a cascade of epithelial-stromal crosstalk involving chronic microbial sensing and hyaluronan-driven signaling. This co-evolution leads to the diversification of cancer-associated fibroblast (CAF) subsets, including inflammatory (iCAF), myofibroblastic (myCAF), and antigen-presenting (apCAF) populations. These subsets collectively orchestrate immune evasion via T-cell exhaustion and physical immune exclusion. Finally, we discuss the clinical implications of the "Reverse Warburg Effect" and exosome-mediated chemoresistance. We emphasize that effective therapeutic strategies must transcend epithelial-centric models to target the stromal axis. By integrating recent advances in single-cell and spatial transcriptomics, we identify novel opportunities for "stromal reprogramming" through metabolic, epigenetic, and senomorphic interventions to prevent and treat IBD-CRC.
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