Academic Journal
Cancer-associated and non-neoplastic fibrosis: Comparative mechanisms and emerging antifibrotic strategies.
| Τίτλος: | Cancer-associated and non-neoplastic fibrosis: Comparative mechanisms and emerging antifibrotic strategies. |
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| Συγγραφείς: | Riccò B; Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy; Division of Oncology, Department of Oncology and Haematology, Modena AOU - Hospital, Modena, Italy; Department of Oncology, IRCCS San Raffaele Scientific Institute Hospital, Milan, Italy. Electronic address: beatrice.ricco3@gmail.com., Grisendi G; Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy., Monaco AL; Rheumatology Unit, AOU S. Anna, Ferrara, Italy., Giuggioli D; Rheumatology Unit, Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy., Clini E; Lung and Respiratory Intensive Care Unit, Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy., Dominici M; Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy; Division of Oncology, Department of Oncology and Haematology, Modena AOU - Hospital, Modena, Italy. Electronic address: massimo.dominici@unimore.it. |
| Πηγή: | Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [Biomed Pharmacother] 2026 Jul; Vol. 200, pp. 119626. Date of Electronic Publication: 2026 Jun 07. |
| Τύπος έκδοσης: | Journal Article; Review |
| Γλώσσα: | English |
| Στοιχεία περιοδικού: | Publisher: Editions Scientifiques Elsevier Country of Publication: France NLM ID: 8213295 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1950-6007 (Electronic) Linking ISSN: 07533322 NLM ISO Abbreviation: Biomed Pharmacother Subsets: MEDLINE |
| Imprint Name(s): | Publication: Paris : Editions Scientifiques Elsevier Original Publication: New York, N.Y. : Masson Pub. USA, Inc., c1982- |
| Ιατρικοί όροι (MeSH): | Antifibrotic Agents*/therapeutic use , Antifibrotic Agents*/pharmacology , Cancer-Associated Fibroblasts*/pathology , Cancer-Associated Fibroblasts*/metabolism , Cancer-Associated Fibroblasts*/drug effects , Idiopathic Pulmonary Fibrosis*/pathology , Idiopathic Pulmonary Fibrosis*/drug therapy , Idiopathic Pulmonary Fibrosis*/metabolism , Neoplasms*/pathology , Neoplasms*/drug therapy , Neoplasms*/metabolism, Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Extracellular Matrix/drug effects ; Fibrosis/drug therapy ; Animals ; Humans ; Signal Transduction |
| Περίληψη: | Fibrosis is a maladaptive tissue-remodeling process characterized by persistent fibroblast activation, excessive extracellular matrix deposition, and progressive tissue stiffening. Beyond non-neoplastic disorders, fibrosis is also a hallmark of several solid tumors, where it promotes immune evasion, impaired drug delivery, and therapeutic resistance, particularly in pancreatic, hepatocellular, colorectal, and triple-negative breast cancers. In this review, we comparatively analyze fibrosis across non-neoplastic and neoplastic conditions, using idiopathic pulmonary fibrosis as a reference model and comparing it with highly fibrotic tumors. We focus on conserved biological pathways, including TGF-β signaling, ECM remodeling, mechanotransduction, and fibroblast-to-myofibroblast activation, as well as on stromal heterogeneity and the role of cancer-associated fibroblast subsets in tumor progression and immune modulation. We also critically discuss current antifibrotic therapeutic strategies targeting ECM components, fibroblast activation, stromal signaling, and tumor-stroma interactions, highlighting both preclinical rationale and translational limitations. Finally, we examine emerging approaches such as mesenchymal stromal cell-based platforms and drug repurposing strategies bridging oncology and fibrotic diseases. Overall, this review underscores how comparative analysis of cancerous and non-cancerous fibrosis may help identify shared therapeutic vulnerabilities, while supporting the development of context-specific antifibrotic interventions. (Copyright © 2026. Published by Elsevier Masson SAS.) |
| Competing Interests: | Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Massimo Dominici reports financial support was provided by Dipartimenti Eccellenti MIUR 2022. Massimo Dominici, Giulia Grisendi, Dilia Giuggioli, Enrico Clini reports financial support was provided by European Union - NextGenerationEU. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The views and opinions expressed are those of the authors only and do not necessarily reflect those of the European Union or the European Commission. Neither the European Union nor the European Commission can be held responsible for them. |
| Contributed Indexing: | Keywords: Cancer-associated fibroblasts; Extracellular matrix; Fibrosis; Idiopathic pulmonary fibrosis; Lung cancer; Mesenchymal stromal cells; Pancreatic cancer |
| Substance Nomenclature: | 0 (Antifibrotic Agents) |
| Entry Date(s): | Date Created: 20260607 Date Completed: 20260619 Latest Revision: 20260624 |
| Update Code: | 20260624 |
| DOI: | 10.1016/j.biopha.2026.119626 |
| PMID: | 42251804 |
| Βάση Δεδομένων: | MEDLINE |
| ISSN: | 1950-6007 |
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| DOI: | 10.1016/j.biopha.2026.119626 |