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Review
. 2023 Jul 24;14(7):230-246.
doi: 10.5306/wjco.v14.i7.230.

Stromal inflammation, fibrosis and cancer: An old intuition with promising potential

Oliver Oey  1   2 , Angela Felicia Sunjaya  3 , Yasir Khan  4 , Andrew Redfern  5
Affiliations
Review

Stromal inflammation, fibrosis and cancer: An old intuition with promising potential

Oliver Oey et al. World J Clin Oncol. .

Abstract

It is now well established that the biology of cancer is influenced by not only malignant cells but also other components of the tumour microenvironment. Chronic inflammation and fibrosis have long been postulated to be involved in carcinogenesis. Chronic inflammation can promote tumorigenesis via growth factor/cytokine-mediated cellular proliferation, apoptotic resistance, immunosuppression; and free-radical-induced oxidative deoxyribonucleic acid damage. Fibrosis could cause a perturbation in the dynamics of the tumour microenvironment, potentially damaging the genome surveillance machinery of normal epithelial cells. In this review, we will provide an in-depth discussion of various diseases characterised by inflammation and fibrosis that have been associated with an increased risk of malignancy. In particular, we will present a comprehensive overview of the impact of alterations in stromal composition on tumorigenesis, induced as a consequence of inflammation and/or fibrosis. Strategies including the application of various therapeutic agents with stromal manipulation potential and targeted cancer screening for certain inflammatory diseases which can reduce the risk of cancer will also be discussed.

Keywords: Cancer; Fibrosis; Inflammation; Stroma; Tumour microenvironment.

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Conflict of interest statement

Conflict-of-interest statement: No conflicts of interest to be reported.

Figures

Figure 1
Figure 1
Schematic showing the links between inflammation, fibrosis and cancer in the tumour microenvironment. NK: Natural killer; HIF-1α: Hypoxia-inducible factor 1alpha; PI3K: Phosphatidylinositide 3-kinase; STAT3: Signal transducer and activator of transcription 3; NF-ĸB: Nuclear factor qB; Wnt: Wingless-related integration site.
See this image and copyright information in PMC

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