Inflammation and Cancer: Molecular Mechanisms and Therapeutic Targets

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Inflammation is a core pathological factor regulating tumor initiation, progression, and therapeutic resistance, and elucidating its molecular crosstalk with tumors is crucial for developing effective clinical therapies. Internal drivers of inflammation-tumor transformation include genomic disorder, epigenetic memory, mitochondrial stress, and metabolic reprogramming, which synergistically initiate carcinogenesis. External factors amplifying tumor progression cover immune dysfunction, stromal fibrosis, microbial dysbiosis, vascular neoplasia, and neurotoxicity, collectively accelerating tumor development. Notably, current therapies such as immunotherapy and chemoradiotherapy often induce inflammatory accumulation, exacerbating chemoresistance and recurrence. However, cell-specific inflammatory signal regulation and the precise balance between anti-inflammatory effects and antitumor efficacy remain understudied, hindering clinical translation of potential strategies. This review systematically organizes the "internal driving force-external attractive force" regulatory network of inflammation-induced tumors, summarizes preclinical validation of inflammatory targets and combined therapy efficacy, and proposes future focus on cell-specific inflammatory signal regulation. It fills the gap in systematically integrating inflammation-tumor interaction mechanisms and provides important

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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