# Inflammation and Cancer: Molecular Mechanisms and Therapeutic Targets

## TL;DR

Chronic inflammation drives cancer through internal and external mechanisms, and targeting these could lead to better cancer treatments.

## Contribution

The paper systematically integrates inflammation–tumor interaction mechanisms and proposes cell-specific inflammatory signal regulation as a future focus.

## Key findings

- Internal drivers like genomic disorder and metabolic reprogramming initiate cancer.
- External factors such as immune dysfunction and microbial dysbiosis accelerate tumor progression.
- Precision therapies targeting inflammation could improve antitumor efficacy and reduce resistance.

## Abstract

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 theoretical/practical guidance for developing precision anti‐inflammatory–antitumor therapies.

Chronic inflammation fuels tumorigenesis via “internal drivers” and “external attractions.” Targeting these core mechanisms with combined therapies/novel deliveries enables precise, potent anti‐inflammatory–antitumor treatment.