Research on cancer development now firmly positions chronic inflammation as a central factor driving tumor initiation, malignant progression, and metastasis. Persistent inflammatory states—from chronic infections to autoimmune conditions—elevate the risk of multiple cancer types, reflecting historic and contemporary observations of immune cell infiltration in tumors. Within the tumor microenvironment, inflammatory cells and cytokines release bioactive factors that enhance malignant cell survival, promote angiogenesis, and contribute to immune evasion. Moreover, epidemiological evidence demonstrates the cancer-lowering effects of anti-inflammatory interventions. Inflammation also provokes metabolic rewiring that supports tumor growth and adaptability. These multifaceted interactions reveal critical knowledge gaps concerning how inflammation orchestrates the cellular and molecular events underlying cancer, particularly concerning mechanisms governing cell death, immune function, and metabolic control.

This Research Topic aims to advance our understanding of how inflammation influences cancer biology through the interconnected regulation of cell death modalities, immune landscape, and metabolic pathways. The central objective is to dissect the dual nature of inflammation-induced cell death forms, such as pyroptosis and necroptosis, which may either promote antitumor immunity or facilitate immune escape and tumor expansion depending on context. The Topic also seeks to clarify how inflammatory cues create an immunosuppressive tumor niche, as well as how inflammatory cytokines and metabolites reshape the metabolic profiles of cancer and immune cells alike. By integrating approaches that span cell death, tumor immunology, and cancer metabolism, we hope to uncover principles that explain when and how inflammation transitions from tumor-promoting to tumor-inhibiting, with the ultimate aim of providing new conceptual frameworks and future therapeutic directions.

Research covered by this Topic is limited to cellular, molecular, and mechanistic studies at the convergence of inflammation, cancer, and their shared downstream pathways, while a focus on foundational biomedical science is prioritized. To gather further insights in these domains, we welcome articles addressing, but not limited to, the following themes:

o The contribution of chronic inflammation to tumor initiation and progression.

o Mechanistic links between inflammatory signals and cell death pathways (apoptosis, necroptosis, pyroptosis) in cancer.

o Crosstalk between the inflammatory tumor microenvironment and immune surveillance or immunosuppression.

o Metabolic reprogramming induced by inflammation in cancer and immune cells.

o Approaches to modulate inflammation from a tumor-promoting to a tumor-restraining state.

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Linking Chronic Inflammation to Cancer: New Insights in Cell Death, Immune Response and Metabolism