Why Does Cancer Metastasize?
7 月 7, 2026Core Framework & Diagram How Does Inflammation Promote Cancer?
7 月 7, 2026
How Does Inflammation Promote Cancer?
Inflammation is life's fire — but burning too long, it can cook normal cells into cancer cells
Have you wondered why hepatitis B patients are more prone to liver cancer? Why long-term H. pylori infection leads to gastric cancer? Why inflammatory bowel disease patients have colorectal cancer risk several times that of ordinary people? Why obesity (essentially a state of chronic low-grade inflammation) correlates with elevated risk for over a dozen cancers?
All these questions point to one answer: chronic inflammation is cancer's 'accomplice.' In 1863, great German pathologist Rudolf Virchow observed large amounts of white blood cells infiltrating cancer tissue and proposed a prescient hypothesis: cancer originates from chronic inflammation. Today's molecular immunology confirms his basic intuition: chronic inflammation pushes normal cells toward cancer through continuous DNA damage, pro-proliferative signals, immunoediting pressure, and immunosuppressive microenvironments.
The World Health Organization estimates approximately twenty to twenty-five percent of global cancer incidence is related to chronic inflammation.
核心要点
01
Chronic inflammation promotes cancer via four mechanisms: persistent DNA damage (ROS/RNS random attack, exceeding DNA repair capacity), pro-proliferative signal activation (IL-6/STAT3, COX-2/PGE2 suppressing apoptosis), immunosuppressive microenvironment shaping (TGF-β, M2-TAMs suppressing immune surveillance), and epigenetic reprogramming (silencing tumor suppressor genes).
02
NF-κB is the 'master switch' connecting inflammation and cancer, simultaneously driving pro-proliferative (Cyclin D1), anti-apoptotic (BCL-2), pro-angiogenic (VEGF), and more inflammatory gene activation — chronic inflammation's self-amplifying cycle ultimately converts 'firefighting tools' into 'cancer-promoting engines.'
03
COX-2/PGE2 suppresses cell apoptosis, letting cells that have accumulated carcinogenic mutations 'not want to die.' COX-2 is highly expressed in eighty percent of colorectal cancers — the molecular basis for NSAIDs (aspirin, celecoxib) showing colorectal cancer protective effects epidemiologically.
04
Obesity is the largest-scale 'chronic inflammation-cancer' case: confirmed associated with elevated risk in thirteen cancer types; three carcinogenic pathways (visceral fat inflammation, high insulin/IGF-1 promoting proliferation, adipose tissue estrogen) synergistically drive multiple cancers.
05
Acute inflammation (brief, intense) has protective effects against cancer. Chronic inflammation (persistent, low-grade) is a definitive cancer promoter — distinguishing the two is crucial. Managing chronic inflammation (controlling weight, regular exercise, treating chronic infections, healthy diet) is a powerful cancer primary prevention strategy.
Art 76
Chronic Inflammation and Cancer
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Art 77
How Does the Tumor 'Turn Off' Immune Switches?
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