TNF: a master switch for inflammation to cancer
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Updated: Jul 4, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
Gautam Sethi1, Bokyung Sung, Bharat B Aggarwal
1Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
Abstract:
Chronic inflammation has long been associated with the development of cancer, ever since Rudolf Virchow's first observation that leukocytes were present in neoplastic tissue more than 130 years ago. Recent evidences have reignited the interest of cancer researchers in the exciting concept of an association between chronic inflammation and cancer. Tumor necrosis factor alpha (TNF-alpha), initially discovered as a result of its antitumor activity, has now been shown to be one of the major mediators of inflammation. Induced by a wide range of pathogenic stimuli, TNF-alpha induces other inflammatory mediators and proteases that orchestrate inflammatory responses. TNF-alpha is also produced by tumors and can act as an endogenous tumor promoter. The role of TNF-alpha has been linked to all steps involved in tumorigenesis, including cellular transformation, promotion, survival, proliferation, invasion, angiogenesis, and metastasis. How TNF-alpha acts as a masterswitch in establishing an intricate link between inflammation and cancer is the focus of this review.
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