Tumour necrosis factor and cancer
By F. Balkwill. Nature Reviews. Cancer, 2009
1,975 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d75917c5588544c74c9b2bb9c3f629937e376df0
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Citations in the corpus
- Oxidative Stress and Lipid Peroxidation Products in Cancer Progression and Therapy (2012, background): “For example, tumour-associated macrophages were shown to induce sublethal oxidative stress in murine mammary tumour cells, possibly through the secretion of the inflammatory cytokine tumour necrosis factor-α (TNF-α) [42].”
- Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability. (2009, background): “Tumor promotion by this cytokine can involve different pathways: TNF enhances tumor growth and invasion, leukocyte recruitment, angiogenesis and facilitate epithelial to mesenchymal transition [8,38,39].”
- Immunity, Inflammation, and Cancer (2010, background): “Although cytokine inhibitors alone are unlikely to cause cancer cell death, several phase I/II clinical trials currently evaluate the efficacy of anti-IL-6 and anti-TNFa drugs as single agents in various cancers (Balkwill, 2009).”
- The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer (2018, background): “Although TNF-α can induce potent necrosis in tumors, it is also an important driver of inflammatory carcinogenesis (Balkwill, 2009).”
- Cancer-related inflammation: common themes and therapeutic opportunities. (2012, background): “[29]).”
- Cell Death Pathways in Photodynamic Therapy of Cancer (2011, background): “All death receptors belong to TNFR superfamily (tumor necrosis factor receptor) [72].”
- Matrix Metalloproteinases: Regulators of the Tumor Microenvironment (2010, background): “For example, given that TNF-α contributes to progression of several sorts of cancer (Balkwill, 2009), inhibiting TNF-α activation using MPIs might dampen the inflammatory milieu at the tumor microenvironment.”