NF-κB functions as a tumour promoter in inflammation-associated cancer

By E. Pikarsky, R. Porat, I. Stein, R. Abramovitch, S. Amit, Shafika Kasem, Elena Gutkovich-Pyest, S. Urieli-Shoval, E. Galun, Y. Ben‐Neriah. Nature, 2004

2,287 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/b229bdd4c169cdf7958313823397a253e4b8e186

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Citations in the corpus

Mortality in COPD: role of comorbidities (2006, background): “A number of additional experimental studies indicate that NF-kB may be essential for promoting inflammation-associated cancers [ 56 , 57].”
Cancer-related inflammation (2008, background): “There is unequivocal evidence that NF-κB is involved in tumour initiation and progression in tissues in which cancer-related inflammation typically occurs (such as the gastrointestinal tract and the liver”
The H19 Non-Coding RNA Is Essential for Human Tumor Growth (2007, background): “. In this specific model of inflammation-induced tumors, we provided evidence that NFκB has a role in HCC progression”
Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability. (2009, background): “[11,17,18].”
NF-κB represses E-cadherin expression and enhances epithelial to mesenchymal transition of mammary epithelial cells: potential involvement of ZEB-1 and ZEB-2 (2007, background): “For example, while NF-kB is not required for the initiation, it is required for the progression of hepatocellular carcinoma (Pikarsky et al., 2004).”
Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “The significance of NF-kB activation in cancer cells is evident from the results obtained in inflammationassociatedmodels of cancer (Karin & Greten, 2005; Pikarsky et al, 2004).”
Novel insights into Notum and glypicans regulation in colorectal cancer (2015, background): “, the NFKB, IL-10, IL-6, TNFA and TGFβ genes [29, 30].”
Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes. (2014, background): “Thus, similar to other models of inflammation-induced liver cancer (Haybaeck et al., 2009; Pikarsky et al., 2004), canonical NF-kB and LTbR signaling are critical, hepatocyte-intrinsic modulators of NASH to HCC transition but have distinct functions with regard to hepatic lipid uptake.”