IKKbeta couples hepatocyte death to cytokine-driven compensatory proliferation that promotes chemical hepatocarcinogenesis.

By S. Maeda, H. Kamata, Jun-Li Luo, H. Leffert, M. Karin. Cell, 2005

1,232 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/1f95f51fa5956008684786f6ba0466cf616571ad

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The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. A. Mantovani
2. M. Karin
3. A. Sica
4. P. Allavena
5. N. Perkins
6. F. Balkwill
7. F. Colotta
8. F. Greten

Citations in the corpus

• Cancer-related inflammation (2008, background): “It should be noted that genetic targeting of NF-κB in liver epithelial cells can have divergent effects in different models of carcinogenesis, possibly depending on the balance between promoting apoptosis that has already been initiated and triggering compensatory cell proliferatio”
• NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma (2011, result): “In contrast to the studies discussed above, NF-κB inhibition by deletion of IKK2 in hepatocytes resulted in increased liver tumor formation in the genotoxic diethylnitrosamine (DEN) tumor model”
• Tumors as organs: complex tissues that interface with the entire organism (2010, unknown): “These cytokines stimulate compensatory proliferation of the surviving hepatocytes, some of which will have carcinogen-induced mutations with the potential to generate transformed progeny (Maeda et al., 2005).”
• Cancer-related inflammation: common themes and therapeutic opportunities. (2012, background): “[34]; in a model where chemical damage led to liver cancer, Kupffer cell-derived TNF was one of the mitogens driving proliferation of hepatocytes in which DNA damage had already been caused by the carcinogenic agent diethylnitrosamine [35].”
• Upsides and Downsides of Reactive Oxygen Species for Cancer: The Roles of Reactive Oxygen Species in Tumorigenesis, Prevention, and Therapy (2012, unknown): “Induction of cell proliferation In vitro studies H2O2 Exogenous Hepatoma PKB [ , ERK [ (195) ROS MMA Bladder COX-2 [ (84) Arsenite Breast c-Myc [, HO-1 [, NF-jB [ (262) Endogenous Lung ERK [ (224) Superoxide Endogenous Hepatoma PI3K/AKT [ (78) ROS Endogenous Breast PTEN Y, PI3K [ (70) Superoxide SOD”
• Mechanisms of Liver Injury. I. TNF-α-induced liver injury: role of IKK, JNK, and ROS pathways (2006, background): “This differential role of IKK/ NF- B in hepatocytes and Kupffer cells was recently demonstrated in the diethylnitrosamine model of hepatocarcinogenesis: a hepatocyte-specific deletion of IKK- increased ROS production, JNK activation, and hepatocyte death (24).”