NF-kappaB and cancer-identifying targets and mechanisms.

By W. Naugler, M. Karin. Current Opinion in Genetics and Development, 2008

616 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/dea944fd7e505445cf40e300be4c9d20500b3443

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Citations in the corpus

MicroRNAs — the micro steering wheel of tumour metastases (2009, background): “NF-κB constitutive activation is common to different types of cancers and, besides having a crucial role in promoting malignant proliferation, evasion from apoptosis and angiogenesis, it has been shown to take part in EMT, inducing genes such as Twist, ZEB1 , ZEB2 , vimentin , MMPs, cathepsin B ”
Inflammatory Networks during Cellular Senescence: Causes and Consequences (2010, background): “Thus, IL-1α triggers the formation of a complex between IL-1R and its coreceptor, activating a signaling cascade that ultimately permits nuclear translocation of NF-κB [66].”
An epigenetic switch involving NF-κB, Lin28, let-7 microRNA, and IL6 links inflammation to cell transformation (2009, positive): “Clinical and epidemiological studies have suggested a strong association between inflammation and different types of cancer, and inflammatory molecules can provide growth signals that promote the proliferation of malignant cells (Balkwill and Mantovani, 2001; Naugler and Karin, 2008; Pierce et al., ”
The eIF2α kinases: their structures and functions (2013, positive): “Considering the link between PERK signaling and cancer progression discussed above and the acknowledged role of NF-κB in promoting the growth of malignant cells [135], PERK’s cytoprotective effects in tumorigenesis may at least partly be mediated by NF-κB activity.”
Role of interleukin-6 in cancer progression and therapeutic resistance (2016, neutral): “well as progression of oncogenesis [18].”