Nuclear factor-kappaB in cancer development and progression.
By M. Karin. Nature, 2006
1,722 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/b94d4b94697c338303bbbf61dfd0aed0eb7e2b01
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Citations in the corpus
- Activation and Function of the MAPKs and Their Substrates, the MAPK-Activated Protein Kinases (2011, background): “p38 can regulate cytokine expression by modulating transcription factors, such as NF- B (180), or at the mRNA level, by modulating their stability and translation through the regulation of MNK1 (44) and MK2/3 (293).”
- Role of interleukin-6 in cancer progression and therapeutic resistance (2016, background): “Pro-inflammatory cytokines (TNF-α, IL-1β) AnƟ-inflammatory molecules: IRAP, TNFsR ProliferaƟon & RegeneraƟon gp130 (IL-6Rβ) IL-6 IL-6Rα(gp80) JAK JAK”
- Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer (2007, background): “As inhibition of NF-kB also has an antitumor consequences (Karin, 2006), YopJ can inhibit concurrently at least two important pathways that promote oncogenesis.”
- miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice (2011, background): “…from detecting statistically significant enrichment, or that the majority of miR-146a targets are regulated by 1198 miR-146a prevents autoimmunity and cancer | Boldin et al. cancer are intimately linked (Balkwill and Mantovani, 2001; Coussens and Werb, 2002; Karin, 2006; Mantovani et al., 2008).”
- Dual Roles of Immune Cells and Their Factors in Cancer Development and Progression (2011, background): “TNF itself also plays an essential role in several models of cancer, and is a critical inflammatory mediator in many autoimmune diseases of both mice and humans primarily acting via induction of NF-κB (5, 6).”
- Immune evasion in cancer: Mechanistic basis and therapeutic strategies. (2015, unknown): “For example, the ris k of overt 125 hepatocellular carcinoma (HCC) appears to be closely linked to the duration of the Hepatitis B 126 and C viral-induced inflammatory state [6-9].”
- Immunity, Inflammation, and Cancer (2010, unknown): “Additional NFκB and STAT3 targets control cell and tissue resistance to stress and injury and include antimicrobial proteins (RegIIIβ, RegIIIγ, Tff3), heat shock proteins, and anti-oxidants, such as superoxide dismutase 2 (SOD2) and ferritin heavy chain (FHC) (Bollrath et al., 2009; Karin, 2006).”
- Inflammation and Cancer (2019, background): “Yet, it is only during the past decade that clear evidence has been obtained that inflammation plays a critical role in tumorigenesis.[1] However, when inflammation becomes chronic or lasts too long, it can prove harmful and may lead to disease.”
- Role of chemokines in tumor growth. (2007, background): “NF-κB may also be involved in regulation of tumor angiogenesis and invasiveness [14].”
- NF‐κB and the link between inflammation and cancer (2012, background): “Recent advances in the development of genetic mouse models of cancer and inflammation-linked cancer have provided invaluable insight into the role individual components of the NF-jB pathway play in the onset, progression and, hopefully, the eventual treatment of human cancers (4, 14, 15).”
- Cancer metastasis: building a framework. (2006, background): “(Karin, 2006).”
- Inflammation and breast cancer. Balancing immune response: crosstalk between adaptive and innate immune cells during breast cancer progression (2007, background): “A growing body of evidence has recently implicated tumor-infiltrating leukocytes as causal players in cancer development [2-8].”
- Tumors as organs: complex tissues that interface with the entire organism (2010, unknown): “The transcription factor NF-kB is a key mediator of inflammation that is important in both inflammatory and cancer cells (Karin, 2006).”
- Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. (2007, background): “Linkage between inflammatory response and cancer is thought to be primarily mediated by activation of NF-kB transcription factors (Karin, 2006).”