We are analyzing https://link.springer.com/article/10.1007/s11010-009-0267-2.

Title:
NF-κB and cancer: how intimate is this relationship | Molecular and Cellular Biochemistry
Description:
NF-κB, a transcription factor first discovered in 1986, is now known to be closely connected to the process of tumorogenesis based on a multiplicity of evidence. (1) NF-κB is activated in response to tobacco, stress, dietary agents, obesity, alcohol, infectious agents, irradiation, and environmental stimuli that account for as much as 95% of all cancers. (2) The transcription factor has been linked with transformation of cells. (3) It is constitutively active in most tumor cells. (4) It has also been linked with the survival of cancer stem cells, an early progenitor cell that has acquired self-renewal potential. (5) NF-κB regulates the expression of most anti-apoptotic gene products associated with the survival of the tumor. (6) It also regulates the gene products linked with proliferation of tumors. (7) The transcription factor controls the expression of gene products linked with invasion, angiogenesis, and metastasis of cancer. (8) While most carcinogens activate NF-κB, most chemopreventive agents suppress its activation. These observations suggest that NF-κB is intimately intertwined with cancer growth and metastasis. The mechanism that leads to constitutive activation of NF-κB in hematological, gastrointestinal, genitourinary, gynecological, thoracic head and neck, breast, and skin cancers, and the ways NF-κB is activated are the topics of discussion in this review.
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Keywords {🔍}

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Topics {✒️}

glycogen synthase kinase-3alpha/beta nuclear factor-kappab-regulated antiapoptotic nf-kappab-regulated gene products suppressing nf-kappab-regulated antiapoptotic nf-kappab-regulated gene expression nuclear factor-kappab-dependent mechanism tnfalpha-induced nf-kappab activation baff-induced nemo-independent processing nf-kappab-regulated antiapoptotic nf-kappab-inducing kinase regulates constitutive nf-kappab/rel activation month download article/chapter nuclear factor-kappab rela nf-kappab-mediated transcription noncanonical nf-kappab pathway blocks nuclear factor-kappab nuclear factor-kappabalpha kinase genes encoding tnf-beta transcription factor nf-kappab constitutive nuclear factor-kappab nuclear factor-kappab activation phosphatidylinositol 3-kinase/akt pathway anti-apoptotic gene products api2-malt1 fusion act induced nf-kappab activation inducible nuclear factor-kappab rela/nuclear factor-kappa pkcalpha-nf-kappab cascade enhances 5-fluorouracil-induced apoptosis peripheral t-cell lymphomas fas-induced cell death nmda receptor-mediated apoptosis constitutive nf-kappab signalling suppresses nf-kappab activation tnf-alpha-mediated apoptosis il1-induced nf-kappa normal fas-induced apoptosis constitutive nf-kappab activation hydrogen peroxide-induced apoptosis guggulsterone inhibits nf-kappab helicobacter pylori-infected mice activation-dependent transcriptional regulation bcr-abl-mediated transformation carcinogens activate nf-κb high-risk myelodysplastic syndrome nf-kappab-responsive genes inducible nuclear factor-kappa doxorubicin-based neoadjuvant chemotherapy inducible nf-kappab activation anthracene-induced mammary carcinogenesis

Questions {❓}

Gilmore TD, Starczynowski DT, Kalaitzidis D (2004) RELevant gene amplification in B-cell lymphomas?
Scotton CJ, Wilson JL, Milliken D, Stamp G, Balkwill FR (2001) Epithelial cancer cell migration: a role for chemokine receptors?

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