IndraLab

Statements



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"Recent evidence also suggests that platelets may play a more active role in promoting metastatic spread outside of the primary tumour 's microenvironment by active signalling to tumour cells through the TGF-B and NF-Kb pathways resulting in a pro metastatic phenotype that facilitates tumour cell extravasation and metastasis formation [XREF_BIBR], and aspirin is known to inhibit the activation of NF-Kb [XREF_BIBR]."

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"Aspirin reduces the production of NF-KB, and at the same time inhibits the breakdown of its inhibitor (Kopp and Ghosh, 1994)."

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"It has been demonstrated, in human and mouse cell lines, that aspirin and sodium salicylate inhibit the activation of NFKB without af- fecting other transcription factors (Kopp and Ghosh, 1994)."

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"Aspirin and sodium salicylate inhibit activation of NF-KB by blocking IkappaB kinase, a key enzyme in NF-kappaB activation."

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"Aspirin and salicylates prevent activation of NFkB [XREF_BIBR], making them potentially very useful."

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"It is pertinent that the NSAIDs aspirin and salicylate have long been known to also inhibit NFkB signaling by blocking IKKbeta activity [XREF_BIBR], most probably via the same thiol-reactive quinone type of irreversible binding interaction."

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"Aspirin and sodium salicylate inhibit activation of NFkB by blocking IkB kinase [48]."

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"It is known that aspirin decreases NFkB activity XREF_BIBR."

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"In addition it has been shown that the anti- inflammatory drug aspirin can inhibit the activation of NF-KB [16]."