IndraLab

Statements


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"According to these findings it was suggested that the decreased miR-146a expression observed in untreated CML cells could contribute to mediate the BCR and ABL induced NFkB constitutive activation; on the other hand, the increased miR-146a expression observed following imatinib treatment, could contribute to mediate the imatinib induced NFkB inhibition [XREF_BIBR]."

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"However, CD40 inhibition alone had no direct effect on human GISTs, whereas imatinib in combination with a CD40 antagonist significantly inhibited GISTs via the nuclear factor kappa B subunit 1 (NFKB1) pathway in mice carrying a mutation in Kit exon 11 (114)."

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"Imatinib treatment inhibit IL-6, IL-8, NF-KB and AP-1 production and modulate intracellular calcium in CML patients."