Ntrol transfected cells; however, cells with reduced IGFBP3 expression were partially resistant to the cytotoxic effects of imatinib. Taken together, this data suggests that IGFBP3 sensitizes GIST882 cells to the anti-tumor effects of imatinib. In contrast to GIST882 cells, GIST-T1 cells have no endogenous IGFBP3 expression and there was no induction of IGFBP3 after imatinib treatment. Therefore,
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