Matches in Nanopublications for { ?s ?p "Mutations in the tumor suppressor gene p53 also protect tumor cells against apoptosis and increase tumor angiogenic activity. Both advantages may be overcome by antiangiogenic therapy. Tumor cells with p53 mutations may become resistant to apoptosis [55], and thus decrease their response to cytotoxic chemotherapy. In mice, p53 mutations may also decrease the response of cancer cells to antiangiogenic therapies [56]. Wild-type p53 normally suppresses tumor angiogenesis by up-regulating thrombospondin-1 [57], inducing degradation of HIF-1-alpha [58], suppressing transcription of VEGF [59] and down-regulating bFGF-binding protein expression [60]." ?g. }
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- _4 value "Mutations in the tumor suppressor gene p53 also protect tumor cells against apoptosis and increase tumor angiogenic activity. Both advantages may be overcome by antiangiogenic therapy. Tumor cells with p53 mutations may become resistant to apoptosis [55], and thus decrease their response to cytotoxic chemotherapy. In mice, p53 mutations may also decrease the response of cancer cells to antiangiogenic therapies [56]. Wild-type p53 normally suppresses tumor angiogenesis by up-regulating thrombospondin-1 [57], inducing degradation of HIF-1-alpha [58], suppressing transcription of VEGF [59] and down-regulating bFGF-binding protein expression [60]." provenance.
- _4 value "Mutations in the tumor suppressor gene p53 also protect tumor cells against apoptosis and increase tumor angiogenic activity. Both advantages may be overcome by antiangiogenic therapy. Tumor cells with p53 mutations may become resistant to apoptosis [55], and thus decrease their response to cytotoxic chemotherapy. In mice, p53 mutations may also decrease the response of cancer cells to antiangiogenic therapies [56]. Wild-type p53 normally suppresses tumor angiogenesis by up-regulating thrombospondin-1 [57], inducing degradation of HIF-1-alpha [58], suppressing transcription of VEGF [59] and down-regulating bFGF-binding protein expression [60]." provenance.