PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28842826-10 2018 Vandetanib produces a significant decrease in vascular and neuronal densities and reduction in the expression of molecules involved in survival and proliferation processes such as phospho-Akt/Akt and phospho-Erk/Erk. vandetanib 0-10 EPH receptor B2 Homo sapiens 208-211 28842826-10 2018 Vandetanib produces a significant decrease in vascular and neuronal densities and reduction in the expression of molecules involved in survival and proliferation processes such as phospho-Akt/Akt and phospho-Erk/Erk. vandetanib 0-10 EPH receptor B2 Homo sapiens 212-215 21470995-7 2011 RESULTS: XL184 and vandetanib most effectively inhibited cell proliferation, RET autophosphorylation in combination with a reduction of RET expression, and ERK phosphorylation in MTC-TT and MZ-CRC-1, respectively. vandetanib 19-29 EPH receptor B2 Homo sapiens 156-159 20139705-0 2010 ZD6474, a dual tyrosine kinase inhibitor of EGFR and VEGFR-2, inhibits MAPK/ERK and AKT/PI3-K and induces apoptosis in breast cancer cells. vandetanib 0-6 EPH receptor B2 Homo sapiens 76-79 19318229-5 2009 ZD6474 and ZD1839 inhibited EGF-induced phosphorylation of EGFR, AKT and ERK, whereas VEGF-induced phosphorylation of VEGFR2 was completely inhibited with 0.1 microM SU11248. vandetanib 0-6 EPH receptor B2 Homo sapiens 73-76 34190716-6 2021 There was no statistically significant difference in ERK activation compared with placebo (P=0.45); however, ERK activation was reduced 74% compared with pretreatment biopsy with vandetinib treatment (P=0.005) without a significant reduction in the placebo group (-29%, P=0.55). vandetanib 179-189 EPH receptor B2 Homo sapiens 109-112 34190716-11 2021 In accordance with the investigational hypothesis, there was a nonsignificant trend with vandetanib treatment of reduction in p-ERK and increased effects in Ret expressing tumors. vandetanib 89-99 EPH receptor B2 Homo sapiens 128-131