PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25982012-4	2015	A co-administration strategy to enhance the brain accumulation of vandetanib by modulating P-gp/Abcb1- and Bcrp1/Abcg2-mediated efflux with mTOR inhibitors, specifically everolimus, was shown to increase the blood-brain barrier penetration.	vandetanib	66-76	mechanistic target of rapamycin kinase	Homo sapiens	140-144	
30555244-0	2018	Vandetanib (ZD6474) induces antiangiogenesis through mTOR-HIF-1 alpha-VEGF signaling axis in breast cancer cells.	vandetanib	0-10	mechanistic target of rapamycin kinase	Homo sapiens	53-57	
30555244-0	2018	Vandetanib (ZD6474) induces antiangiogenesis through mTOR-HIF-1 alpha-VEGF signaling axis in breast cancer cells.	vandetanib	12-18	mechanistic target of rapamycin kinase	Homo sapiens	53-57	
30555244-9	2018	Vandetanib can reduce both mRNA and protein level of mTOR, HIF-1 alpha, and VEGF.	vandetanib	0-10	mechanistic target of rapamycin kinase	Homo sapiens	53-57	
30555244-12	2018	Conclusion: In short, our study showed that vandetanib can control angiogenesis of breast cancer in culture via mTOR, HIF-1 alpha, and VEGF signaling pathway.	vandetanib	44-54	mechanistic target of rapamycin kinase	Homo sapiens	112-116	
27207748-8	2016	When the mTOR inhibitor everolimus was added to continued vandetanib treatment, the patient achieved a second 25% reduction of tumor volume (RECIST 1.1) for 8 months.	vandetanib	58-68	mechanistic target of rapamycin kinase	Homo sapiens	9-13	
23799852-7	2013	RESULTS: ZD6474-induced autophagy was dependent on signalling through the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway.	vandetanib	9-15	mechanistic target of rapamycin kinase	Homo sapiens	104-133	
23799852-7	2013	RESULTS: ZD6474-induced autophagy was dependent on signalling through the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway.	vandetanib	9-15	mechanistic target of rapamycin kinase	Homo sapiens	144-148	
33721621-1	2021	BACKGROUND: Preclinical studies suggest that combining vandetanib (VAN), a multi-tyrosine kinase inhibitor of rearranged during transfection (RET) proto-oncogene, vascular endothelial growth factor receptor (VEGFR), and epidermal growth factor receptor (EGFR), with everolimus (EV), a mammalian target of rapamycin (mTOR) inhibitor, may improve antitumor activity.	vandetanib	55-65	mechanistic target of rapamycin kinase	Homo sapiens	285-314	
16995874-4	2006	ZD6474 treatment also blocked the mammalian target of rapamycin (mTOR), which lies downstream of Akt and ERK.	vandetanib	0-6	mechanistic target of rapamycin kinase	Homo sapiens	34-63	
16995874-4	2006	ZD6474 treatment also blocked the mammalian target of rapamycin (mTOR), which lies downstream of Akt and ERK.	vandetanib	0-6	mechanistic target of rapamycin kinase	Homo sapiens	65-69	
16995874-5	2006	Interestingly, when ZD6474 was combined with sunitinib (SU11248; Sutent, Pfizer, Kalamazoo, MI, USA), a class III and V receptor tyrosine kinase inhibitor, the ZD6474-mediated growth inhibition was potentiated in association with further down-regulation of the mTOR targets p-p70S6K and p-4E-BP-1.	vandetanib	20-26	mechanistic target of rapamycin kinase	Homo sapiens	261-265	
33721621-1	2021	BACKGROUND: Preclinical studies suggest that combining vandetanib (VAN), a multi-tyrosine kinase inhibitor of rearranged during transfection (RET) proto-oncogene, vascular endothelial growth factor receptor (VEGFR), and epidermal growth factor receptor (EGFR), with everolimus (EV), a mammalian target of rapamycin (mTOR) inhibitor, may improve antitumor activity.	vandetanib	55-65	mechanistic target of rapamycin kinase	Homo sapiens	316-320	
33721621-1	2021	BACKGROUND: Preclinical studies suggest that combining vandetanib (VAN), a multi-tyrosine kinase inhibitor of rearranged during transfection (RET) proto-oncogene, vascular endothelial growth factor receptor (VEGFR), and epidermal growth factor receptor (EGFR), with everolimus (EV), a mammalian target of rapamycin (mTOR) inhibitor, may improve antitumor activity.	vandetanib	67-70	mechanistic target of rapamycin kinase	Homo sapiens	285-314	
33721621-1	2021	BACKGROUND: Preclinical studies suggest that combining vandetanib (VAN), a multi-tyrosine kinase inhibitor of rearranged during transfection (RET) proto-oncogene, vascular endothelial growth factor receptor (VEGFR), and epidermal growth factor receptor (EGFR), with everolimus (EV), a mammalian target of rapamycin (mTOR) inhibitor, may improve antitumor activity.	vandetanib	67-70	mechanistic target of rapamycin kinase	Homo sapiens	316-320