PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31227006-15	2019	CONCLUSIONS: Strategies restoring miR-126-3p expression or targeting VEGF-A or ADAM9 could restrain growth and metastasis of dabrafenib-resistant melanomas and increase their drug sensitivity.	dabrafenib	125-135	vascular endothelial growth factor A	Homo sapiens	69-75	
31227006-0	2019	miR-126-3p down-regulation contributes to dabrafenib acquired resistance in melanoma by up-regulating ADAM9 and VEGF-A.	dabrafenib	42-52	vascular endothelial growth factor A	Homo sapiens	112-118	
27748799-9	2016	Upregulated phosphorylation of MEK was observed in RAS mutated cells after dabrafenib treatment and caused VEGF upregulation, but was not related to the cellular proliferation.	dabrafenib	75-85	vascular endothelial growth factor A	Homo sapiens	107-111	
27572607-11	2016	Moreover, this inhibitor given in combination with dabrafenib efficiently counteracted the stimulating effects of the BRAFi on invasiveness and VEGF-A and MMP-9 secretion.	dabrafenib	51-61	vascular endothelial growth factor A	Homo sapiens	144-150	
25589619-6	2015	Dabrafenib and trametinib in BRAF V600E/K, and trametinib in BRAF wild-type tumor cells induced apoptosis markers, upregulated HLA molecule expression, and downregulated certain immunosuppressive factors such as PD-L1, IL1, IL8, NT5E, and VEGFA.	dabrafenib	0-10	vascular endothelial growth factor A	Homo sapiens	239-244	
27572607-8	2016	Dabrafenib reduced invasiveness, VEGFR-2 expression and VEGF-A secretion in A375 cells, whereas it increased invasiveness, VEGF-A and MMP-9 release in A375R cells.	dabrafenib	0-10	vascular endothelial growth factor A	Homo sapiens	56-62	
27572607-9	2016	In these latter cells, the stimulating effects of dabrafenib on the invasive capacity were markedly impaired by the anti-VEGF-A antibody bevacizumab, or by AKT1 silencing.	dabrafenib	50-60	vascular endothelial growth factor A	Homo sapiens	121-127