PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20053726-4	2010	Sunitinib treatment resulted in the activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase and upregulation of proapoptotic genes, Bak and Bim, and inhibited the expression of survivin, an antiapoptotic protein.	Sunitinib	0-9	caspase 3	Homo sapiens	50-59	
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	caspase 3	Homo sapiens	188-197	
34216806-5	2021	RESULTS: Our study showed that treatment with sunitinib and photoirradiation at 8 mW/cm2 for 30 min resulted in the production intracellular reactive oxygen species (ROS), which is indicated by the increase in mRNA expression levels of PAI-1, NF-kappabeta, and Caspase-3.	Sunitinib	46-55	caspase 3	Homo sapiens	261-270	
16916320-5	2006	SU11248 (10 or 20 nM, 48 h) activated caspase-3 and induced apoptosis of GIST-T1 cells as measured by caspase assay, annexin V staining and cleavage of poly (ADP-ribose) polymerase.	Sunitinib	0-7	caspase 3	Homo sapiens	38-47	
33597889-7	2021	In vivo studies further confirmed that crizotinib and sunitinib decreased mitochondrial membrane potential and activated apoptosis-associated proteins (cleaved-PARP, cleaved caspase3, cytochrome c, Bcl2 and Bax).	Sunitinib	54-63	caspase 3	Homo sapiens	174-182	
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	caspase 3	Homo sapiens	318-327	
31248045-5	2019	The therapeutic benefit of the TRAIL/sunitinib combination was associated with increased apoptosis marked by enhanced caspase-3 cleavage and DNA fragmentation.	Sunitinib	37-46	caspase 3	Homo sapiens	118-127	
29435010-5	2018	The inhibition of autophagy by CQ enhanced sunitinib-induced apoptosis, which was characterized by the activation of caspase-3, caspase-9, Bcl-2 and p53.	Sunitinib	43-52	caspase 3	Homo sapiens	117-126	
27288242-11	2016	Besides, sunitinib boosted cortical and hippocampal p53 and executioner caspase-3 and decreased nuclear factor kappa B and Bcl-2 levels promoting apoptotic cell death.	Sunitinib	9-18	caspase 3	Homo sapiens	72-81	
28885866-5	2018	Of particular interest is the novel use of tyrosine kinase inhibitors (sunitinib and its derivatives) for the prevention and treatment of age-related ocular diseases via inhibition of the caspase-3, dual-leucine zipper kinase (DLK) and leucine zipper-bearing kinase (LZK) pathways.	Sunitinib	71-80	caspase 3	Homo sapiens	188-197	
28870911-5	2017	Apoptotic death induced by sunitinib in MCF7 cells was mediated by activation of caspase-3 and p53 mRNA and protein expression and an increase in the percentage of apoptotic cells (40%) as determined by flow cytometry.	Sunitinib	27-36	caspase 3	Homo sapiens	81-90	
24751611-8	2014	Furthermore, chloroquine augmented sunitinib-induced apoptosis by decreasing survivin level and increasing caspase 3 activity.	Sunitinib	35-44	caspase 3	Homo sapiens	107-116