PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30410673-11	2018	Ponatinib sensitivity was restored following Axl inhibition or shRNA-mediated-knockdown of Axl, suggesting that Axl was the primary driver of resistance and a potential target for therapy in this setting.	ponatinib	0-9	AXL receptor tyrosine kinase	Homo sapiens	45-48	
30410673-11	2018	Ponatinib sensitivity was restored following Axl inhibition or shRNA-mediated-knockdown of Axl, suggesting that Axl was the primary driver of resistance and a potential target for therapy in this setting.	ponatinib	0-9	AXL receptor tyrosine kinase	Homo sapiens	91-94	
30410673-11	2018	Ponatinib sensitivity was restored following Axl inhibition or shRNA-mediated-knockdown of Axl, suggesting that Axl was the primary driver of resistance and a potential target for therapy in this setting.	ponatinib	0-9	AXL receptor tyrosine kinase	Homo sapiens	91-94	
27856601-4	2017	We investigated the therapeutic potential of Axl inhibition in CML.Experimental Design: We used primary cells from patients with CML and TKI-sensitive and -resistant BCR-ABL1+ CML cell lines and a novel ponatinib-resistant cell line KCL-22 PonR.	ponatinib	203-212	AXL receptor tyrosine kinase	Homo sapiens	45-48