PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16444746-1	2006	BACKGROUND: The objective of this study was to evaluate the ability of the clinically available histone deacetylase (HDAC) inhibitor valproate to enhance the cytotoxicity of the Bcr-Abl inhibitor imatinib in imatinib-resistant cell lines.	Valproic Acid	133-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185	
16444746-5	2006	Coexposure of cells to valproate and imatinib was associated with repression of several genes involved in Bcr-Abl transformation.	Valproic Acid	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113	
16444746-6	2006	In particular, the combination valproate-imatinib downregulated the expression of Bcr-Abl and the antiapoptotic protein Bcl-2, which is particularly overexpressed in imatinib-resistant clones.	Valproic Acid	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89