PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17477881-2	2007	BIN1 re-expression in the DU145 prostate cancer cell line after 5-aza-2"-deoxycytidine treatment was recently reported but no methylation of the BIN1 promoter CpG island was found in DU145.	Decitabine	64-86	bridging integrator 1	Homo sapiens	0-4	
28152502-8	2017	In addition, treatment with the de-methylation agent Decitabine (DAC) could restore Bin1 expression and evidently restrained ESCC cell malignant behaviors, particularly the epithelial mesenchymal transition (EMT) via reactivating the PTEN/AKT signaling pathway to inhibit matrix metalloproteinase (MMP)-2 and MMP-9 expression in vitro and in vivo.	Decitabine	53-63	bridging integrator 1	Homo sapiens	84-88	
28152502-8	2017	In addition, treatment with the de-methylation agent Decitabine (DAC) could restore Bin1 expression and evidently restrained ESCC cell malignant behaviors, particularly the epithelial mesenchymal transition (EMT) via reactivating the PTEN/AKT signaling pathway to inhibit matrix metalloproteinase (MMP)-2 and MMP-9 expression in vitro and in vivo.	Decitabine	65-68	bridging integrator 1	Homo sapiens	84-88	
28152502-9	2017	In conclusion, these results demonstrated that Bin1 methylation could augment the malignant biological behaviors of ESCC and predict the poor prognosis for ESCC patients, thus indicating the potential clinical application value of DAC-based de-methylation therapy in ESCC.	Decitabine	231-234	bridging integrator 1	Homo sapiens	47-51