PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25116350-0	2014	Up-regulation of P21 inhibits TRAIL-mediated extrinsic apoptosis, contributing resistance to SAHA in acute myeloid leukemia cells.	Vorinostat	93-97	H3 histone pseudogene 16	Homo sapiens	17-20	
25116350-2	2014	In this study we examined the effect of altered p21 expression on the sensitivity of acute myeloid leukemia cells in response to HDAC inhibitor SAHA treatment and investigated the underlying mechanism.	Vorinostat	144-148	H3 histone pseudogene 16	Homo sapiens	48-51	
25116350-8	2014	Enforced expression of p21 in HL60 cells reduced sensitivity to SAHA and blocked TRAIL-mediated apoptosis.	Vorinostat	64-68	H3 histone pseudogene 16	Homo sapiens	23-26	
25116350-9	2014	Conversely, p21 silencing in NB4 cells enhanced SAHA-mediated apoptosis and lethality.	Vorinostat	48-52	H3 histone pseudogene 16	Homo sapiens	12-15	
25116350-10	2014	Finally, we found that combined treatment with SAHA and rapamycin down-regulated p21 and enhanced apoptosis in AML cells.	Vorinostat	47-51	H3 histone pseudogene 16	Homo sapiens	81-84	
25116350-11	2014	CONCLUSION: We conclude that up-regulated p21 expression mediates resistance to SAHA via inhibition of TRAIL apoptotic pathway.	Vorinostat	80-84	H3 histone pseudogene 16	Homo sapiens	42-45	
25116350-12	2014	P21 may serve as a candidate biomarker to predict responsiveness or resistance to SAHA-based therapy in AML patients.	Vorinostat	82-86	H3 histone pseudogene 16	Homo sapiens	0-3	
25116350-13	2014	In addition, rapamycin may be an effective agent to override p21-mediated resistance to SAHA in AML patients.	Vorinostat	88-92	H3 histone pseudogene 16	Homo sapiens	61-64