PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23063977-1	2012	The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis.	Azacitidine	68-73	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	222-227	
25319547-0	2014	5-azacytidine inhibits nonsense-mediated decay in a MYC-dependent fashion.	Azacitidine	0-13	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	52-55	
25319547-5	2014	Moreover, this activity of 5-azacytidine depends on the induction of MYC expression, thus providing a link between the effect of this drug and one of the key cellular pathways that are known to affect NMD activity.	Azacitidine	27-40	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	69-72	
25061731-9	2014	5-Azacytidine suppressed the proliferation of pancreatic cancer cells by inhibiting the Wnt/beta-catenin signaling pathway, particularly the expression of beta-catenin, c-myc, and cyclinD1.	Azacitidine	0-13	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	169-174	
10914736-8	2000	Western blot analyses revealed that 5-aza-CR reactivated p16 expression and repressed c-Myc expression in TSU-PR1 cells but not in DU-145 cells.	Azacitidine	36-44	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	86-91	
23300844-5	2012	Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes.	Azacitidine	9-14	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	212-215	
22672838-9	2012	Finally, EMSA and ChIP confirmed that the methylation of the CGCG (-695 to -692) site prevented c-Myc from binding of the site and demethylation treatment of the 5" flanking region of MYCT1 by 5-aza induced the increased occupation of the core promoter by c-Myc (p < 0.01).	Azacitidine	193-198	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	96-101	
22672838-9	2012	Finally, EMSA and ChIP confirmed that the methylation of the CGCG (-695 to -692) site prevented c-Myc from binding of the site and demethylation treatment of the 5" flanking region of MYCT1 by 5-aza induced the increased occupation of the core promoter by c-Myc (p < 0.01).	Azacitidine	193-198	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	256-261	
10914736-10	2000	These findings suggest that 5-aza-CR inhibits telomerase activity via transcriptional repression of hTERT, in which p16 and c-Myc may play a key role.	Azacitidine	28-36	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	124-129	
25487600-0	2015	Overexpression of GYS1, MIF, and MYC is associated with adverse outcome and poor response to azacitidine in myelodysplastic syndromes and acute myeloid leukemia.	Azacitidine	93-104	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	33-36	
34405020-8	2021	5-Aza also increased p53 and p21 transcription through promoter demethylation, and decreased the expression of oncogene c-Myc in 22RV1 and LNCaP cells.	Azacitidine	0-5	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	120-125	
34405020-11	2021	Thus, in responsible for its apoptotic induction and DNA damage, the mechanism of the antitumor activities of 5-Aza may involve in an increase of tumor suppressive maspin, upregulation of wild type p53-mediated p21 expression and a decrease of oncogene c-Myc level in 22RV1 and LNCaP cells, and enhancing the tumor suppressive maspin expression in DU145 cells.	Azacitidine	110-115	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	253-258	
2425967-0	1986	Methylation and expression of c-myc and c-abl oncogenes in human leukemic K562 cells before and after treatment with 5-azacytidine.	Azacitidine	117-130	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	30-35	
34837933-9	2021	In addition, mRNA analyses demonstrated that MOLT4 and jurkat cells, expressed p53 gene more than 10-fold higher compared with untreated cells in three independent experiments while the cells suppressed the expression of a subset of functionally related genes including MYC, BCL2, APEX, SIRT1, SNAIL1 and vimentin to some extent, following 5-AZA treatment.	Azacitidine	340-345	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	270-273