PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31196146-4	2019	Here, we demonstrate that cardiac glycoside proscillaridin A specifically targets MYC overexpressing leukemia cells and leukemia stem cells by causing MYC degradation, epigenetic reprogramming and leukemia differentiation through loss of lysine acetylation.	Glycosides	34-43	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	82-85	
32759815-10	2020	Our pursuits led us to the discovery that cardiac glycosides also decrease levels of c-MYC.	Glycosides	50-60	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	85-90	
31196146-4	2019	Here, we demonstrate that cardiac glycoside proscillaridin A specifically targets MYC overexpressing leukemia cells and leukemia stem cells by causing MYC degradation, epigenetic reprogramming and leukemia differentiation through loss of lysine acetylation.	Glycosides	34-43	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	151-154	
18794087-11	2008	CONCLUSIONS: We conclude that cardiac glycosides can dramatically suppress the transcription of KLKs and that these effects may be linked to proto-oncogene (c-myc/fos) expression.	Glycosides	38-48	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	157-162	
23150017-0	2013	Identification of cardiac glycoside molecules as inhibitors of c-Myc IRES-mediated translation.	Glycosides	26-35	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	63-68	
23150017-4	2013	This screen identified a series of cardiac glycosides as inhibitors of IRES-mediated translation using, in particular, the oncogene mRNA c-Myc IRES.	Glycosides	43-53	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	137-142