PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30012673-4	2018	Here, we demonstrate that BMX expression in prostate cancer is suppressed directly by AR via binding to the BMX gene and that BMX expression is subsequently rapidly increased in response to ADT.	1,4-androstadiene-3,17-dione	190-193	BMX non-receptor tyrosine kinase	Homo sapiens	26-29	
30012673-8	2018	These data indicate that increased BMX in response to ADT contributes to enhanced tyrosine kinase signaling and the subsequent emergence of CRPC, and that combination therapies targeting AR and BMX may be effective in a subset of patients.Significance: The tyrosine kinase BMX is negatively regulated by androgen and contributes to castration-resistant prostate cancer by enhancing the phosphorylation and activation of multiple receptor tyrosine kinases following ADT.	1,4-androstadiene-3,17-dione	54-57	BMX non-receptor tyrosine kinase	Homo sapiens	35-38