PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35209965-12	2022	Mechanistically, afatinib effectively reduced the protein expression levels of HER2 and HER3 and inhibited EGFR phosphorylation, thereby enhancing the effect of MDV3100 and suppressing CRPC.	enzalutamide	161-168	epidermal growth factor receptor	Homo sapiens	107-111	
34681618-8	2021	Afatinib diminished AKT phosphorylation at 30 min and 6 h in the EGFR- and EGFRvIII-overexpressing cells, respectively, and decreased AR phosphorylation in EGFR-overexpressing cells at 4 h. Afatinib or MK2206 combination therapy with the AR antagonist enzalutamide in the EGFR and EGFRvIII-overexpressing cells had synergistic efficacy.	enzalutamide	252-264	epidermal growth factor receptor	Homo sapiens	65-69	
34681618-8	2021	Afatinib diminished AKT phosphorylation at 30 min and 6 h in the EGFR- and EGFRvIII-overexpressing cells, respectively, and decreased AR phosphorylation in EGFR-overexpressing cells at 4 h. Afatinib or MK2206 combination therapy with the AR antagonist enzalutamide in the EGFR and EGFRvIII-overexpressing cells had synergistic efficacy.	enzalutamide	252-264	epidermal growth factor receptor	Homo sapiens	156-160	
34681618-8	2021	Afatinib diminished AKT phosphorylation at 30 min and 6 h in the EGFR- and EGFRvIII-overexpressing cells, respectively, and decreased AR phosphorylation in EGFR-overexpressing cells at 4 h. Afatinib or MK2206 combination therapy with the AR antagonist enzalutamide in the EGFR and EGFRvIII-overexpressing cells had synergistic efficacy.	enzalutamide	252-264	epidermal growth factor receptor	Homo sapiens	272-276	
25713333-6	2015	Furthermore, mechanistic analysis reveals that AR activation upregulates secretion of the EGFR ligand amphiregulin (AREG), an effect abrogated by enzalutamide in vitro and in vivo.	enzalutamide	146-158	epidermal growth factor receptor	Homo sapiens	90-94	
31566139-9	2019	CONCLUSION: By targeting AR and EGFR using a potent AR inhibitor such as Enzalutamide, we postulate the possible crosstalk between EGFR and AR pathways in GC.	enzalutamide	73-85	epidermal growth factor receptor	Homo sapiens	32-36	
31566139-9	2019	CONCLUSION: By targeting AR and EGFR using a potent AR inhibitor such as Enzalutamide, we postulate the possible crosstalk between EGFR and AR pathways in GC.	enzalutamide	73-85	epidermal growth factor receptor	Homo sapiens	131-135	
26487496-9	2015	Constitutive and Tam-induced phosphorylation of EGFR and ERK1/2 was blocked by the AR antagonist Enzalutamide, suggesting that AR-mediated EGFR activation was a mechanism of resistance in these cells.	enzalutamide	97-109	epidermal growth factor receptor	Homo sapiens	48-52	
26487496-9	2015	Constitutive and Tam-induced phosphorylation of EGFR and ERK1/2 was blocked by the AR antagonist Enzalutamide, suggesting that AR-mediated EGFR activation was a mechanism of resistance in these cells.	enzalutamide	97-109	epidermal growth factor receptor	Homo sapiens	139-143	
26487496-10	2015	Constitutive ERalpha phosphorylation and transcriptional activity was inhibited by Enzalutamide and the EGFR inhibitor gefitinib, demonstrating that AR-mediated EGFR signaling activated ERalpha.	enzalutamide	83-95	epidermal growth factor receptor	Homo sapiens	161-165	
29340039-6	2017	Amongst the pathways enriched in the enzalutamide-resistant cells were those associated with MEK, EGFR, RAS, and NFKB.	enzalutamide	37-49	epidermal growth factor receptor	Homo sapiens	98-102