PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29728077-11	2018	Consequently, sequential treatment with Adriamycin/Cyclophosphamide (AC) cytotoxic drugs to generate resistant cells indicated that BT-474 NRP-1 cells increased sensitivity to treatment by inactivating NRP-1/ITGB3/FAK/Akt/NF-kB p65 signaling compared to wild-type BT-474 resistant cells.	Cyclophosphamide	51-67	neuropilin 1	Homo sapiens	139-144	
31106153-7	2019	In vitro validation of the former result showed an increase in the secreted and cellular NRP-1 levels in resistant MDA-MB-231 cells to the most common NAC regimen Adriyamicin/cyclophosphamide+Paclitaxel (AC+PAC).	Cyclophosphamide	175-191	neuropilin 1	Homo sapiens	89-94	
31883395-7	2020	Adriyamicin/cyclophosphamide and Paclitaxel resistant MDA-MB-231 cells activated NRP-1/TNC/Integrin beta3/FAK/NF-kappaBp65 axis and displayed a decrease in breast cancer resistant protein (BCRP/ABCB2).	Cyclophosphamide	12-28	neuropilin 1	Homo sapiens	81-86	
31883395-8	2020	In turn, resistant MCF7 cells to Adriamycin/cyclophosphamide (4xAC), induced HER2 expression which converted MCF7 subtype from being a luminal A to luminal B-HER2 type, upregulated NRP-1, ER-alpha, and EGFR and activated PI3K/AKT/NF-kappaBp65 axis.	Cyclophosphamide	44-60	neuropilin 1	Homo sapiens	181-186	
29728077-11	2018	Consequently, sequential treatment with Adriamycin/Cyclophosphamide (AC) cytotoxic drugs to generate resistant cells indicated that BT-474 NRP-1 cells increased sensitivity to treatment by inactivating NRP-1/ITGB3/FAK/Akt/NF-kB p65 signaling compared to wild-type BT-474 resistant cells.	Cyclophosphamide	51-67	neuropilin 1	Homo sapiens	202-207	
29728077-12	2018	CONCLUSIONS: We thus report a novel mechanism correlating high baseline NRP-1 with upregulated TNC/ITGB3 signaling, but decreased ABCG2 expression, which sensitizes BT-474 NRP-1 cells to Adriamycin/Cyclophosphamide.	Cyclophosphamide	198-214	neuropilin 1	Homo sapiens	72-77