PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26018318-7	2015	Overexpression of Twist in the two cell lines markedly increased GDF15 expression, cell invasion, matrix metalloproteinase-2 expression/activity and the half maximal inhibitory concentration (IC50) values of cisplatin, which was eradicated by GDF15 knockdown or the selective p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 (10 microM).	Cisplatin	208-217	growth differentiation factor 15	Homo sapiens	243-248	
26018318-0	2015	Twist promotes invasion and cisplatin resistance in pancreatic cancer cells through growth differentiation factor 15.	Cisplatin	28-37	growth differentiation factor 15	Homo sapiens	84-116	
26018318-8	2015	By contrast, Twist knockdown significantly decreased GDF15 expression, cell invasion, matrix metalloproteinase-2 expression/activity and the IC50 values of cisplatin, which was completely reversed by overexpression of GDF15.	Cisplatin	156-165	growth differentiation factor 15	Homo sapiens	218-223	
26018318-10	2015	In conclusion, the present study, for the first time, to the best of our knowledge, demonstrated that Twist promotes PC cell invasion and cisplatin chemoresistance through inducing GDF15 expression via a p38 MAPK-dependent mechanism.	Cisplatin	138-147	growth differentiation factor 15	Homo sapiens	181-186	
25590623-0	2015	Growth differentiation factor 15 (GDF-15) plasma levels increase during bleomycin- and cisplatin-based treatment of testicular cancer patients and relate to endothelial damage.	Cisplatin	87-96	growth differentiation factor 15	Homo sapiens	0-32	
25590623-0	2015	Growth differentiation factor 15 (GDF-15) plasma levels increase during bleomycin- and cisplatin-based treatment of testicular cancer patients and relate to endothelial damage.	Cisplatin	87-96	growth differentiation factor 15	Homo sapiens	34-40	
10506617-2	1999	We describe the two largest reported, randomized, parallel trials designed to determine whether the addition of chemotherapy influences duration and quality of life in localized, unresectable (mitomycin, ifosfamide, cisplatin [MIC]1 trial) and extensive (MIC2 trial) disease.	Cisplatin	216-225	growth differentiation factor 15	Homo sapiens	227-232	
34826159-2	2022	The results indicated that OSCC cells overexpressing GDF15 were sensitive to docetaxel, cisplatin, and 5-fluorouracil through a caspase-9-dependent pathway both in vitro and in vivo.	Cisplatin	88-97	growth differentiation factor 15	Homo sapiens	53-58	
30146065-3	2018	Growth differentiation factor 15 (GDF15) expression was increased in cisplatin- or hypoxia-treated HCC cells.	Cisplatin	69-78	growth differentiation factor 15	Homo sapiens	0-32	
30146065-3	2018	Growth differentiation factor 15 (GDF15) expression was increased in cisplatin- or hypoxia-treated HCC cells.	Cisplatin	69-78	growth differentiation factor 15	Homo sapiens	34-39	
34826159-1	2022	The aim of this study was to: 1) explore the potential mechanism of cancer cell sensitivity to cisplatin, docetaxel, and 5-fluorouracil (TPF) in oral squamous cell carcinoma (OSCC) patients overexpressing growth differentiation factor 15 (GDF15); and 2) identify potential alternative agents for patients who might not benefit from inductive TPF chemotherapy.	Cisplatin	95-104	growth differentiation factor 15	Homo sapiens	205-237	
34826159-1	2022	The aim of this study was to: 1) explore the potential mechanism of cancer cell sensitivity to cisplatin, docetaxel, and 5-fluorouracil (TPF) in oral squamous cell carcinoma (OSCC) patients overexpressing growth differentiation factor 15 (GDF15); and 2) identify potential alternative agents for patients who might not benefit from inductive TPF chemotherapy.	Cisplatin	95-104	growth differentiation factor 15	Homo sapiens	239-244	
31629959-8	2020	Therefore, GDF15, LRG1, and SPP1 may be applied as novel candidate urinary markers of kidney injury after cisplatin treatment.	Cisplatin	106-115	growth differentiation factor 15	Homo sapiens	11-16