PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24939178-7	2014	Together, our data provide a novel explanation that high level of IL6 stimulated SOD2 expression that, at least partially, contributed to the low level of ROS that would likely result in a sustained increase in the expression of IGF-1R through abolishment of beta-arrestin1 in docetaxel resistant cells.	Docetaxel	277-286	superoxide dismutase 2	Homo sapiens	81-85	
24939178-0	2014	Regulation of SOD2 and beta-arrestin1 by interleukin-6 contributes to the increase of IGF-1R expression in docetaxel resistant prostate cancer cells.	Docetaxel	107-116	superoxide dismutase 2	Homo sapiens	14-18	
24939178-2	2014	Proteomics-based analysis in this study revealed that SOD2, associated with downregulation of reactive oxygen species (ROS), was significantly up-regulated in docetaxel-resistant (PC3/Doc) cells if compared to sensitive cells, and the expression of redox-regulated genes such as IGF-1R, CXCR4, and BCL2 was increased as well.	Docetaxel	159-168	superoxide dismutase 2	Homo sapiens	54-58	
21056653-9	2011	MnSOD also induces up-regulation of Bcl-2 and prevents docetaxel-, etoposide-, or TNF-induced cell death.	Docetaxel	55-64	superoxide dismutase 2	Homo sapiens	0-5