PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31726100-0	2020	Destabilization of ROR1 enhances activity of Ibrutinib against chronic lymphocytic leukemia in vivo.	ibrutinib	45-54	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	19-23	
31726100-5	2020	Based on our previous finding that a humanized monoclonal antibody against ROR1 increases the activity of Ibrutinib against CLL, which is currently undergoing evaluation in clinical trials for the treatment of B-cell lymphoid malignancies, we then provided evidence that treatment with HSP90 inhibitor (17-DMAG) enhances anti-CLL activity of Ibrutinib in vitro and in vivo, by down-modulating ROR1.	ibrutinib	106-115	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	75-79	
31726100-5	2020	Based on our previous finding that a humanized monoclonal antibody against ROR1 increases the activity of Ibrutinib against CLL, which is currently undergoing evaluation in clinical trials for the treatment of B-cell lymphoid malignancies, we then provided evidence that treatment with HSP90 inhibitor (17-DMAG) enhances anti-CLL activity of Ibrutinib in vitro and in vivo, by down-modulating ROR1.	ibrutinib	106-115	heat shock protein 90 alpha family class A member 1	Homo sapiens	286-291	
31726100-5	2020	Based on our previous finding that a humanized monoclonal antibody against ROR1 increases the activity of Ibrutinib against CLL, which is currently undergoing evaluation in clinical trials for the treatment of B-cell lymphoid malignancies, we then provided evidence that treatment with HSP90 inhibitor (17-DMAG) enhances anti-CLL activity of Ibrutinib in vitro and in vivo, by down-modulating ROR1.	ibrutinib	106-115	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	393-397	
31726100-5	2020	Based on our previous finding that a humanized monoclonal antibody against ROR1 increases the activity of Ibrutinib against CLL, which is currently undergoing evaluation in clinical trials for the treatment of B-cell lymphoid malignancies, we then provided evidence that treatment with HSP90 inhibitor (17-DMAG) enhances anti-CLL activity of Ibrutinib in vitro and in vivo, by down-modulating ROR1.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	303-310	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	75-79	
31726100-5	2020	Based on our previous finding that a humanized monoclonal antibody against ROR1 increases the activity of Ibrutinib against CLL, which is currently undergoing evaluation in clinical trials for the treatment of B-cell lymphoid malignancies, we then provided evidence that treatment with HSP90 inhibitor (17-DMAG) enhances anti-CLL activity of Ibrutinib in vitro and in vivo, by down-modulating ROR1.	ibrutinib	342-351	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	75-79	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	ibrutinib	50-59	heat shock protein 90 alpha family class A member 1	Homo sapiens	92-97	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	ibrutinib	50-59	Bruton tyrosine kinase	Homo sapiens	168-171	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	ibrutinib	50-59	BLK proto-oncogene, Src family tyrosine kinase	Homo sapiens	173-176	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	ibrutinib	50-59	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	178-181	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	ibrutinib	50-59	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	185-188	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	ibrutinib	50-59	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	198-202	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	110-117	heat shock protein 90 alpha family class A member 1	Homo sapiens	92-97	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	110-117	Bruton tyrosine kinase	Homo sapiens	168-171	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	110-117	BLK proto-oncogene, Src family tyrosine kinase	Homo sapiens	173-176	
31726100-7	2020	However, immunoblotting validation confirmed that Ibrutinib treatment dramatically deprived HSP90 inhibitors, 17-DMAG, AUY922 or PU-H71, of inducing the degradation of BTK, BLK, LCK or LYN, but not ROR1.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	110-117	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	178-181	
31726100-8	2020	Collectively, our data suggested that depletion of ROR1 induced by targeting HSP90 might facilitate the enhancement of Ibrutinib activity against CLL.	ibrutinib	119-128	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	51-55	
31726100-8	2020	Collectively, our data suggested that depletion of ROR1 induced by targeting HSP90 might facilitate the enhancement of Ibrutinib activity against CLL.	ibrutinib	119-128	heat shock protein 90 alpha family class A member 1	Homo sapiens	77-82