PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30956968-0	2019	Coexistence of BCR/ABL1-positive chronic myeloid leukemia and JAK2 V617F-mutated myelofibrosis successfully treated with dasatinib and ruxolitinib.	ruxolitinib	135-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-23	
34167562-7	2021	RESULTS: All NOTCH1-signaling-dependent T-ALL cell lines were sensitive to MRK-560 and its combination with ruxolitinib or imatinib in JAK1- or ABL1-dependent cell lines synergistically inhibited leukemia proliferation.	ruxolitinib	108-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-148	
29296813-6	2017	In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2.	ruxolitinib	249-260	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-122	
29296813-6	2017	In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2.	ruxolitinib	249-260	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121	
26298727-10	2016	Ruxolitinib is a promising agent in chronic myeloid leukemia treatment by blocking JAK/STAT pathway known as downstream of BCR-ABL and triggering autophagy.	ruxolitinib	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130	
28749919-5	2017	In this review, we outline the age-related and geographic incidence of Ph-like ALL, the association with worse clinical outcomes, and early evidence for the use of ruxolitinib (a Janus kinase 2 inhibitor) and dasatinib (a tyrosine kinase inhibitor targeting ABL1).	ruxolitinib	164-175	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	258-262	
26430722-0	2015	Concomitant JAK2 V617F-positive polycythemia vera and BCR-ABL-positive chronic myelogenous leukemia treated with ruxolitinib and dasatinib.	ruxolitinib	113-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61	
26459144-0	2016	Expansion of a BCR-ABL clone in a JAK2 V617F myeloproliferative neoplasm treated by ruxolitinib.	ruxolitinib	84-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22	
25207766-8	2014	Cell lines and human leukemic cells expressing ABL1, ABL2, CSF1R, and PDGFRB fusions were sensitive in vitro to dasatinib, EPOR and JAK2 rearrangements were sensitive to ruxolitinib, and the ETV6-NTRK3 fusion was sensitive to crizotinib.	ruxolitinib	170-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51	
25499760-3	2015	Using a mouse model of Ph+ ALL that accurately mimics the genetics, clinical behavior, and therapeutic response of the human disease, we show that a combination of 2 agents approved by the US Food and Drug Administration (dasatinib and ruxolitinib, which inhibit BCR-ABL and Janus kinases, respectively), significantly extends survival by targeting parallel signaling pathways.	ruxolitinib	236-247	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	263-270	
24280282-4	2014	Taken together, our data provide a rationale for the therapeutic combination of TKIs and Ruxolitinib with the aim to eradicate primary BCR-ABL+ cells homed in BM niches.	ruxolitinib	89-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142