PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23187745-8	2012	The homoharringtonine derivative omacetaxine mepesuccinate, which inhibits protein synthesis, has also demonstrated clinical activity in CML, including in patients with TKI resistance due to T315I and in patients who have TKI resistance despite no evidence of ABL mutations.	Homoharringtonine	4-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-263	
24159169-0	2013	Activity of omacetaxine mepesuccinate against ponatinib-resistant BCR-ABL-positive cells.	Homoharringtonine	12-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73	
31789418-0	2020	Homoharringtonine promotes BCR-ABL degradation through the p62-mediated autophagy pathway.	Homoharringtonine	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34	
31789418-3	2020	In the present study, HHT treatment demonstrated induction of apoptosis in imatinib-resistant K562G cells by using MTS assay and western blotting, and BCR-ABL protein was reduced.	Homoharringtonine	22-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158	
27268912-3	2016	Omacetaxine mepesuccinate inhibits protein translation through prevention of the initial elongation step of protein synthesis and its use benefits CML patients possessing the BCR-ABL oncogene.	Homoharringtonine	0-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182	
24516334-3	2014	Omacetaxine mepesuccinate has been recently approved by the US Food and Drug Administration to treat patients with chronic myeloid leukemia who failed to respond to multiple tyrosine kinase inhibitors and/or acquired the BCR-ABL-T315I mutation.	Homoharringtonine	0-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228	
23187745-8	2012	The homoharringtonine derivative omacetaxine mepesuccinate, which inhibits protein synthesis, has also demonstrated clinical activity in CML, including in patients with TKI resistance due to T315I and in patients who have TKI resistance despite no evidence of ABL mutations.	Homoharringtonine	33-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-263	
21294709-4	2011	The advent of resistance to imatinib and other TKIs in CML patients (often due to the presence of an ABL mutation at position 315) has led to a revived clinical interest in omacetaxine in CML patients who failed TKIs.	Homoharringtonine	173-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104	
20673586-5	2011	In T315I and F317L mutated patients, CML-resistance appears to be promoted by SFKs kinase protein reactivation once the BCR-ABL mutated clone has decreased on Omacetaxine.	Homoharringtonine	159-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127	
21030353-0	2010	The durable clearance of the T315I BCR-ABL mutated clone in chronic phase chronic myelogenous leukemia patients on omacetaxine allows tyrosine kinase inhibitor rechallenge.	Homoharringtonine	115-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42	
21030353-2	2010	PATIENTS AND METHODS: We have investigated the affect of subcutaneous omacetaxine (OMA, or homo-harringtonine) cycles on unmutated and T315I-mutated BCR-ABL transcripts in a series of 8 TKI-resistant chronic-phase CML patients and we have addressed the question of whether the administration of OMA could resensitize patients to TKIs.	Homoharringtonine	70-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156	
18028486-6	2008	The combination of homoharringtonine that reduces Mcl-1 enhanced the killing by ABT-737 strongly in Bcr-Abl(+) cells even with T315I mutation.	Homoharringtonine	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107	
17881650-0	2007	Interferon-alpha or homoharringtonine as salvage treatment for chronic myeloid leukemia patients who acquire the T315I BCR-ABL mutation.	Homoharringtonine	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126