PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34680392-4	2021	Here, using a panel of human AML cell lines and primary AML patient specimens harboring IDH mutations, we showed that the production of an oncometabolite (R)-2-HG by IDH mutant enzymes induces vitamin D receptor-related transcriptional changes, priming these AML cells to differentiate with pharmacological doses of ATRA and/or VD.	Tretinoin	316-320	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	166-169	
29274134-10	2018	Further studies addressing its biology and clinical significance may be especially relevant in the era of IDH inhibitors and recent work showing efficacy of ATRA therapy in NPM1 and IDH1-mutated AML.	Tretinoin	157-161	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	182-186	
34850159-2	2022	In these IDH-mutant gliomas, retinoic acid-related gene expression is commonly silenced by DNA hypermethylation.	Tretinoin	29-42	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	9-12	
34850159-5	2022	This was the rationale for a preclinical evaluation combining the DNA demethylating agent, 5-Azacytidine (5-Aza), and retinoic acid pathway activation with all-trans retinoic acid (atRA) in IDH-mutant glioma.	Tretinoin	181-185	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	190-193	
32882760-9	2020	IDH-associated changes in histone methylation markers decreased after AG-221 and ATRA combination treatment.	Tretinoin	81-85	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	0-3	
26951332-4	2016	We show that treatment with all-trans retinoic acid (ATRA) at clinically achievable doses markedly enhanced terminal granulocytic differentiation in AML cell lines, primary patient samples, and a xenograft mouse model carrying mutant IDH1.	Tretinoin	38-51	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	234-238	
26951332-4	2016	We show that treatment with all-trans retinoic acid (ATRA) at clinically achievable doses markedly enhanced terminal granulocytic differentiation in AML cell lines, primary patient samples, and a xenograft mouse model carrying mutant IDH1.	Tretinoin	53-57	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	234-238	
26951332-5	2016	Moreover, treatment with a cell-permeable form of 2-HG sensitized wild-type IDH1 AML cells to ATRA-induced myeloid differentiation, whereas inhibition of 2-HG production significantly reduced ATRA effects in mutant IDH1 cells.	Tretinoin	192-196	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	215-219	
26951332-6	2016	ATRA treatment specifically decreased cell viability and induced apoptosis of mutant IDH1 blasts in vitro.	Tretinoin	0-4	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	85-89	
26951332-7	2016	ATRA also reduced tumor burden of mutant IDH1 AML cells xenografted in NOD-Scid-IL2rgamma(null)mice and markedly increased overall survival, revealing a potent antileukemic effect of ATRA in the presence of IDH1 mutation.	Tretinoin	0-4	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	41-45	
26951332-7	2016	ATRA also reduced tumor burden of mutant IDH1 AML cells xenografted in NOD-Scid-IL2rgamma(null)mice and markedly increased overall survival, revealing a potent antileukemic effect of ATRA in the presence of IDH1 mutation.	Tretinoin	183-187	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	41-45	
22945948-14	2012	Because RBP1 is involved in retinoic acid synthesis, our results suggest that dysregulation of retinoic acid metabolism may contribute to glioma formation along the IDH1/IDH2-mutant pathway.	Tretinoin	95-108	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	165-169