PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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