PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9009083-7 1997 NB4 cells did not express EVI-1 under basal conditions, but expressed EVI-1 after ATRA-induced differentiation. Tretinoin 82-86 MDS1 and EVI1 complex locus Homo sapiens 70-75 26036413-1 2015 Article title: The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid. Tretinoin 119-132 MDS1 and EVI1 complex locus Homo sapiens 28-32 25486480-0 2014 The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid. Tretinoin 104-117 MDS1 and EVI1 complex locus Homo sapiens 13-17 25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 153-176 MDS1 and EVI1 complex locus Homo sapiens 53-57 25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 153-176 MDS1 and EVI1 complex locus Homo sapiens 303-307 25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 178-182 MDS1 and EVI1 complex locus Homo sapiens 53-57 25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 178-182 MDS1 and EVI1 complex locus Homo sapiens 303-307 25486480-7 2014 In line with the gene expression results, EVI1 enhanced cell cycle arrest, differentiation, and apoptosis in response to ATRA, and knockdown of GDF15 counteracted some of these effects. Tretinoin 121-125 MDS1 and EVI1 complex locus Homo sapiens 42-46 19843176-0 2009 Zinc finger transcription factor ecotropic viral integration site 1 is induced by all-trans retinoic acid (ATRA) and acts as a dual modulator of the ATRA response. Tretinoin 92-105 MDS1 and EVI1 complex locus Homo sapiens 33-67 19843176-0 2009 Zinc finger transcription factor ecotropic viral integration site 1 is induced by all-trans retinoic acid (ATRA) and acts as a dual modulator of the ATRA response. Tretinoin 107-111 MDS1 and EVI1 complex locus Homo sapiens 33-67 19843176-3 2009 Here we describe the identification of a retinoic acid response element that was located in the most distal of several alternative first exons of the human EVI1 gene and was constitutively bound by canonical retinoid receptors in NTERA-2 teratocarcinoma cells. Tretinoin 41-54 MDS1 and EVI1 complex locus Homo sapiens 156-160 19843176-4 2009 Furthermore, it was the target of negative feedback by EVI1 on the induction of its own promoter by retinoic acid. Tretinoin 100-113 MDS1 and EVI1 complex locus Homo sapiens 55-59 19843176-6 2009 Extending its role as a modulator of the retinoic acid response, EVI1 had the opposite effect on the RARbeta retinoic acid response element, whose induction by all-trans retinoic acid it enhanced through a mechanism that involved almost all of its known functional domains. Tretinoin 41-54 MDS1 and EVI1 complex locus Homo sapiens 65-69 19843176-7 2009 Augmentation of the retinoic acid response by EVI1 was also observed for the endogenous RARbeta gene. Tretinoin 20-33 MDS1 and EVI1 complex locus Homo sapiens 46-50 19843176-8 2009 Thus, we have established EVI1 as a novel type of modulator of the retinoic acid response, which can both enhance and repress induction by this agent in a promoter-specific manner. Tretinoin 67-80 MDS1 and EVI1 complex locus Homo sapiens 26-30 26582376-0 2016 Primary acute myeloid leukemia cells with overexpression of EVI-1 are sensitive to all-trans retinoic acid. Tretinoin 93-106 MDS1 and EVI1 complex locus Homo sapiens 60-65 26582376-3 2016 Because treatment of acute promyelocytic patients with all-trans retinoic acid (ATRA) has improved the survival of these patients substantially, we investigated whether ATRA might also be effective for the subgroup of AML patients with EVI-1 overexpression. Tretinoin 169-173 MDS1 and EVI1 complex locus Homo sapiens 236-241 26582376-4 2016 Here, we show that a substantial part of the EVI-1-positive AML cases respond to ATRA by induction of differentiation and decreased clonogenic capacity of myeloid blasts. Tretinoin 81-85 MDS1 and EVI1 complex locus Homo sapiens 45-50 26582376-5 2016 Most importantly, we demonstrate that in vivo treatment of primary EVI-1-positive AML with ATRA leads to a significant reduction in leukemic engraftment. Tretinoin 91-95 MDS1 and EVI1 complex locus Homo sapiens 67-72 26582376-6 2016 Altogether, our results show that a considerable part of the EVI-1-positive primary AML cases are sensitive to ATRA, suggesting that combining ATRA with the currently used conventional chemotherapy might be a promising treatment strategy decreasing relapse rates and enhancing complete remissions in this poor prognostic subgroup of AML patients. Tretinoin 111-115 MDS1 and EVI1 complex locus Homo sapiens 61-66 26582376-6 2016 Altogether, our results show that a considerable part of the EVI-1-positive primary AML cases are sensitive to ATRA, suggesting that combining ATRA with the currently used conventional chemotherapy might be a promising treatment strategy decreasing relapse rates and enhancing complete remissions in this poor prognostic subgroup of AML patients. Tretinoin 143-147 MDS1 and EVI1 complex locus Homo sapiens 61-66 9009083-8 1997 When NB4 cells were exposed to ATRA and transferred to cultures with N,N"-hexamethylene-bis-acetamide (HMBA), differentiation occurred but EVI-1 RNA was not detected, indicating that EVI-1 expression was not required for terminal, NB4 differentiation. Tretinoin 31-35 MDS1 and EVI1 complex locus Homo sapiens 183-188 9009083-13 1997 In conclusion, this study demonstrates the EVI-1 gene is consistently expressed in APL cells either constitutively or after ATRA treatment. Tretinoin 124-128 MDS1 and EVI1 complex locus Homo sapiens 43-48 9009083-14 1997 ATRA represents the first biologically active agent shown to specifically regulate EVI-1 expression in blood cells. Tretinoin 0-4 MDS1 and EVI1 complex locus Homo sapiens 83-88 9009083-15 1997 In contrast to previous studies in AML and MDS, the pattern of EVI-1 expression suggests it may facilitate rather than inhibit myeloid differentiation during ATRA treatment. Tretinoin 158-162 MDS1 and EVI1 complex locus Homo sapiens 63-68 33003409-8 2020 Taken together, our results suggest that in the P19 cells, PRDM3 contributed to neurogenesis and its expression was stimulated by the synergism between GATA6 and the retinoic acid signaling pathway. Tretinoin 166-179 MDS1 and EVI1 complex locus Homo sapiens 59-64 32998330-0 2020 Evi1 Counteracts Anti-Leukemic and Stem Cell Inhibitory Effects of All-Trans Retinoic Acid on Flt3-ITD/Npm1c-Driven Acute Myeloid Leukemia Cells. Tretinoin 67-90 MDS1 and EVI1 complex locus Homo sapiens 0-4 32998330-3 2020 atRA promoted stemness of MLL-AF9-driven AML in an Evi1-dependent manner but had the opposite effect in Flt3-ITD/Nup98-Hoxd13-driven AML. Tretinoin 0-4 MDS1 and EVI1 complex locus Homo sapiens 51-55 31822659-0 2019 All-trans retinoic acid enhances, and a pan-RAR antagonist counteracts, the stem cell promoting activity of EVI1 in acute myeloid leukemia. Tretinoin 10-23 MDS1 and EVI1 complex locus Homo sapiens 108-112 31822659-1 2019 Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. Tretinoin 185-205 MDS1 and EVI1 complex locus Homo sapiens 0-34 31822659-1 2019 Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. Tretinoin 185-205 MDS1 and EVI1 complex locus Homo sapiens 36-40 31822659-1 2019 Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. Tretinoin 207-211 MDS1 and EVI1 complex locus Homo sapiens 0-34 31822659-1 2019 Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. Tretinoin 207-211 MDS1 and EVI1 complex locus Homo sapiens 36-40 32699982-0 2019 Efficacy of All-Trans-Retinoic Acid in High-Risk Acute Myeloid Leukemia with Overexpression of EVI1. Tretinoin 12-35 MDS1 and EVI1 complex locus Homo sapiens 95-99 32699982-1 2019 INTRODUCTION: EVI1 (MECOM)-positive acute myeloid leukemia (AML) cells have shown in vitro sensitivity to all-trans-retinoic acid (ATRA) by inducing differentiation, cell death, and decreased leukemic engraftment. Tretinoin 106-129 MDS1 and EVI1 complex locus Homo sapiens 14-18 32699982-1 2019 INTRODUCTION: EVI1 (MECOM)-positive acute myeloid leukemia (AML) cells have shown in vitro sensitivity to all-trans-retinoic acid (ATRA) by inducing differentiation, cell death, and decreased leukemic engraftment. Tretinoin 106-129 MDS1 and EVI1 complex locus Homo sapiens 20-25 32699982-1 2019 INTRODUCTION: EVI1 (MECOM)-positive acute myeloid leukemia (AML) cells have shown in vitro sensitivity to all-trans-retinoic acid (ATRA) by inducing differentiation, cell death, and decreased leukemic engraftment. Tretinoin 131-135 MDS1 and EVI1 complex locus Homo sapiens 14-18 32699982-1 2019 INTRODUCTION: EVI1 (MECOM)-positive acute myeloid leukemia (AML) cells have shown in vitro sensitivity to all-trans-retinoic acid (ATRA) by inducing differentiation, cell death, and decreased leukemic engraftment. Tretinoin 131-135 MDS1 and EVI1 complex locus Homo sapiens 20-25 32699982-2 2019 METHODS: In this pilot study, we investigated the response to ATRA in 13 high-risk AML patients with overexpression of EVI1. Tretinoin 62-66 MDS1 and EVI1 complex locus Homo sapiens 119-123 32699982-4 2019 CONCLUSION: These primary results tend to confirm in vitro results and suggest that addition of ATRA might be of benefit in the treatment of patients with EVI1-positive AML. Tretinoin 96-100 MDS1 and EVI1 complex locus Homo sapiens 155-159 27129260-4 2016 We document that overexpression of EVI1 abrogates retinoic acid-induced maturation of EML cells into committed myeloid cells, a process that can be documented by the down-regulation of stem cell antigen-1 and acquisition of responsiveness to granulocyte-macrophage colony-stimulating factor. Tretinoin 50-63 MDS1 and EVI1 complex locus Homo sapiens 35-39