PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30728460-4 2019 We found that 5-azacytidine (5-aza-CR) induces LOXL4 upregulation, with LOXL4 subsequently binding the basic domain of p53 via its low-isoelectric point region. Azacitidine 14-27 tumor protein p53 Homo sapiens 119-122 33600210-0 2021 Eprenetapopt Plus Azacitidine in TP53-Mutated Myelodysplastic Syndromes and Acute Myeloid Leukemia: A Phase II Study by the Groupe Francophone des Myelodysplasies (GFM). Azacitidine 18-29 tumor protein p53 Homo sapiens 33-37 33600210-1 2021 PURPOSE: TP53-mutated (TP53m) myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) have very poor outcome irrespective of the treatment received, including 40% responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a median overall survival (OS) of approximately 6 months. Azacitidine 217-228 tumor protein p53 Homo sapiens 9-13 33600210-1 2021 PURPOSE: TP53-mutated (TP53m) myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) have very poor outcome irrespective of the treatment received, including 40% responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a median overall survival (OS) of approximately 6 months. Azacitidine 217-228 tumor protein p53 Homo sapiens 23-27 33600210-1 2021 PURPOSE: TP53-mutated (TP53m) myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) have very poor outcome irrespective of the treatment received, including 40% responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a median overall survival (OS) of approximately 6 months. Azacitidine 230-233 tumor protein p53 Homo sapiens 9-13 33600210-1 2021 PURPOSE: TP53-mutated (TP53m) myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) have very poor outcome irrespective of the treatment received, including 40% responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a median overall survival (OS) of approximately 6 months. Azacitidine 230-233 tumor protein p53 Homo sapiens 23-27 33001991-0 2020 Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine. Azacitidine 73-84 tumor protein p53 Homo sapiens 10-14 33001991-2 2020 Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear. Azacitidine 329-340 tumor protein p53 Homo sapiens 10-14 33001991-2 2020 Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear. Azacitidine 329-340 tumor protein p53 Homo sapiens 199-203 33001991-2 2020 Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear. Azacitidine 329-340 tumor protein p53 Homo sapiens 199-203 32482751-0 2020 To target the untargetable: elucidation of synergy of APR-246 and azacitidine in TP53 mutant myelodysplastic syndromes and acute myeloid leukemia. Azacitidine 66-77 tumor protein p53 Homo sapiens 81-85 33449813-0 2021 Eprenetapopt (APR-246) and Azacitidine in TP53-Mutant Myelodysplastic Syndromes. Azacitidine 27-38 tumor protein p53 Homo sapiens 42-46 33449813-13 2021 CONCLUSION: Combination treatment with eprenetapopt and azacitidine is well-tolerated yielding high rates of clinical response and molecular remissions in patients with TP53-mutant MDS and oligoblastic AML. Azacitidine 56-67 tumor protein p53 Homo sapiens 169-173 31488557-0 2020 Synergistic effects of PRIMA-1Met (APR-246) and Azacitidine in TP53-mutated myelodysplastic syndromes and acute myeloid leukemia. Azacitidine 48-59 tumor protein p53 Homo sapiens 63-67 31488557-1 2020 Myelodysplastic syndromes and acute myeloid leukemia with TP53 mutations are characterized by frequent relapses, poor or short responses, and poor survival with the currently available therapies including chemotherapy and 5-azacitidine. Azacitidine 222-235 tumor protein p53 Homo sapiens 58-62 31488557-3 2020 We show here that low doses of APR on its own or in combination with 5-azacitidine reactivate the p53 pathway and induce an apoptosis program. Azacitidine 69-82 tumor protein p53 Homo sapiens 98-101 31488557-4 2020 Functionally, we demonstrate that APR exerts these activities on its own and that it synergizes with 5-azacitidine in TP53-mutated Myelodysplastic syndromes / acute myeloid leukemia cell lines and in TP53-mutated primary cells from Myelodysplastic syndromes / acute myeloid leukemia patients. Azacitidine 101-114 tumor protein p53 Homo sapiens 118-122 31990086-8 2020 Decrease of TP53-mutated clone was correlated with response to AZA, confirming AZA efficacy in this subgroup. Azacitidine 63-66 tumor protein p53 Homo sapiens 12-16 31990086-8 2020 Decrease of TP53-mutated clone was correlated with response to AZA, confirming AZA efficacy in this subgroup. Azacitidine 79-82 tumor protein p53 Homo sapiens 12-16 30728460-4 2019 We found that 5-azacytidine (5-aza-CR) induces LOXL4 upregulation, with LOXL4 subsequently binding the basic domain of p53 via its low-isoelectric point region. Azacitidine 29-37 tumor protein p53 Homo sapiens 119-122 30728460-8 2019 In conclusion, we found that 5-aza-CR-induced LOXL4 upregulation reactivates wild-type p53 and triggers cell death, which blocks liver cancer development. Azacitidine 29-37 tumor protein p53 Homo sapiens 87-90 28802167-10 2017 Induction of p53 by 5-Aza-dC was tested in vitro using cancer cells. Azacitidine 20-25 tumor protein p53 Homo sapiens 13-16 31048321-11 2019 Targeting CLPB synergizes with venetoclax and the venetoclax/azacitidine combination in AML in a p53-independent manner.See related commentary by Savona and Rathmell, p. 831.This article is highlighted in the In This Issue feature, p. 813. Azacitidine 61-72 tumor protein p53 Homo sapiens 97-100 29648492-0 2018 Azacitidine effectively reduces TP53-mutant leukemic cell burden in secondary acute myeloid leukemia after cord blood transplantation. Azacitidine 0-11 tumor protein p53 Homo sapiens 32-36 29143344-5 2017 Cells transfected with siRNAs targeting p16 and MGMT as well as cells stimulated with 5-Aza-dC were arrested in S phase, and the expression of p53, p21, and Rb was up-regulated more significantly. Azacitidine 86-91 tumor protein p53 Homo sapiens 143-146 28916527-4 2017 5-aza reduced expression of HPV genes, stabilized p53, and induced p53-dependent apoptosis in HNSCC cells and tumors. Azacitidine 0-5 tumor protein p53 Homo sapiens 50-53 28916527-4 2017 5-aza reduced expression of HPV genes, stabilized p53, and induced p53-dependent apoptosis in HNSCC cells and tumors. Azacitidine 0-5 tumor protein p53 Homo sapiens 67-70 28476801-12 2017 CONCLUSION: AzaC significantly increases the sensitivity of MCF7 cells to Dox via activation of ERK1/2, P53, BAX and caspase-3. Azacitidine 12-16 tumor protein p53 Homo sapiens 104-107 28476801-8 2017 These observations were accompanied by activation of ERK1/2 and p38MAPK, as well as up-regulation of BAX and P53 in the AzaC/Dox group. Azacitidine 120-124 tumor protein p53 Homo sapiens 109-112 28505595-8 2017 Functional mapping of transcripts uniquely regulated by the azacitidine-panobinostat combination in MV4;11 cells identified p53 as an upstream regulator. Azacitidine 60-71 tumor protein p53 Homo sapiens 124-127 28505595-9 2017 A comparison of the uniquely modulated transcripts by azacitidine-panobinostat combination in MV4;11 cells versus AML-193 and THP-1 cells, bearing mutated p53, also revealed p53 as the topmost upstream regulator. Azacitidine 54-65 tumor protein p53 Homo sapiens 174-177 28505595-10 2017 Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML. Azacitidine 73-84 tumor protein p53 Homo sapiens 30-33 28505595-10 2017 Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML. Azacitidine 73-84 tumor protein p53 Homo sapiens 127-130 27029827-6 2017 The combination of Aza+SAHA significantly increased p53 protein binding to DNA in pax5 promoter region (p<0.01). Azacitidine 19-22 tumor protein p53 Homo sapiens 52-55 27029827-7 2017 More efficient binding of the transcription factor p53 to pax5 promoter region is likely because SAHA increased accessibility of the chromatin conformation and Aza-demethylated DNA was more permissive, allowing transcription factors to bind. Azacitidine 160-163 tumor protein p53 Homo sapiens 51-54 27029827-8 2017 CONCLUSION: Our study not only explained an underlying mechanism, that pax5 re-expression was induced by Aza+SAHA combination in H460 cells via p53, but also demonstrated a pattern showing that the combination of demethylating agent and HDAC inhibitor can re-activate tumor suppressor gene (TSG) which is associated with the enhancement of transcription factors binding to the promoter region of the TSG. Azacitidine 105-108 tumor protein p53 Homo sapiens 144-147 28484169-8 2017 In the case of TP53 mutations, prognosis is poor for both hematopoietic stem cell transplantation and AZA treatment, although, patients with TP53 mutations have been shown to respond favorably to decitabine administration for 10 days. Azacitidine 102-105 tumor protein p53 Homo sapiens 15-19 26651421-0 2016 A new prognostic index to make short-term prognoses in MDS patients treated with azacitidine: A combination of p53 expression and cytogenetics. Azacitidine 81-92 tumor protein p53 Homo sapiens 111-114 26651421-6 2016 Here, we propose a new prognostic index to make short-term prognoses of MDS patients in the era of Aza treatment; high: p53-positive and poor cytogenetics, low: p53-negative and absence of poor cytogenetics, and intermediate: the others. Azacitidine 99-102 tumor protein p53 Homo sapiens 120-123 26651421-8 2016 In conclusion, p53 expression was a significant prognostic factor in MDS patients treated with Aza. Azacitidine 95-98 tumor protein p53 Homo sapiens 15-18 25934763-0 2015 Correction to "5-aza-Cytidine Is a Potent Inhibitor of DNA Methyltransferase 3a and Induces Apoptosis in HCT-116 Colon Cancer Cells via Gadd45- and p53-Dependent Mechanisms". Azacitidine 15-29 tumor protein p53 Homo sapiens 148-151 24836762-0 2014 Prognostic value of TP53 gene mutations in myelodysplastic syndromes and acute myeloid leukemia treated with azacitidine. Azacitidine 109-120 tumor protein p53 Homo sapiens 20-24 25134538-5 2014 Furthermore, we assessed the expression of p53 and p73 isoforms in 5-aza-dC-treated T-47D cells and p53 knockout cells. Azacitidine 67-72 tumor protein p53 Homo sapiens 43-46 25134538-11 2014 We also demonstrate that p53 likely contributes to 5-aza-dC-induced DeltaNp73 transcriptional inactivation in breast cancer cells. Azacitidine 51-56 tumor protein p53 Homo sapiens 25-28 24836762-2 2014 However, the impact of TP53 mutations in MDS treated with azacitidine (AZA) remains unclear. Azacitidine 58-69 tumor protein p53 Homo sapiens 23-27 24836762-3 2014 We analyzed TP53 mutations in 62 patients with high risk MDS or AML treated with AZA. Azacitidine 81-84 tumor protein p53 Homo sapiens 12-16 24836762-9 2014 Thus, TP53 mutations strongly correlated with poorer survival in higher risk MDS and AML treated with AZA. Azacitidine 102-105 tumor protein p53 Homo sapiens 6-10 23924947-7 2013 5-aza-dC induced p53-dependent tumor cell senescence and a high number of DNA double-strand breaks. Azacitidine 0-5 tumor protein p53 Homo sapiens 17-20 23924947-8 2013 In contrast, 5-aza-CR downregulated p53, induced caspase activation and apoptosis. Azacitidine 13-21 tumor protein p53 Homo sapiens 36-39 24319226-2 2013 For example, 5-azacytidine and decitabine produce remissions and better overall survival in MDS with high-risk chromosome abnormalities at a surprisingly high rate, consistent with experimental observations that noncytotoxic DNA methyltransferase depletion by 5-azacytidine/decitabine can trigger cell cycle exit independently of p53, thus circumventing a basis for resistance to apoptosis-based DNA-damaging therapy. Azacitidine 13-26 tumor protein p53 Homo sapiens 330-333 24319226-2 2013 For example, 5-azacytidine and decitabine produce remissions and better overall survival in MDS with high-risk chromosome abnormalities at a surprisingly high rate, consistent with experimental observations that noncytotoxic DNA methyltransferase depletion by 5-azacytidine/decitabine can trigger cell cycle exit independently of p53, thus circumventing a basis for resistance to apoptosis-based DNA-damaging therapy. Azacitidine 260-273 tumor protein p53 Homo sapiens 330-333 19531575-6 2009 Top-I, Sp1, and p53 expression modulated by 5-aza were measured by real-time PCR. Azacitidine 44-49 tumor protein p53 Homo sapiens 16-19 22893484-7 2012 5-AZA down-regulated MCL-1, known to mediate resistance to ABT-737, in a p53-independent manner. Azacitidine 0-5 tumor protein p53 Homo sapiens 73-76 23300844-3 2012 We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. Azacitidine 27-32 tumor protein p53 Homo sapiens 82-85 23300844-5 2012 Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Azacitidine 9-14 tumor protein p53 Homo sapiens 25-28 23300844-6 2012 Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. Azacitidine 52-57 tumor protein p53 Homo sapiens 15-18 23300844-7 2012 In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. Azacitidine 63-68 tumor protein p53 Homo sapiens 31-34 23300844-9 2012 Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Azacitidine 74-79 tumor protein p53 Homo sapiens 138-141 21903246-4 2011 Wild-type (wt) p53 was transiently transfected into the mutant p53 (m p53) SKOV3 cells which were treated with 5-azaC. Azacitidine 111-117 tumor protein p53 Homo sapiens 15-18 21903246-4 2011 Wild-type (wt) p53 was transiently transfected into the mutant p53 (m p53) SKOV3 cells which were treated with 5-azaC. Azacitidine 111-117 tumor protein p53 Homo sapiens 63-66 21903246-4 2011 Wild-type (wt) p53 was transiently transfected into the mutant p53 (m p53) SKOV3 cells which were treated with 5-azaC. Azacitidine 111-117 tumor protein p53 Homo sapiens 63-66 19531575-11 2009 In contrast, 5-aza down-regulated Top-I expression in the p53 wild-type LS174T cells in a p53-dependent manner, thereby reducing SN38 cytotoxicity. Azacitidine 13-18 tumor protein p53 Homo sapiens 90-93 19531575-12 2009 In conclusion, 5-aza modulates Top-I expression by several mechanisms involving Sp1, p16, and p53. Azacitidine 15-20 tumor protein p53 Homo sapiens 94-97 19531575-13 2009 If confirmed in other models, these results suggest that p16 and p53 status affects the 5-aza-irinotecan interaction. Azacitidine 88-93 tumor protein p53 Homo sapiens 65-68 19531575-11 2009 In contrast, 5-aza down-regulated Top-I expression in the p53 wild-type LS174T cells in a p53-dependent manner, thereby reducing SN38 cytotoxicity. Azacitidine 13-18 tumor protein p53 Homo sapiens 58-61 34768330-0 2021 Lymphocytic Infiltrate and p53 Protein Expression as Predictive Markers of Response and Outcome in Myelodysplastic Syndromes Treated with Azacitidine. Azacitidine 138-149 tumor protein p53 Homo sapiens 27-30 16007224-6 2005 Treatment of Weri-Rb1 cell line by 5-Aza-dC induced an increase in expression level of pRb2/p130, E2F1, p73 and p53. Azacitidine 35-40 tumor protein p53 Homo sapiens 112-115 15547111-0 2005 5-Aza-cytidine is a potent inhibitor of DNA methyltransferase 3a and induces apoptosis in HCT-116 colon cancer cells via Gadd45- and p53-dependent mechanisms. Azacitidine 0-14 tumor protein p53 Homo sapiens 133-136 15547111-4 2005 In this study, we investigated the p53 dependence of apoptotic, cell cycle, and growth inhibitory effects of 5-aza-CR, as well as the influence on the expression level of DNMT1, DNMT3a, and DNMT3b in the colon cancer cell line HCT-116. Azacitidine 109-117 tumor protein p53 Homo sapiens 35-38 15547111-5 2005 Exposure to 5-aza-CR induced the up-regulation of genes promoting cell cycle arrest and DNA repair (p21(WAF1) and GADD45) or apoptosis (p53, RIPK2, Bak1, caspase 5, and caspase 6). Azacitidine 12-20 tumor protein p53 Homo sapiens 136-139 8790940-4 1996 Although the mutated p53 is selectively expressed in the immortalized cells, expression of the wild-type p53 was induced by treatment of the cells with a hypomethylating reagent, 5-azacytidine, indicating that the wild-type p53 allele might be inactivated by hypermethylation of DNA. Azacitidine 179-192 tumor protein p53 Homo sapiens 105-108 8790940-4 1996 Although the mutated p53 is selectively expressed in the immortalized cells, expression of the wild-type p53 was induced by treatment of the cells with a hypomethylating reagent, 5-azacytidine, indicating that the wild-type p53 allele might be inactivated by hypermethylation of DNA. Azacitidine 179-192 tumor protein p53 Homo sapiens 105-108 15547111-11 2005 Our data demonstrate that 5-aza-CR action in HCT-116 is mediated by p53 and its downstream effectors p21(WAF1) and GADD45. Azacitidine 26-34 tumor protein p53 Homo sapiens 68-71 34768330-8 2021 Our results suggest the possible role of lymphocytic infiltrate and p53+ elements as predictive markers in MDS treated with azacitidine, disclosing new chapters in the understanding of MDS evolution and treatment. Azacitidine 124-135 tumor protein p53 Homo sapiens 68-71 35368106-7 2022 Notably, 6 of 7 pts (86%) who received either allo-SCT3 or a combination therapy of DLIs, 5-azacytidine and venetoclax achieved CR despite poor cytogenetics post-allo-SCT2 (e.g. TP53). Azacitidine 90-103 tumor protein p53 Homo sapiens 178-182 34405020-8 2021 5-Aza also increased p53 and p21 transcription through promoter demethylation, and decreased the expression of oncogene c-Myc in 22RV1 and LNCaP cells. Azacitidine 0-5 tumor protein p53 Homo sapiens 21-24 34405020-11 2021 Thus, in responsible for its apoptotic induction and DNA damage, the mechanism of the antitumor activities of 5-Aza may involve in an increase of tumor suppressive maspin, upregulation of wild type p53-mediated p21 expression and a decrease of oncogene c-Myc level in 22RV1 and LNCaP cells, and enhancing the tumor suppressive maspin expression in DU145 cells. Azacitidine 110-115 tumor protein p53 Homo sapiens 198-201 34070172-8 2021 In the subgroup analyses, patients with mutated TP53 (HR, 4.71, p = 0.009) showed a better RFS in the azacytidine arm. Azacitidine 102-113 tumor protein p53 Homo sapiens 48-52 35576022-0 2022 Selinexor synergizes with azacitidine to eliminate myelodysplastic syndrome cells through p53 nuclear accumulation. Azacitidine 26-37 tumor protein p53 Homo sapiens 90-93 34854834-6 2022 Early phase clinical trials combining the anti-CD47 mAb magrolimab with the hypomethylating agent azacitidine have showed synergistic activities, deep and durable responses, as well as a tolerable safety profile in these patients, including those with TP53 mutations. Azacitidine 98-109 tumor protein p53 Homo sapiens 252-256 35216478-10 2022 Among a number of non-canonical approaches to TP53-mutated AML, the anti-CD47 antibody magrolimab in combination with azacitidine showed promising results in a phase 1b trial. Azacitidine 118-129 tumor protein p53 Homo sapiens 46-50