PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27003313-1 2016 BACKGROUND: The archetypal DNA methyltransferase inhibitors, 5-azacytidine (AZA) and 5-aza-2"-deoxycytidine (DAC) are potent antineoplastic agents used in the treatment of mainly, blood malignancies. Azacitidine 76-79 arylacetamide deacetylase Homo sapiens 109-112 29795051-1 2018 Higher-risk myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) of the elderly exhibit several commonalities, including first line treatment with hypomethylating agents (HMA) like azacitidine (AZA) or decitabine (DAC). Azacitidine 192-203 arylacetamide deacetylase Homo sapiens 225-228 27036028-7 2016 Indeed, different cytotoxicities of AZA and DAC toward human colorectal cancer cell lines were observed, in which cells were more sensitive to AZA. Azacitidine 143-146 arylacetamide deacetylase Homo sapiens 44-47 26960675-3 2016 Two drugs, azacitidine (AZA) and decitabine (DAC), defined, because of their proven mechanism of action, as DNA methyltransferase inhibitors (DNMTIs), or hypomethylating agents (HMAs), have proven effective in improving peripheral cytopenias and quality of life, reducing or eliminating transfusion need, delaying leukemic evolution, and (only for AZA) prolonging overall survival (OS). Azacitidine 348-351 arylacetamide deacetylase Homo sapiens 45-48 28210112-4 2010 In the relatively DAC-insensitive cell line A549, both AZA and DAC caused DNA methyltransferase I depletion and DNA hypomethylation; however, only AZA significantly induced markers of DNA damage and apoptosis, suggesting that mechanisms in addition to, or other than, DNA hypomethylation are important for AZA-induced cell death. Azacitidine 55-58 arylacetamide deacetylase Homo sapiens 18-21 23940695-1 2013 Treatment with the demethylating drugs 5-azacytidine (AZA) and decitabine (DAC) is now recognised as an effective therapy for patients with Myelodysplastic Syndromes (MDS), a range of disorders arising in clones of hematopoietic progenitor cells. Azacitidine 39-52 arylacetamide deacetylase Homo sapiens 75-78 21554144-8 2011 Both DAC- and AZA-treated patients received similar number of treatment cycles (mean: 4.8 vs. 5.6 in DAC vs. AZA, p > 0.05), with means of 4.6 days per cycle for patients receiving DAC and 7.4 days for those receiving AZA (p = 0.003). Azacitidine 14-17 arylacetamide deacetylase Homo sapiens 101-104 21554144-8 2011 Both DAC- and AZA-treated patients received similar number of treatment cycles (mean: 4.8 vs. 5.6 in DAC vs. AZA, p > 0.05), with means of 4.6 days per cycle for patients receiving DAC and 7.4 days for those receiving AZA (p = 0.003). Azacitidine 14-17 arylacetamide deacetylase Homo sapiens 101-104 21554144-11 2011 CONCLUSIONS: In MDS patients treated with an HMA, treatment with DAC was associated with less frequent transfusions than with AZA treatment. Azacitidine 126-129 arylacetamide deacetylase Homo sapiens 65-68 18931345-4 2009 Sensitivity to DAC showed a low correlation (R = 0.44, P = .11) to that of 5-azacytidine (AZA), but a good correlation to that of cytarabine (Ara-C; R = 0.89, P < .001). Azacitidine 75-88 arylacetamide deacetylase Homo sapiens 15-18 18931345-4 2009 Sensitivity to DAC showed a low correlation (R = 0.44, P = .11) to that of 5-azacytidine (AZA), but a good correlation to that of cytarabine (Ara-C; R = 0.89, P < .001). Azacitidine 90-93 arylacetamide deacetylase Homo sapiens 15-18 16273408-2 2005 5-Aza-2"-deoxycytidine (decitabine, DAC) is a nucleoside analog, which, at low doses, acts as a hypomethylating agent and is fivefold to tenfold more active than 5-azacytidine (azacitidine, Vidaza)--currently the only approved drug for treatment of myelodysplastic syndrome (MDS). Azacitidine 162-175 arylacetamide deacetylase Homo sapiens 36-39 16273408-2 2005 5-Aza-2"-deoxycytidine (decitabine, DAC) is a nucleoside analog, which, at low doses, acts as a hypomethylating agent and is fivefold to tenfold more active than 5-azacytidine (azacitidine, Vidaza)--currently the only approved drug for treatment of myelodysplastic syndrome (MDS). Azacitidine 177-188 arylacetamide deacetylase Homo sapiens 36-39 33669837-4 2021 By measuring the cell retention of fluorescein-linked annexin V and propidium iodide, we showed an apoptotic mode of death for MOLM-13 cells after treatment with either DAC or AZA, for MOLM-13/DAC cells after treatment with AZA, and for MOLM-13/AZA cells after treatment with DAC. Azacitidine 176-179 arylacetamide deacetylase Homo sapiens 193-196 33669837-4 2021 By measuring the cell retention of fluorescein-linked annexin V and propidium iodide, we showed an apoptotic mode of death for MOLM-13 cells after treatment with either DAC or AZA, for MOLM-13/DAC cells after treatment with AZA, and for MOLM-13/AZA cells after treatment with DAC. Azacitidine 176-179 arylacetamide deacetylase Homo sapiens 193-196 33669837-4 2021 By measuring the cell retention of fluorescein-linked annexin V and propidium iodide, we showed an apoptotic mode of death for MOLM-13 cells after treatment with either DAC or AZA, for MOLM-13/DAC cells after treatment with AZA, and for MOLM-13/AZA cells after treatment with DAC. Azacitidine 224-227 arylacetamide deacetylase Homo sapiens 169-172 32784599-5 2020 Although these inhibitors, mainly nucleoside analogues such as 5-azacytidine (5-aza) and decitabine (DAC), cause re-expression of tumor suppressor genes, inhibition of tumor cell growth, and increased apoptosis in BC experimental models and clinical trials, they also show important drawbacks that prevent their use as a valuable option for the treatment of BC. Azacitidine 63-76 arylacetamide deacetylase Homo sapiens 101-104 32784599-5 2020 Although these inhibitors, mainly nucleoside analogues such as 5-azacytidine (5-aza) and decitabine (DAC), cause re-expression of tumor suppressor genes, inhibition of tumor cell growth, and increased apoptosis in BC experimental models and clinical trials, they also show important drawbacks that prevent their use as a valuable option for the treatment of BC. Azacitidine 63-68 arylacetamide deacetylase Homo sapiens 101-104