Relevant bibliographies by topics / Azacytidin (AZA)

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Academic literature on the topic 'Azacytidin (AZA)'

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Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Azacytidin (AZA)"

1

Pískala, Alois, Naeem B. Hanna, Milena Masojídková, Miroslav Otmar, Pavel Fiedler, and Karel Ubik. "Synthesis of N4-Alkyl-5-azacytidines and Their Base-Pairing with Carbamoylguanidines - A Contribution to Explanation of the Mutagenicity of 2'-Deoxy-5-azacytidine." Collection of Czechoslovak Chemical Communications 68, no. 4 (2003): 711–43. http://dx.doi.org/10.1135/cccc20030711.

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A series of N4-alkyl-5-azacytidines 3a-3h were prepared by treatment of the 4-methoxy analogue 4 with the respective amines. In the case of propyl-, butyl-, sec-butyl-, benzyl- or furfurylamine, aggregates of azacytidines 3a-3e with their hydrolytic products 5a-5e were isolated. Similar aggregates were obtained with 1-methyl-5-azacytosine (6) and 2-(methylcarbamoyl)guanidine (7). Compound 7 was prepared by the reaction of guanidine with methyl isocyanate; the reaction of 2 or 3 equivalents gave the di- or tricarbamoyl derivatives 11 and 12, respectively. Cyclization of 7 and 11 with DMF dimethyl acetal afforded azacytosines 6 and 13, respectively. Aggregates of guanosine with 5-azacytosine nucleosides 1, 2 and 15 or of 5-aza-5,6-dihydrocytosine nucleosides 16 and 17 with 5-azacytidine (1) and its 2'-deoxy congener 2 have been prepared by co-crystallization of the respective pairs of nucleosides. The anomers of (deoxyribosylcarbamoyl)guanidine 20a and 20b have been prepared by hydrolysis of the deoxy nucleoside 2. An aggregate of the picrate (8a) of (ribosylcarbamoyl)guanidine 8 with cytidine (9) has been obtained by co-crystallization of both components. Reaction of the methoxy nucleoside 4 with tert-butylamine gave, by contrast to the above mentioned amines, the α-anomer of O-methylribosylisobiuret 22, which was cyclized by DMF dimethyl acetal to the α-anomer of N4,N4-dimethyl-5-azacytidine 24. The connection of the base-pairing ability of carbamoylguanidines with the mutagenicity of 2'-deoxy-5-azacytidine (2) as well as the mechanism of inhibition of DNA methyltransferase by this nucleoside analogue is discussed. In contrast to the unsubstituted 5-azacytidine (1) or its N4-methyl derivatives, none of the N4-alkyl derivatives exhibited any antibacterial or antitumor activity at 100 μg/ml or 10 μmol/l concentrations, respectively.
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2

Wang, C., and EA McCulloch. "Sensitivity to 5-azacytidine of blast progenitors in acute myeloblastic leukemia." Blood 69, no. 2 (February 1, 1987): 553–59. http://dx.doi.org/10.1182/blood.v69.2.553.553.

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Abstract In a previous study, we showed that the blast stem cells of acute myeloblastic leukemia (AML) were more sensitive to cytosine arabinoside (ara-C) when growing in suspension culture than during colony formation in methylcellulose. We suggested that the difference might be explained by considering the cellular mechanisms responsible for growth in suspension and colony formation. In the former, the clonogenic cells increase in number (self-renewal); in the latter, most of the divisions are terminal. The increased sensitivity to ara-C in suspension might then be attributed to its ability to inhibit self-renewal to a greater degree than cell division generally. A test of this hypothesis would be to compare the survival curves in suspension and in methylcellulose using a drug that spared or stimulated self-renewal. Such an agent is 5- azacytidine (5-aza) and has the additional advantage that its analogue, 6-azacytidine (6-aza) has no effect on self renewal. The data supported the hypothesis, since clonogenic AML blasts were much less sensitive to 5-aza in suspension than in methylcellulose. The effect of 6-aza, while qualitatively similar, was much less marked. Controls showed that the difference in survival curves could not be explained on a kinetic basis or by the secretion of growth factors by 5-aza-treated cells. We suggest that a comparison of the effects of drugs in suspension and in methylcellulose may be useful in preclinical screening of putative anti- AML compounds.
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Wang, C., and EA McCulloch. "Sensitivity to 5-azacytidine of blast progenitors in acute myeloblastic leukemia." Blood 69, no. 2 (February 1, 1987): 553–59. http://dx.doi.org/10.1182/blood.v69.2.553.bloodjournal692553.

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In a previous study, we showed that the blast stem cells of acute myeloblastic leukemia (AML) were more sensitive to cytosine arabinoside (ara-C) when growing in suspension culture than during colony formation in methylcellulose. We suggested that the difference might be explained by considering the cellular mechanisms responsible for growth in suspension and colony formation. In the former, the clonogenic cells increase in number (self-renewal); in the latter, most of the divisions are terminal. The increased sensitivity to ara-C in suspension might then be attributed to its ability to inhibit self-renewal to a greater degree than cell division generally. A test of this hypothesis would be to compare the survival curves in suspension and in methylcellulose using a drug that spared or stimulated self-renewal. Such an agent is 5- azacytidine (5-aza) and has the additional advantage that its analogue, 6-azacytidine (6-aza) has no effect on self renewal. The data supported the hypothesis, since clonogenic AML blasts were much less sensitive to 5-aza in suspension than in methylcellulose. The effect of 6-aza, while qualitatively similar, was much less marked. Controls showed that the difference in survival curves could not be explained on a kinetic basis or by the secretion of growth factors by 5-aza-treated cells. We suggest that a comparison of the effects of drugs in suspension and in methylcellulose may be useful in preclinical screening of putative anti- AML compounds.
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Motoji, T., T. Hoang, D. Tritchler, and EA McCulloch. "The effect of 5-azacytidine and its analogues on blast cell renewal in acute myeloblastic leukemia." Blood 65, no. 4 (April 1, 1985): 894–901. http://dx.doi.org/10.1182/blood.v65.4.894.894.

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Abstract Blast cells from patients with acute myeloblastic leukemia were exposed to 5-azacytidine (5-aza) and its analogues 5-aza 2′-deoxycytidine (5- aza-dr) and 6-azacytidine (6-aza). Simple negative exponential survival curves were obtained for the three drugs, but the sensitivity varied; 5- aza-dr was most toxic, 6-aza was least toxic, and 5-aza was intermediate. Colonies surviving drug exposure were replated; 5-aza and 5-aza-dr were found to increase secondary plating efficiency, whereas 6- aza was inactive. The findings provide indirect evidence for a role for DNA methylation in the regulation of blast cell self-renewal.
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5

Motoji, T., T. Hoang, D. Tritchler, and EA McCulloch. "The effect of 5-azacytidine and its analogues on blast cell renewal in acute myeloblastic leukemia." Blood 65, no. 4 (April 1, 1985): 894–901. http://dx.doi.org/10.1182/blood.v65.4.894.bloodjournal654894.

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Blast cells from patients with acute myeloblastic leukemia were exposed to 5-azacytidine (5-aza) and its analogues 5-aza 2′-deoxycytidine (5- aza-dr) and 6-azacytidine (6-aza). Simple negative exponential survival curves were obtained for the three drugs, but the sensitivity varied; 5- aza-dr was most toxic, 6-aza was least toxic, and 5-aza was intermediate. Colonies surviving drug exposure were replated; 5-aza and 5-aza-dr were found to increase secondary plating efficiency, whereas 6- aza was inactive. The findings provide indirect evidence for a role for DNA methylation in the regulation of blast cell self-renewal.
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6

Potter, Victoria T., Victoria J. Tindell, Rachel Kesse-Adu, Janet Hayden, Patience Pasipanodya, Laura Reiff-Zall, Judith C. W. Marsh, et al. "Comparative Analysis of An Azacytidine Versus Azacytidine-HSCT Approach for the Treatment of Older Patients with AML/MDS." Blood 116, no. 21 (November 19, 2010): 2375. http://dx.doi.org/10.1182/blood.v116.21.2375.2375.

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Abstract Abstract 2375 While allogeneic HSCT remains the only curative option for patients with MDS, it is associated with considerable morbidity and mortality. 5-azacytidine (5-aza) has been shown to improve the overall survival (OS) of patients with int-2/high risk MDS when compared with best supportive care and conventional chemotherapy. The feasibility of 5-aza in the pre-transplant setting has been demonstrated allowing disease remission induction whilst minimising the toxicity of “induction” chemotherapy. However the additional benefit gained by patients receiving HSCT post 5-aza as compared to patients who receive continuous 5-aza therapy remains to be determined. We report on our single centre experience on the use of 5-aza in a cohort of 71 patients receiving 5-aza as de-novo therapy for high risk MDS/AML. The patients were classified into 2 cohorts. 41 patients received 5-aza in a non-intensive group (defined as patients with advanced age or significant co-morbidities precluding them from HSCT) and 30 patients received 5-aza induction therapy with the intention of proceeding to an allogeneic HSCT (intensive group). Patients in the non-intensive group were significantly older at start of 5-aza therapy than the intensive group (median age: 72 yrs vs 62 yrs, p=<0.01). There was no difference in the proportion of patients with advanced disease (int-2/high IPSS or AML) between groups (non-intensive: 80% vs intensive: 76%, p=0.76). Similarly, there was no significant difference in blast percentage at diagnosis or karyotype risk group between the non-intensive and intensive groups. In the intensive group, the median no. of cycles of 5-aza administered was 7(range 1–30). Out of 30 patients, 15(50%) patients did not proceed to transplant. 14 of these patients had disease progression while on 5-aza, out of which 11 patients received conventional chemotherapy. None of these 11 patients proceeded to HSCT primarily as a result of refractory MDS/AML or chemotherapy toxicity. 15(50%) patients attained a morphological remission (<5% bone marrow blasts) post-5-aza and eventually received a RIC HSCT (including two patients who received umbilical cord blood transplants). All transplanted patients had durable engraftment and the incidence of GVHD at 1 year post-transplant was 50%. At last follow-up, 6 patients who received HSCT were still alive. The actuarial OS at 1 yr post transplant was 35%+/&minus;7%. Among the 41 patients in the non-intensive group, the median number of cycles of 5-aza received was 7 (range:1-46). At last follow-up, 8 patients (19%) were alive with 7 patients receiving ongoing 5 aza. The main reason for cessation of therapy was disease progression. In summary, only 50% of patients commencing 5-aza in the intensive group were subsequently able to receive an allogeneic HSCT. While the non-intensive group consisted of older patients, the median OS from start of 5-azacytidine was 22 months for both intensive and non-intensive groups. The 1 yr and 2 yr actuarial OS was 57%+/&minus;8% and 24%+/&minus;8% for the non-intensive group and 76%+/&minus;8% and 17%+/&minus;8% for the intensive group (p=0.76). While the development of RIC regimens has facilitated the expansion of allogeneic HSCT to older patients with AML/MDS, these findings suggest that in certain patients with co-morbidities, non-intensive novel therapies may be a preferable therapeutic option. Further studies in older AML/MDS patients to evaluate the benefit of novel agents such as 5-azacytidine when compared with HSCT are warranted. Disclosures: Mufti: Celgene: Consultancy, Honoraria, Research Funding, Speakers Bureau.
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Sripayap, Piyanuch, Tadashi Nagai, Mitsuyo Uesawa, Hiroyuki Kobayashi, Tomonori Tsukahara, Ken Ohmine, Kazuo Muroi, Gary Baley, and Keiya Ozawa. "Overcoming Resistance to 5-Azacytidine in Acute Myelogenous Leukemia." Blood 120, no. 21 (November 16, 2012): 1370. http://dx.doi.org/10.1182/blood.v120.21.1370.1370.

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Abstract Abstract 1370 Background: The DNA methylation inhibitor 5-azacytidine (AZA), which is approved for treatment of myelodysplastic syndrome, is also a potential agent for treatment of leukemia; however, drug resistance is an ongoing problem, and mechanisms underlying developing resistance to AZA are poorly understood. Therefore, clarifying the resistance mechanisms is central to establish effective countermeasures. Methods: To probe the mechanisms of resistance to AZA and to develop an effective method for overcoming them, we first generated two AZA-resistant cell lines, THP-1/AR and HL60/AR, from the human acute myelogenous leukemia cell lines THP-1 and HL60. We then studied variations between the parental and resistant lines. Results: AZA increased the percentages of sub-G1 and G2/M-phase cells in the AZA-sensitive parental cell lines; whereas, it had no similar effect in the resistant lines. Consistent with these results, the AZA-induced increases in the levels of cleaved forms of caspase 3, caspase 7, caspase 9, and PARP seen in sensitive cells were diminished in resistant cells. Furthermore, AZA markedly elevated the level of phospho JNK/SAPK in sensitive cells, but not in resistant cells. These results suggest that AZA induced apoptosis as well as G2/M arrest due to activation of JNK/SAPK signaling, and that induction of these changes was prevented in resistant cells. We also found that the activity as well as protein levels of DNA methyltransferases (DNMTs), which are the main target molecules of AZA, were suppressed by AZA in sensitive cells. However, in resistant cells, this effect was abrogated; and accordingly, AZA-induced up-regulation of p16 gene expression was also negated. These findings thus suggest that resistance was acquired by a DNMT-dependent mechanism. There was no remarkable difference between resistant cells and sensitive cells in the levels of uridine-cytidine kinase 2 (UCK2), which is a key enzyme for conversion of AZA to active form. However, several point mutations were found restrictedly in exon 4 of the UCK2 gene in both resistant cells. These results raised the possibility that the AZA activation process was perturbed due to reduction of UCK activity; and consequently, AZA failed to suppress DNMT in resistant cells. In addition, by microarray analysis, we identified eleven genes that were expressed at significantly different levels in resistant cells versus sensitive cells. Finally, we showed that the histone deacetylase inhibitor romidepsin induced p16 gene expression and increased the levels of apoptosis-related molecules, while suppressing growth in both sensitive and resistant cell lines. An isobologram analysis demonstrated that simultaneous administration of AZA and romidepsin resulted in an additive inhibitory effect on both AZA-sensitive and AZA-resistant cell growth. These results suggest that romidepsin can overcome AZA resistance; therefore, the combination of AZA and romidepsin not only augments the anti-leukemia effect but also prevents acquisition of resistance to AZA. Conclusions: Newly established 5-azacytidine-resistant cell lines THP-1/AR and HL60/AR are good models to analyze the mechanisms of drug resistance to 5-azacytidine. Using these cell lines, we revealed that acquisition of resistance is primarily caused by a DNMT-dependent mechanism, which can be surmounted with addition of romidepsin. It is likely that the combination of AZA and romidepsin can prevent patients from acquiring resistance to AZA while augmenting its anti-leukemia therapeutic effect. Disclosures: No relevant conflicts of interest to declare.
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Yalamalle, V. R., D. M. Ithape, A. Kumar, K. Bhagat, S. Ghosh, and M. Singh. "Seed treatment with 5-azacytidine reduces ageing-induced damage in onion seeds." Seed Science and Technology 48, no. 3 (December 31, 2020): 407–12. http://dx.doi.org/10.15258/sst.2020.48.3.09.

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The effect of treating aged onion seeds with 5-azacytidine (5-aza) on germination and vigour was evaluated. Seeds of two onion varieties, 'Bhima Raj' (BRJ) and 'Bhima Red' (BRD) were treated with 0, 10, 25 or 50 μg mL–1 5-azacytidine (a DNA demethylating agent). In comparison with the control treatment (0 μg mL–1 5-azacytidine), treatment with 5-azacytidine enhanced seed germination, seedling length, seedling dry weight and seed vigour indices. 5-azacytidine treatment also increased the activity of superoxide dismutase (SOD) and total antioxidant capacity (TAC). Seed treatment with 5-azacytidine has the potential to enhance the viability and vigour of aged onion seeds. This study provides phenotypic and biochemical data for further exploring the role of DNA methylation in understanding the process of seed ageing.
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Bakanay, S. M., E. Karakiliç, S. Civriz-Bozdag, M. Arat, M. Ozcan, G. Gurman, O. Ilhan, M. Beksac, N. Konuk, and O. Arslan. "5-azacytidine treatment results in myelodysplastic syndrome." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e18003-e18003. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e18003.

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e18003 Background: Myelodysplastic syndrome (MDS) is a clonal disease of hematopoiesis characterized by dysplasia in one or more series. 5-azacytidine (5-AZA) which is one of the methyl transferase inhibitors, targets the epigenetic changes in MDS and has been used for the last few years. Phase III studies which compare 5-AZA with supportive therapies report response rates up to 60%. Methods: In this study the aim was to retrospectively analyze the response rates of 26 MDS patients who were treated with 5-AZA between years 2002–2008. The patients were; median age 58 (21–84); male/female = 16/10; RAEB-I (7 patients); RAEB-II (18 patients); ve CMML (1 patient); secondary MDS (2 patients). According to an international prognostic scoring system, 6 patients were intermediate-1; 9 patients were intermediate-2; and 11 patients were high risk. Nine patients received 5-AZA as first-line therapy. The median leukocyte counts, absolute neutrophil counts (ANC), hemoglobin values, and thrombocyte counts at the begining of the cycles were; 2.4 (0.5–23)x10e9/L, 0.7 (0.1–16.5)x10e9/L, 8.6(5.3–11.4) gr/dl, 41(4–35)x10e9/L, respectively. The karyotype analysis revealed del5q in 3 patients; -7/del7q in 6 patients; trisomy 8 in 7 patients, del20q, del11q and complex karyotype (del7q+del5q+delY) in 1 patient each. The median cycles completed were 2 (1–6). Results: Seven patient were not elligible for response evaluation. Nine patients (47%) did not respond to the therapy and 8 of them were lost. Ten patients (53%) responded to the therapy with complete remission (n=4), partial remission (n = 2) and hematological improvement (n = 4). The responders and non-responders were similar in terms of median age, sex and pretreatment leukocyte, ANC and hemoglobin levels. However, there was statistically significant difference in terms of initial thrombocyte counts, total number of cycles received and serum ferritin levels. The patients who received 5-AZA as first line therapy had beter response than others (71% versus 29%). Conclusions: The observed response to 5-AZA therapy was similar to the reported rates in the literature. The most important factors for response were initial thrombocyte counts, total number of cycles, other therapies received before 5-AZA and the serum ferritin levels. No significant financial relationships to disclose.
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Locatelli, Silvia L., Roberto Papait, Giuseppa Careddu, Ada Koschorke, Giuliano G. Stirparo, Monica Balzarotti, Luca Castagna, Armando Santoro, and Carmelo Carlo-Stella. "Upregulation of Cereblon Expression By the DNA Methyltransferase Inhibitor Azacytidine Strongly Enhances Lenalidomide Cytotoxicity in Germinal Center B-Cell-like (GCB) and Activated B-Cell-like (ABC) Diffuse Large B-Cell Lymphoma (DLBCL)." Blood 124, no. 21 (December 6, 2014): 2253. http://dx.doi.org/10.1182/blood.v124.21.2253.2253.

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Abstract INTRODUCTION: Lenalidomide monotherapy exerts clinical activity in relapsed/refractory Diffuse Large B-cell Lymphoma (DLBCL) with better response rate and progression-free survival being recorded in activated B-cell-like (ABC) rather than germinal center B-cell-like (GCB)-DLBCL. Reasons for such a difference are likely due to different expression of key molecules involved in mediating activity of Lenalidomide, such as Interferon regulatory factor 4(IRF4) and cereblon (CRBN). Evidences supporting the key role of DNA methylation and histone modifications in regulating genome stability and gene expression in DLBCL prompted us to investigate the capacity of Azacytidine in modulating Lenalidomide activity, thereby sensitizing GCB-DLBCL to Lenalidomide and enhancing Lenalidomide efficacy in ABC-DLBCL. METHODS: DLBCL cell lines with ABC (U-2932, RIVA) or GCB (SU-DHL4, SU-DHL6) genotype were used to investigate the effects of Lenalidomide and Azacytidine on cell growth and cell death. Western blotting (WB) and immunofluorescence analysis were used to assess modulating effects of the two-drug combination on molecular determinants of Lenalidomide activity. Additionally, we studied CRBN, IRF4 and CRBN binding proteins expression, such as Ikaros and Aiolos (IKZF1 and IKZF3) by real time polymerase chain reaction (RT-PCR) in response to drug treatment. RESULTS: Graded concentrations of Lenalidomide (0.1-100 µM) inhibited cell proliferation by 20% to 40% and increased cell death up to 30% to 40% in ABC-DLBCL cell lines, whereas had minimal effects on GCB-DLBCL cell lines. Untreated ABC-DLBCL but not GCB-DLBCL consistently showed a high expression of CRBN and IRF4. Upon Lenalidomide treatment (3 days) CRBN was significantly upregulated and IRF4 downregulated in ABC-DLBCL, but not GCB-DLBCL cells. Since DNA methylation regulates gene expression in DLBCL cell lines, we next examined whether Azacytdine could modulate CRBN and IRF4 expression and in turn enhance responsiveness to Lenalidomide. Exposure of both ABC- and GCB-DLBCL cell lines to Azacytidine (up to 72 hours) induced a marked increase of CRBN and IRF4 transcripts; addition of Lenalidomide strongly increased Azacytidine-induced increase of CRBN and significantly downregulated IRF4 expression; the combined treatment induced a marked downregulation of Ikaros and Aiolos protein levels. At the cellular level, the concomitant Azacytidine (10 μM)/Lenalidomide (10 μM) treatment inhibited in a synergistic manner the mean (±SEM) cell growth of both ABC-DLBCL (Lena: -16 ± 4%; AZA: -22 ± 2%; AZA/Lena: -70 ± 1%, P<0.001) and GCB-DLBCL (Lena: -17 ± 3%; AZA: -40 ± 4%; AZA/Lena: -82 ± 2%, P<0.001). Additionally, the two drug exposure was associated with a 3-fold decrease of S phase cells(Lena: 28 ± 2%; AZA: 22 ± 0.8%; AZA/Lena: 9 ± 1%, P<0.001); a marked p21 overexpression, and a 3- to 4-fold cell death increase (P<0.001) in both ABC- and GCB-DLBCL. CONCLUSIONS: Our results indicate that Azacytidine sensitizes GCB-DLBCL to the cytotoxic effects of Lenalidomide and enhances Lenalidomide efficacy against ABC-DLBCL resulting in synergistic anti-proliferative and pro-apoptotic effects in both ABC- and GCB-DLBCL cell lines. Cytotoxicity of the two drug combination is mediated by signaling events involving CRBN upregulation and IRF4 downregulation leading to CRBN-binding proteins downregulation. Azacytidine-dependent activation of CRBN and IRF4 expression allow to hypothesize a methylation-driven regulation of these genes. These results might provide a rationale for clinical studies using Azacytidine and Lenalidomide combination in ABC- and GCB-DLBCL. Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Azacytidin (AZA)"

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Chen, Ping. "Pharmacokinetic-Pharmacodynamic Studies Of 5-Azacytidine In Combination With Gti-2040." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1221854928.

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Křtěnová, Petra. "Epigenetická regulace genu PU.1 v rezistenci na léčbu 5-azacytidinem u akutní myeloidní leukémie." Master's thesis, 2017. http://www.nusl.cz/ntk/nusl-355665.

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Hematopoiesis is a highly orchestrated process, in which a single hematopoietic stem cell (HSC) gives a rise to all blood cellular components. For myeloid and lymphoid development precise controlled expression of the PU.1 transcription factor is needed. Deletion of PU.1 gene in mouse is lethal and its dysregulation during hematopoietic differentiation is associated with blood malignancies including acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS). MDS and AML are serious blood disorders characterized by expansion of immature blood cells and lack of differentiated functional cells. Not only genetic but also epigenetic aberrations represent a very important field for studying pathophysiology of leukemia genesis and dysregulation of the PU.1 gene represents intensively studied candidate mechanism. Modern therapy of selected MDS and subset of AML patients is based on treatment with DNA hypomethylating agent Azacytidine (AZA) interfering in PU.1 gene regulatory mechanism. However, poor response or resistance to this therapy often occurs. In this thesis we present data obtained from AZA-resistant clones of MDS/AML cell line OCI-M2. We analysed DNA methylation and DNA hydroxymethylation at the key regulatory element of the PU.1 gene (URE). We found that these epigenetic modifications at URE...
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Mnasri, Nourhen. "Le médicament épigénétique 5-Azacytidine stabilise l’ARN messager du récepteur des lipoprotéines de basse densité (LDLR) via une voie IRE1α/EGFR/ERK1/2- dépendante." Thèse, 2017. http://hdl.handle.net/1866/20259.

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Book chapters on the topic "Azacytidin (AZA)"

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Balansky, R. "Effects of 5-Azacytidine(5-AzC), 5-Bromodeoxyuridine(BrdU) and Diethyldithiocarbamate (DEDTC) on Diethylnitrosamine (DEN)-Induced Carcinogenesis in Rats." In Chemical Carcinogenesis 2, 579–86. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3694-9_55.

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Conference papers on the topic "Azacytidin (AZA)"

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Wilson, Andrew, Lanzi Sinaise, Jade M. Readus, Michelle Park, Anum S. Lalani, Jeanette Saskowski, and Dineo Khabele. "Abstract 1016: Combination low dose 5-azacytidine (AZA) and romidepsin (FK228) therapy re-sensitizes ovarian cancer cells to cisplatin." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1016.

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Smit, Evelyn, Nithya Krishnan, Jeffrey Conroy, Jianmin Wang, Song Lui, and Anna Woloszynska-Read. "Abstract 424: The transcriptomic and methylomic changes caused by subtoxic doses of 5-azacytidine and 5-aza-2’-deoxycytidine." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-424.

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Verschraegen, Claire, Carolyn Muller, Julie Bauman, Teresa Rutledge, and Dennie Jones. "Abstract A184: A phase I study of 5‐azacytidine (AZA) and erlotinib (E) for patients (pt) with advanced solid tumors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a184.

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Pískala, Alois, Naeem B. Hanna, Milena Masojídková, Miroslav Otmar, and Pavel Fiedler. "Synthesis of N4-alkyl-5-azacytidines and their base pairing with carbamoylguanidines – a contribution to explanation of the mutagenicity of 5-aza-2'-deoxycytidine." In XIth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 1999. http://dx.doi.org/10.1135/css199902248.

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Serdjebi, Cindy, Joseph Ciccolini, Alexandre Evrard, Cedric Mercier, Nicolas André, Laetitia Dahan, Gerard Milano, Jean-François Seitz, Bruno Lacarelle, and L'Houcine Ouafik. "Abstract 1869: Severe toxicities in patients undergoing gemcitabine, ARA-C, capecitabine, or azacytidine treatments: Is deregulated cytidine deaminase the bad guy." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1869.

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