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Decitabine

Q: What are the different variations or types of Decitabine?

Decitabine is available in different formulations and administration routes, such as intravenous (IV) infusion and subcutaneous injection. Researchers are also exploring novel delivery methods and combination therapies to optimize its efficacy and safety profile.

Q: What are some common usage challenges with Decitabine?

One of the key challenges with Decitabine is determining the optimal dosing and administration regimen. The drug's effectiveness can be influenced by factors such as patient characteristics, disease stage, and prior treatments. Researchers must carefully evaluate the latest literature to identify the most effective protocols for their specific research goals.

Q: What are some specific applications of Decitabine?

Decitabine has shown promise in the treatment of various cancers, including myelodysplastic syndrome and acute myeloid leukemia. It is also being investigated for its potential in enhancing immune response and combating solid tumors. Reseachers are continuously exploring new avenues for Decitabine's therapeutic applications to improve patient outcomes.

Decitabine, a synthetic nucleoside analog, is a potent antineoplastic agent used in the treatment of various cancers, including myelodysplastic syndrome and acute myeloid leukemia.
It functions by inhibiting DNA methyltransferase, leading to demethylation and reactivation of silenced tumor suppressor genes.
Decitabine has shown promise in enhancing treatment outcomes and improving patient quality of life, though its optimal dosing and administration regimens continue to be an area of active research.
PubCompare.ai's AI-driven platform can help researchers identify the most effective Decitabine protocols by analyzing the latest literature, preprints, and patent data, ensuring reproducibility and accuracy in this vital field of oncology research.

Most cited protocols related to «Decitabine»

Cisplatin-Resistant Ovarian Cancer Cell Line Development

All cells were maintained in RPMI 1640 media with 2 mM L-glutamine, 50 U/ml penicillin, 50 mg/ml streptomycin, and 10% fetal bovine serum, at 30°C and 5% CO₂. 5-aza-2'-deoxycytidine (5-aza-dC) was purchased from Sigma (St. Louis, MO) and zebularine [1-(β-D-ribofuranosyl)-1,2-dihydropyrimidin-2-one] was a kind gift from Dr. Victor Marquez (Developmental Therapeutics Program, National Cancer Institute, Frederick, MD). A2780 ovarian cancer cells were obtained from ATCC (Manassas, VA), restriction enzymes from New England Biolabs (Beverly, MA), and cell culture reagents from Invitrogen (Carlsbad, CA). Using serial dilution cell seeding, a single clone of the cisplatin-sensitive, epithelial ovarian cancer cell line A2780 was cultured for multiple cycles ("treatment rounds") with incrementally increasing doses of cis-diamminedichloroplatinum(II) dichloride (CDDP, cisplatin) (Sigma). 5-aza-dC or zebularine treatment was performed after cell seeding for 48 hours prior to cisplatin treatment [31 (link)]. MTT assays were used to determine both GI₅₀values and growth curves of the cells, as we have described previously [31 (link)]. Briefly, 96-well dishes were plated with 2,000 cells per well one day before cisplatin treatment. The next day, cells were treated with various dosages of cisplatin (0.5 μM to 100 μM) for three hours and allowed to recover for three days. Following drug treatments, total viable cell numbers were determined by 4-hr treatments with 3-(4.5-dimethylthiazol-2-yl)-2.5-diphenyl tetrazolium bromide (MTT) assay, with cell viability (as determined by MTT metabolism to formazan) determined by measuring absorbance at 600 nm using a Bio-Tek (Winooski, VT) microplate spectrophotometer. Dose-response curves were then generated and 50% growth inhibitory (GI₅₀) dose values determined by Microsoft Excel or Prism 4.0 (GraphPad Software, San Diego, CA), using sigmoidal dose (variable slope) curve fitting, as we have described previously [31 (link),32 (link)].

Li M., Balch C., Montgomery J.S., Jeong M., Chung J.H., Yan P., Huang T.H., Kim S, & Nephew K.P. (2009). Integrated analysis of DNA methylation and gene expression reveals specific signaling pathways associated with platinum resistance in ovarian cancer. BMC Medical Genomics, 2, 34.

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Publication 2009

Azacitidine Biological Assay Bromides Cell Culture Techniques Cell Lines Cells Cell Survival Cisplatin Clone Cells Decitabine diphenyl DNA Restriction Enzymes Fetal Bovine Serum Formazans Glutamine Hyperostosis, Diffuse Idiopathic Skeletal Metabolism Ovarian Cancer Ovarian Neoplasm Penicillins Pharmaceutical Preparations prisma Psychological Inhibition pyrimidin-2-one beta-ribofuranoside Streptomycin Technique, Dilution Tetrazolium Salts

Comprehensive Cancer Cell Profiling

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Publication 2015

Antibodies Biological Assay Bromodeoxyuridine cDNA Microarrays Cell Cycle Cell Proliferation Cells Coculture Techniques Cytoplasm Decitabine DNA, Complementary Fractionation, Chemical Genome hydrogen sulfite Immunofluorescence Immunoprecipitation Immunoprecipitation, Chromatin Luciferases Microarray Analysis Nuclear Protein Protein Arrays Reverse Transcriptase Polymerase Chain Reaction Ubiquitination

Investigating Uremic Toxin Effects

Ten-week-old B-6 mice with ½-nephrectomy were used in this study. The experimental mice received intraperitoneal injection with IS (Sigma, St Louis, MO; n=8) or PCS (Kureha, Tokyo, Japan; n=8) at a dosage of 100 mg/kg/day for 4 weeks. The control mice (n=8) received daily phosphate-buffered saline injection for 4 weeks at the same volume that was administered to the experimental mice. At the end of study, the body weight of study animal was recorded, and the serum levels of blood urea nitrogen and creatinine were analyzed. The renal cortex was microdissected for further analysis. In the 5Aza-2dc treatment study, the IS- and PCS-injected mice received intraperitoneal injection with 5Aza-2dc (Sigma) simultaneously at a dosage of 0.35 mg/kg per 48 h for 4 weeks (n=8 for each group). All animal experiments were approved by the experimental animal ethics committee at the Chang Gung Memorial Hospital. The flow diagram for animal study is summarized in Figure 10.

Sun C.Y., Chang S.C, & Wu M.S. (2012). Suppression of Klotho expression by protein-bound uremic toxins is associated with increased DNA methyltransferase expression and DNA hypermethylation. Kidney International, 81(7), 640-650.

Publication 2012

Animal Ethics Committees Animals Body Weight Creatinine Decitabine Injections, Intraperitoneal Kidney Cortex Mice, House Nephrectomy Phosphates Saline Solution Serum Urea Nitrogen, Blood

Engineered Glioblastoma TICs and Xenografts

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Publication 2015

Azacitidine Caimans Cell Lines Clone Cells Decitabine Glioblastoma GMX 1778 Neoplasms Patients Sulfoxide, Dimethyl Xenografting

Transcriptional Profiling of Epigenetic Regulators

RNeasy Mini Kit (Qiagen, Ontario, Toronto, Canada) was used for RNA extraction as per the manufacturer’s protocol. Preparation of cDNA and qRT-PCR were carried out as described previously [40 (link)-42 (link)]. Transcript levels of Mecp2 (total), Mecp2e1 [NCBI: NM_001081979.1], Mecp2e2 [NCBI: NM_010788.3], Dnmt genes (Dnmt1, Dnmt3a and Dnmt3b), neuronal genes (Tubulin III (Tub III), NeuN), astrocytic genes (Gfap, S100b), and oligodendrocyte-specific genes (Cnpase, Mbp) were examined by using gene-specific primers (Table 2), as described previously [37 (link),43 (link)]. The relative expression and fold changes were calculated as described previously [37 (link)]. Two-way analysis of variance (ANOVA) and the Student t-test were used to calculate significant differences between untreated control and decitabine-treated samples.

Liyanage V.R., Zachariah R.M, & Rastegar M. (2013). Decitabine alters the expression of Mecp2 isoforms via dynamic DNA methylation at the Mecp2 regulatory elements in neural stem cells. Molecular Autism, 4, 46.

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Publication 2013

2',3'-Cyclic-Nucleotide Phosphodiesterases Astrocytes Decitabine DNA, Complementary DNA Modification Methylases DNMT1 protein, human DNMT3B protein, human Genes Glial Fibrillary Acidic Protein MECP2 protein, human Neurons Oligodendroglia Oligonucleotide Primers Student Tubulin

Most recents protocols related to «Decitabine»

Interferon Response in T Cells

Fig. S1 shows the characterization of the IFN response of T cells to cGAMP stimulation, IFNα2a pretreatment, and Sendai virus infection. Fig. S2 shows the impact of RELA on IFN response to cGAMP in CD4⁺ T cells MDDCs, MDMs, and THP-1 cells. Fig. S3 shows the impact of IRF3, TSA, 5AZA, and RELA K5R on IFN response to cGAMP, viability, and signaling in CD4⁺ T cells. Fig. S4 shows the impact of IRF3, 5AZA, and RELA K5R on IFN response to cGAMP in CD4⁺ T cells. Fig. S5 shows the functional impact of iCD4+ T cells in the context of HIV infection and anti-tumor response. Table S1 provides a complete list of differentially expressed genes.

Jeremiah N., Ferran H., Antoniadou K., De Azevedo K., Nikolic J., Maurin M., Benaroch P, & Manel N. (2023). RELA tunes innate-like interferon I/III responses in human T cells. The Journal of Experimental Medicine, 220(5), e20220666.

Publication 2023

CD4 Positive T Lymphocytes cyclic guanosine monophosphate-adenosine monophosphate Decitabine Genes, vif HIV Infections Interferon alfa 2a IRF3 protein, human Macular Edema, Cystoid methylene dimethanesulfonate Neoplasms RELA protein, human Sendai virus T-Lymphocyte THP-1 Cells

Quantifying Viral Infectivity and Interferon Response

For HIV infections, 4 d after lentivirus transduction and 2 d following 5AZA treatment, 0.07 million cells in 70 μl media were infected with 70 μl BFP-reporter single-round HIV-1 or HIV-2 with 8 μg/ml protamine and fresh 5AZA (2 μM). Cells were pretreated with B18R or control supernatants (10%) for 48 h prior to viral infections. Fresh B18R or control supernatants were added at the time of infection and left untouched for 48 h. Serial dilutions of viruses at 1/3 were performed. GHOST X4R5 cells were infected in parallel to control the viral titer of the inoculum. Cells and supernatants were harvested 48 h after infection.
For Sendai virus infections, 100,000 cells in 100 μl were infected with 100 μl of Sendai virus 200 HA/ml (Charles River, Cantell Strain) with 8 μg/ml protamine. Culture supernatants for IFN quantification were harvested 18–24 h after infection. Cells for RNA and protein extraction were harvested 6 h following infection.

Publication 2023

Cells Decitabine HIV-1 Infection Lentivirus protamine 2 Protamines Proteins Red Cell Ghost Rivers Sendai virus Strains Technique, Dilution Virus Virus Diseases

Azacitidine, Decitabine, and Venetoclax in AML

This is a single-center, retrospective cohort review that included patients aged 18 years or greater with a diagnosis of AML that received azacitidine or decitabine with or without VEN between June 1, 2017 and December 5, 2019 at The Ohio State University Comprehensive Cancer Center - The James Cancer Hospital. To be eligible for inclusion in the efficacy analysis, patients had to receive either 28 days of VEN or reach cycle 2, day 1 of azacitidine or decitabine. To be eligible for inclusion in the safety analysis, patients had to receive at least one dose of either azacitidine or decitabine and VEN, if applicable. Protected populations including pregnant or imprisoned patients, and patients enrolled on a clinical trial were excluded. This study protocol was approved by the Institutional Review Board. This study was conducted in compliance with the ethical standards of the responsible institution on human subjects as well as with the Helsinki Declaration.

Freeman T., Williams K., Puto M., Waller A., McLaughlin E.M., Blachly J.S, & Roddy J. (2023). Real-World Experience of Adults With Acute Myeloid Leukemia on Hypomethylating Agents With or Without Venetoclax at a Comprehensive Cancer Center. World Journal of Oncology, 14(1), 40-50.

Publication 2023

Azacitidine Decitabine Diagnosis Ethics Committees, Research Malignant Neoplasms Patients Population Group Safety

Exploratory Analysis of CR Rates

As an exploratory study, the primary aim of the analysis was to present descriptive estimates of the CR rates for both treatment groups. Secondary outcomes including the ORR, the clinical benefit rate, OS, time to response, time to treatment failure, and adverse events were also analyzed. Patients with incomplete medical records were not a part of the analysis.
All data were collected utilizing Research Electronic Data Capture (REDCap^®) [16 ]. Patient demographics and outcomes were reported for each treatment group and compared using Fisher’s exact test or two-sample t-tests, as appropriate. Efficacy outcomes (CR rate, ORR, and clinical benefit rate) were compared between groups for patients treated with 28 days of VEN and reached cycle 2, day 1 of azacitidine or decitabine. Differences in response to therapy were also compared by the presence or absence of various genetic aberrations. Kaplan-Meier curves were generated for each treatment group for OS, time to response and time to treatment failure. Patients were censored at the date of their last physician visit.
Safety outcomes were reported for all patients who have received at least one dose of VEN, azacitidine or decitabine including frequencies of toxicities, adverse events, and any dose delays or reductions. These outcomes were compared between treatment groups using Fisher’s exact tests. Duration of neutropenia was compared using the Wilcoxon rank-sum test. As a sensitivity analysis, response to therapy was also analyzed, including patients who did not meet the required minimum therapy but had at least one dose of VEN, azacitidine or decitabine. P-values reported are for descriptive purposes, and given the exploratory nature of the study, strong conclusions should not be inferred from the results of the statistical tests. All analyses were performed using SAS version 9.4 (SAS Institute Inc., Cary, NC).

Publication 2023

Azacitidine Birth Decitabine Hypersensitivity Leukopenia Patients Physicians Safety Therapeutics

DNA Methylation Profiling in Non-M3 AML Patients

Twenty-eight non-M3 AML patients who were monitored at the Hematology Department of the Chinese People’s Liberation Army General Hospital between August 2014 and June 2016 were enrolled in this study and underwent DNA methylation sequencing, as described previously [13 (link)]. Three of these patients had the t(8;21) translocation. A methylation sequencing dataset comprising 33 bone marrow samples was generated, including 23 non-paired de novo samples, 2 paired t(8;21) de novo/complete remission (CR) samples, and 3 paired non-t(8;21) de novo/CR samples. All de novo AML samples were collected before treatment, while CR samples were obtained after the first round of treatment with the DCAG regimen, which involved decitabine (20 mg/m² on days 1–5), Ara-C (10 mg/m² every 12 h on days 1–5), aclarubicin (20 mg on days 1, 3, and 5), and granulocyte colony-stimulating factor (300 μg/d from d0 to neutrophil recovery). All patients were diagnosed and assessed according to the AML guidelines of the National Comprehensive Cancer Network (version 1.2017; http://www.nccn.org/). As described previously [13 (link)], specimen collection was conducted only after written informed consent was obtained from each participant. Patient characteristics are summarized in Tables 1 and 2.Table 1

Characteristics of the de novo patient study cohort (n = 28)

Characteristic	Value
Age at diagnosis, years	49.07 ± 17.94
Sex, no. (%)
Male	11 (39)
Female	17 (61)
Bone marrow blast, no. (%)	67.55 ± 23.74
AML FAB subtype, no. (%)
M1	1 (3.57)
M2	5 (17.86)
M4	10 (35.71)
M5	11 (39.29)
M6	1 (3.57)
2017 NCCN cytogenetic risk classification, no. (%)
Good	5 (17.86)
Intermediate	20 (71.43)
Poor	3 (10.71)
2017 NCCN molecular risk classification, no. (%)
Good	12 (42.86)
Intermediate	7 (25.00)
Poor	9 (32.14)
Mutation, no. (%)
t(8;21)	3 (10.71)
inv(16)	2 (7.14)
NPM1	4 (14.29)
FLT3	6 (21.43)
DNMT3A	3 (10.71)
IDH1 or IDH2	4 (14.29)
KRAS or NRAS	4 (14.29)
TP53	2 (7.14)
biCEBPA	7 (25.00)

Table 2

Characteristics of the de novo/CR paired samples (n = 5)

	Age (years)	Sex	Bone marrow blast at diagnosis %	Cytogenetics at diagnosis	Risk classification	Induction regimen
Pair 1	59	Female	45.2	Normal karyotype	Intermediate	DCAG
Pair 2	34	Female	67.2	46, XX, inv(16)	Good	DCAG
Pair 3	60	Female	56.4	46, XX, t(11;20)	Intermediate	DCAG
Pair 4	73	Female	81	46, XX, t(8;21)	Good	DCAG
Pair 5	50	Female	83.2	45, XX, − X, t(8;21)	Good	DCAG

He S., Li Y., Shi X., Wang L., Cai D., Zhou J, & Yu L. (2023). DNA methylation landscape reveals LIN7A as a decitabine-responsive marker in patients with t(8;21) acute myeloid leukemia. Clinical Epigenetics, 15, 37.

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Publication 2023

Aclarubicin Ara-C Bone Marrow Chinese Decitabine Diagnosis DNA Methylation Granulocyte Colony-Stimulating Factor K-ras Genes Malignant Neoplasms Marrow Methylation Mutation Neutrophil Patients Specimen Collection Translocation, Chromosomal Treatment Protocols

Top products related to «Decitabine»

5 aza 2 deoxycytidine by Merck Group

Sourced in United States, Germany, United Kingdom, France

5-aza-2′-deoxycytidine is a chemical compound used in laboratory research. It is a synthetic analog of the natural nucleoside 2'-deoxycytidine, with a nitrogen atom substituted at the 5-position of the pyrimidine ring. This modification alters the chemical properties of the compound compared to the natural nucleoside.

Decitabine by Merck Group

Sourced in United States, Germany, China, Macao

Decitabine is a medication used in the treatment of various hematological malignancies. It is a DNA hypomethylating agent that works by inhibiting DNA methyltransferase, resulting in DNA demethylation and potential reactivation of silenced tumor suppressor genes. Decitabine is available as an injectable solution.

5 aza 2 deoxycytidine 5 aza dc by Merck Group

Sourced in United States, Macao, Spain, Japan, Germany

5-aza-2'-deoxycytidine (5-aza-dC) is a synthetic nucleoside analogue. It inhibits DNA methyltransferase enzymes, which are responsible for the addition of methyl groups to DNA.

Fetal bovine serum (fbs) by Thermo Fisher Scientific

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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.

Dimethyl sulfoxide (dmso) by Merck Group

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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.

Decitabine by Selleck Chemicals

Sourced in United States, China

Decitabine is a cytosine analog used as a pharmaceutical ingredient in various lab applications. It functions as a DNA methyltransferase inhibitor.

5 aza 2 deoxycytidine 5 aza by Merck Group

Sourced in United States, Germany, Sao Tome and Principe

5-aza-2′-deoxycytidine (5-Aza) is a synthetic nucleoside analog that can inhibit DNA methylation. It is a widely used tool compound in epigenetic research.

5 aza dc by Merck Group

Sourced in United States, Germany, China, Italy, United Kingdom, Japan, Canada, Macao

5-aza-dC is a chemical compound commonly used in scientific research. It is a modified cytosine nucleoside that inhibits DNA methyltransferase enzymes, which are responsible for DNA methylation. The primary function of 5-aza-dC is to facilitate the study of epigenetic processes and their implications in various biological systems.

Penicillin streptomycin by Thermo Fisher Scientific

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Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.

Trichostatin a tsa by Merck Group

Sourced in United States, Germany, United Kingdom, Spain

Trichostatin A (TSA) is a laboratory reagent used in biological research. It is a histone deacetylase (HDAC) inhibitor, which means it can block the activity of HDAC enzymes. TSA is commonly used as a tool to study the role of histone acetylation in cellular processes.

What is Decitabine and how does it work?

Decitabine is a synthetic nucleoside analog that functions as a potent antineoplastic agent. It works by inhibiting DNA methyltransferase, leading to demethylation and reactivation of silenced tumor suppressor genes. This process can enhance treatment outcomes and improve patient quality of life in various cancers, including myelodysplastic syndrome and acute myeloid leukemia.

What are the different variations or types of Decitabine?

What are some common usage challenges with Decitabine?

How can PubCompare.ai help researchers with their Decitabine research?

PubCompare.ai's AI-driven platform can assist researchers in optimizing their Decitabine research by helping them screen protocol literature more efficiently and leverage AI to pinpiont critical insights. The platform can highlight key differences in protocol effectiveness, enabling researchers to choose the best option for reproducibility and accuracy in their Decitabine studies. This can help researchers identify the most effective Decitabine protocols from the latest literature, preprints, and patent data.

What are some specific applications of Decitabine?

More about "Decitabine"

Decitabine, also known as 5-aza-2′-deoxycytidine (5-aza-dC), is a potent synthetic nucleoside analog that has shown promise in the treatment of various cancers, including myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).
This antineoplastic agent works by inhibiting DNA methyltransferase, leading to the demethylation and reactivation of silenced tumor suppressor genes.
Researchers have explored the optimal dosing and administration regimens of Decitabine, often in combination with other compounds like Trichostatin A (TSA), to enhance treatment outcomes and improve patient quality of life.
PubCompare.ai's AI-driven platform can help identify the most effective Decitabine protocols by analyzing the latest literature, preprints, and patent data, ensuring reproducibility and accuracy in this vital field of oncology research.
By leveraging the insights gained from 5-aza-2′-deoxycytidine (5-aza-dC), FBS, DMSO, and Penicillin/streptomycin, researchers can further optimize their Decitabine studies and unlock new possibilities in cancer treatment.
With PubCompare.ai's powerful tools, researchers can take their Decitabine research to new heights, driving progress in the fight against cancer.