A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent.
Clonal hematopoietic stem cell disorders characterized by dysplasia in one or more hematopoietic cell lineages. They predominantly affect patients over 60, are considered preleukemic conditions, and have high probability of transformation into ACUTE MYELOID LEUKEMIA.
Antimetabolites that are useful in cancer chemotherapy.
A myelodysplastic-myeloproliferative disease characterized by monocytosis, increased monocytes in the bone marrow, variable degrees of dysplasia, but an absence of immature granulocytes in the blood.
A CHROMATOGRAPHY method using supercritical fluid, usually carbon dioxide under very high pressure (around 73 atmospheres or 1070 psi at room temperature) as the mobile phase. Other solvents are sometimes added as modifiers. This is used both for analytical (SFC) and extraction (SFE) purposes.
Providing an investigational therapy to a patient who is not eligible to receive that therapy in a clinical trial, but who has a serious or life-threatening illness for which other treatments are not available. Compassionate use trials allow patients to receive promising but not yet fully studied or approved therapies when no other treatment option exists. Also called expanded access trial.
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
Forceful administration under the skin of liquid medication, nutrient, or other fluid through a hollow needle piercing the skin.
A severe sometimes chronic anemia, usually macrocytic in type, that does not respond to ordinary antianemic therapy.
Drug treatment designed to further diminish the disease toward complete remission following INDUCTION CHEMOTHERAPY. It helps to consolidate the gains during induction chemotherapy and may be followed by MAINTENANCE CHEMOTHERAPY.
Initial drug treatment designed to bring about REMISSION INDUCTION. It is typically a short-term and high-dose drug treatment that is followed by CONSOLIDATION CHEMOTHERAPY and then MAINTENANCE CHEMOTHERAPY.
Chronic refractory anemia with granulocytopenia, and/or thrombocytopenia. Myeloblasts and progranulocytes constitute 5 to 40 percent of the nucleated marrow cells.
Process that is gone through in order for a drug to receive approval by a government regulatory agency. This includes any required pre-clinical or clinical testing, review, submission, and evaluation of the applications and test results, and post-marketing surveillance of the drug.
Addition of methyl groups to DNA. DNA methyltransferases (DNA methylases) perform this reaction using S-ADENOSYLMETHIONINE as the methyl group donor.
Enzymes that are part of the restriction-modification systems. They are responsible for producing a species-characteristic methylation pattern, on either adenine or cytosine residues, in a specific short base sequence in the host cell's own DNA. This methylated sequence will occur many times in the host-cell DNA and remain intact for the lifetime of the cell. Any DNA from another species which gains entry into a living cell and lacks the characteristic methylation pattern will be recognized by the restriction endonucleases of similar specificity and destroyed by cleavage. Most have been studied in bacterial systems, but a few have been found in eukaryotic organisms.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
Continuance of life or existence especially under adverse conditions; includes methods and philosophy of survival.
International organizations which provide health-related or other cooperative services.
The systematic study of the global gene expression changes due to EPIGENETIC PROCESSES and not due to DNA base sequence changes.
An agency of the PUBLIC HEALTH SERVICE concerned with the overall planning, promoting, and administering of programs pertaining to maintaining standards of quality of foods, drugs, therapeutic devices, etc.
A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
Therapeutic act or process that initiates a response to a complete or partial remission level.
The extent to which the active ingredient of a drug dosage form becomes available at the site of drug action or in a biological medium believed to reflect accessibility to a site of action.
The introduction of whole blood or blood component directly into the blood stream. (Dorland, 27th ed)
Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.
Quaternary salts derived from tetrazoles. They are used in tests to distinguish between reducing sugars and simple aldehydes, for detection of dehydrogenase in tissues, cells, and bacteria, for determination of corticosteroids, and in color photography. (From Mall's Dictionary of Chemistry, 5th ed, p455)
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
The highest dose of a biologically active agent given during a chronic study that will not reduce longevity from effects other than carcinogenicity. (from Lewis Dictionary of Toxicology, 1st ed)
The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.
Disease having a short and relatively severe course.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
Transfer of HEMATOPOIETIC STEM CELLS from BONE MARROW or BLOOD between individuals within the same species (TRANSPLANTATION, HOMOLOGOUS) or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). Hematopoietic stem cell transplantation has been used as an alternative to BONE MARROW TRANSPLANTATION in the treatment of a variety of neoplasms.
The return of a sign, symptom, or disease after a remission.

Methylation-associated silencing of the tissue inhibitor of metalloproteinase-3 gene suggest a suppressor role in kidney, brain, and other human cancers. (1/1745)

Tissue inhibitor of metalloproteinase-3 (TIMP-3) antagonizes matrix metalloproteinase activity and can suppress tumor growth, angiogenesis, invasion, and metastasis. Loss of TIMP-3 has been related to the acquisition of tumorigenesis. Herein, we show that TIMP-3 is silenced in association with aberrant promoter-region methylation in cell lines derived from human cancers. TIMP-3 expression was restored after 5-aza-2'deoxycytidine-mediated demethylation of the TIMP-3 proximal promoter region. Genomic bisulfite sequencing revealed that TIMP-3 silencing was related to the overall density of methylation and that discrete regions within the TIMP-3 CpG island may be important for the silencing of this gene. Aberrant methylation of TIMP-3 occurred in primary cancers of the kidney, brain, colon, breast, and lung, but not in any of 41 normal tissue samples. The most frequent TIMP-3 methylation was found in renal cancers, which originate in the tissue that normally expresses the highest TIMP-3 levels. This methylation correlated with a lack of detectable TIMP-3 protein in these tumors. Together, these data show that methylation-associated inactivation of TIMP-3 is frequent in many human tumors.  (+info)

Re-expression of endogenous p16ink4a in oral squamous cell carcinoma lines by 5-aza-2'-deoxycytidine treatment induces a senescence-like state. (2/1745)

We have previously reported that a set of oral squamous cell carcinoma lines express specifically elevated cdk6 activity. One of the cell lines, SCC4, contains a cdk6 amplification and expresses functional p16ink4a, the other cell lines express undetectable levels of p16ink4a, despite a lack of coding-region mutations. Two of the cell lines, SCC15 and SCC40 have a hypermethylated p16ink4A promoter and a third cell line, SCC9, has a mutation in the p16ink4a promoter. Using the demethylation agent 5-aza-2'-deoxycytidine, we showed that the p16ink4a protein was re-expressed after a 5-day treatment with this chemical. One cell line, SCC15 expressed high levels of p16ink4a. In this line, cdk6 activity was decreased after 5-aza-2'deoxycytidine treatment, and the hypophosphorylated, growth suppressive form of the retinoblastoma tumor suppressor protein pRB was detected. Expression of p16ink4a persisted, even after the drug was removed and the cells expressed senescence-associated beta-galactosidase activity. Ectopic expression of p16ink4a with a recombinant retrovirus in this cell line also induced a similar senescence-like phenotype. Hence, it was possible to restore a functional pRB pathway in an oral squamous cell carcinoma line by inducing re-expression of endogenous p16ink4a in response to treatment with a demethylating agent.  (+info)

5-Aza-2'-deoxycytidine is chemopreventive in a 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone-induced primary mouse lung tumor model. (3/1745)

Carcinogenesis is a multistep process in which many alterations in both genetic and epigenetic controls lead to a growth advantage for neoplastic cells. Hypermethylation has been established as the basis of genomic imprinting, but recent studies have also shown that alterations in genomic methylation patterns may contribute to tumorigenesis. The chemical 5-aza-2'-deoxycytidine (5-aza-dC) has been used both in vitro and in vivo to inhibit DNA methylation. In this study, we investigated the chemopreventive efficacy of 5-aza-dC in a well-established primary mouse lung tumor model. Five-week-old male (C3H/HeJ x A/J) F1 hybrid mice were treated for 24 consecutive weeks with 5-aza-dC, three times per week i.p. Lung tumors were induced with two consecutive weekly doses of 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone starting 1 week after initial treatment with 5-aza-dC. We demonstrated that 5-aza-dC exhibits a chemopreventive effect in this primary mouse lung tumor model which, like human lung adenocarcinomas, harbors an activating K-ras mutation. Treatment with 5-aza-dC resulted in a 23% reduction in tumor incidence, as well as a 42% reduction in tumor multiplicity. This work supports further investigation of methylation inhibitors likes 5-aza-dC for early intervention, prevention and treatment of lung cancer.  (+info)

5-azacytidine induces transgene silencing by DNA methylation in Chinese hamster cells. (4/1745)

The cytosine analog 5-azacytidine (5-AzaC) is a demethylating agent that is also known to induce mutagenesis in mammalian cells. In this study, the mutagenic potential of this drug was tested in the G10 and G12 transgenic Chinese hamster cell lines, which have a single bacterial gpt gene integrated into the genome at different sites, with its expression driven by a simian virus 40 (SV40) promoter. We show that the mutation frequencies following a 48-h exposure to different concentrations of 5-AzaC were 10 to 20 times higher than those of any of the other numerous mutagens that have been tested in the G10-G12 system. Moreover, the mutation frequencies were much higher in the G10 cell line than in the G12 cells. Detailed molecular analysis of the 6-thioguanine (6-TG)-resistant variants demonstrated that transgene silencing by de novo DNA methylation and increased chromatin condensation in the SV40 promoter was the major factor responsible for this high level of 6-TG resistance. As would be expected, exposure to 5-AzaC lowered the overall genomic DNA methylation levels, but it unexpectedly caused hypermethylation and increased chromatin condensation of the transgene in both the G10 and G12 cell lines. These results provide the first evidence that 5-AzaC may also induce transgene-specific DNA methylation, a phenomenon that can further be used for the elucidation of the mechanism that controls silencing of foreign DNA.  (+info)

Methylation of CpG in a small region of the hMLH1 promoter invariably correlates with the absence of gene expression. (5/1745)

Microsatellite instability (MSI) has been described in tumors from patients with hereditary nonpolyposis colorectal cancer, sporadic colorectal cancer, and other types of cancers. MSI is caused by the dysfunction of mismatch repairs genes. Loss of expression and mutation in one of the major mismatch repair genes, hMLH1, and the methylation of CpG sites in its promoter occur frequently in primary tumors and cell lines of colorectal cancer with MSI. To understand the mechanisms involved in the silencing of hMLH1 expression by methylation, we examined the methylation status of all CpG sites in the hMLH1 promoter in 24 colorectal cancer cell lines by the NaHSO3-sequencing method. We identified a small proximal region (-248 to -178, relative to the transcription start site) in the promoter in which the methylation status invariably correlates with the lack of hMLH1 expression. This correlation was further supported by the observation that cell lines that showed methylation-suppressed hMLH1 expression can be induced to reexpress hMLH1 by a methyl transferase inhibitor, 5-aza-2'-deoxycytidine, and the small region that we identified exhibited significant demethylation in all cell lines examined.  (+info)

A role for methylation of the hMLH1 promoter in loss of hMLH1 expression and drug resistance in ovarian cancer. (6/1745)

Experimental evidence from several sources has identified a link between mismatch repair deficiency and cytotoxic drug resistance. Selection for cisplatin resistance in the human ovarian cancer cell line A2780, results in loss of expression of the mismatch repair protein hMLH1 in most (90%) of the resultant cisplatin-resistant cell lines. Here we demonstrate that the cisplatin sensitive parental cell line displays methylation of the promoter of only one hMLH1 allele, but that the resistant cell lines all exhibit hyper-methylation of the promoters of both hMLH1 alleles. Full methylation of all sites tested was found to be invariably associated with loss of hMLH1 expression, whereas a partial increase in methylation appears compatible with either loss or maintenance of expression. In addition treatment of two of the resistant cell lines with 5-azacytidine, a known inhibitor of methylation, results in re-expression of hMLH1. Clonogenic assays demonstrate that the 5-azacytidine treated cells show increased sensitivity to cisplatin. Furthermore, 12.5% (3/ 24) of ovarian tumours show hypermethylation of the hMLH1 promoter. Expression of hMLH1 is absent in the tumours that are hypermethylated, while all the unmethylated tumours still express the protein. This analysis suggests that methylation of the hMLH1 promoter may be a common mechanism for loss of hMLH1 expression, and possibly for cisplatin-resistance, in ovarian cancer.  (+info)

Hypermethylation of the DAP-kinase CpG island is a common alteration in B-cell malignancies. (7/1745)

Death-associated protein kinase (DAP-Kinase) is a novel serine/threonine kinase whose expression is required for gamma interferon-induced apoptosis. A previous study suggested that DAP-Kinase expression may be lost epigenetically in cancer cell lines, because treatment of several nonexpressing cell lines with 5-aza-2'-deoxycytidine resulted in the expression of DAP-Kinase. Using methylation-specific polymerase chain reaction (MSP), we examined the DAP-Kinase CpG island for hypermethylation in cancer. Normal lymphocytes and lymphoblastoid cell lines are unmethylated in the 5' CpG island of DAP-Kinase. However, in primary tumor samples, all Burkitt's lymphomas and 84% of the B-cell non-Hodgkin's lymphomas were hypermethylated in the DAP-Kinase CpG island. In contrast, none of the T-cell non-Hodgkin's lymphoma samples and 15% or less of leukemia samples examined had hypermethylated DAP-Kinase alleles. U937, an unmethylated, DAP-Kinase-expressing leukemia cell line, was treated with gamma interferon and underwent apoptosis; however, Raji, a fully methylated, DAP-Kinase nonexpressing Burkitt's lymphoma cell line, only did so when treated with 5-aza-2'-deoxycytidine followed by gamma interferon. Our findings in cell lines and primary tumors suggest that hypermethylation of the DAP-Kinase gene and loss of gamma interferon-mediated apoptosis may be important in the development of B-cell malignancies and may provide a promising biomarker for B-cell-lineage lymphomas.  (+info)

Characterization of the GAGE genes that are expressed in various human cancers and in normal testis. (8/1745)

The GAGE-1 gene was identified previously as a gene that codes for an antigenic peptide, YRPRPRRY, which was presented on a human melanoma by HLA-Cw6 molecules and recognized by a clone of CTLs derived from the patient bearing the tumor. By screening a cDNA library from this melanoma, we identified five additional, closely related genes named GAGE-2-6. We report here that further screening of this library led to the identification of two more genes, GAGE-7B and -8. GAGE-1, -2, and -8 code for peptide YRPRPRRY. Using another antitumor CTL clone isolated from the same melanoma patient, we identified antigenic peptide, YYWPRPRRY, which is encoded by GAGE-3, -4, -5, -6, and -7B and which is presented by HLA-A29 molecules. Genomic cloning of GAGE-7B showed that it is composed of five exons. Sequence alignment showed that an additional exon, which is present only in the mRNA of GAGE-1, has been disrupted in gene GAGE-7B by the insertion of a long interspersed repeated element retroposon. These GAGE genes are located in the p11.2-p11.4 region of chromosome X. They are not expressed in normal tissues, except in testis, but a large proportion of tumors of various histological origins express at least one of these genes. Treatment of normal and tumor cultured cells with a demethylating agent, azadeoxycytidine, resulted in the transcriptional activation of GAGE genes, suggesting that their expression in tumors results from a demethylation process.  (+info)

Azacitidine is a medication that is primarily used to treat myelodysplastic syndrome (MDS), a type of cancer where the bone marrow does not produce enough healthy blood cells. It is also used to treat acute myeloid leukemia (AML) in some cases.

Azacitidine is a type of drug known as a hypomethylating agent, which means that it works by modifying the way that genes are expressed in cancer cells. Specifically, azacitidine inhibits the activity of an enzyme called DNA methyltransferase, which adds methyl groups to the DNA molecule and can silence the expression of certain genes. By inhibiting this enzyme, azacitidine can help to restore the normal function of genes that have been silenced in cancer cells.

Azacitidine is typically given as a series of subcutaneous (under the skin) or intravenous (into a vein) injections over a period of several days, followed by a rest period of several weeks before the next cycle of treatment. The specific dosage and schedule may vary depending on the individual patient's needs and response to treatment.

Like all medications, azacitidine can have side effects, which may include nausea, vomiting, diarrhea, constipation, fatigue, fever, and decreased appetite. More serious side effects are possible, but relatively rare, and may include bone marrow suppression, infections, and liver damage. Patients receiving azacitidine should be closely monitored by their healthcare provider to manage any side effects that may occur.

Myelodysplastic syndromes (MDS) are a group of diverse bone marrow disorders characterized by dysplasia (abnormal development or maturation) of one or more types of blood cells or by ineffective hematopoiesis, resulting in cytopenias (lower than normal levels of one or more types of blood cells). MDS can be classified into various subtypes based on the number and type of cytopenias, the degree of dysplasia, the presence of ring sideroblasts, and cytogenetic abnormalities.

The condition primarily affects older adults, with a median age at diagnosis of around 70 years. MDS can evolve into acute myeloid leukemia (AML) in approximately 30-40% of cases. The pathophysiology of MDS involves genetic mutations and chromosomal abnormalities that lead to impaired differentiation and increased apoptosis of hematopoietic stem and progenitor cells, ultimately resulting in cytopenias and an increased risk of developing AML.

The diagnosis of MDS typically requires a bone marrow aspiration and biopsy, along with cytogenetic and molecular analyses to identify specific genetic mutations and chromosomal abnormalities. Treatment options for MDS depend on the subtype, severity of cytopenias, and individual patient factors. These may include supportive care measures, such as transfusions and growth factor therapy, or more aggressive treatments, such as chemotherapy and stem cell transplantation.

Antimetabolites are a class of antineoplastic (chemotherapy) drugs that interfere with the metabolism of cancer cells and inhibit their growth and proliferation. These agents are structurally similar to naturally occurring metabolites, such as amino acids, nucleotides, and folic acid, which are essential for cellular replication and growth. Antimetabolites act as false analogs and get incorporated into the growing cells' DNA or RNA, causing disruption of the normal synthesis process, leading to cell cycle arrest and apoptosis (programmed cell death).

Examples of antimetabolite drugs include:

1. Folate antagonists: Methotrexate, Pemetrexed
2. Purine analogs: Mercaptopurine, Thioguanine, Fludarabine, Cladribine
3. Pyrimidine analogs: 5-Fluorouracil (5-FU), Capecitabine, Cytarabine, Gemcitabine

These drugs are used to treat various types of cancers, such as leukemias, lymphomas, breast, ovarian, and gastrointestinal cancers. Due to their mechanism of action, antimetabolites can also affect normal, rapidly dividing cells in the body, leading to side effects like myelosuppression (decreased production of blood cells), mucositis (inflammation and ulceration of the gastrointestinal tract), and alopecia (hair loss).

Chronic myelomonocytic leukemia (CMML) is a type of cancer that affects the blood-forming cells of the bone marrow. It is characterized by an overproduction of white blood cells, specifically monocytes and myeloid cells. These abnormal cells accumulate in the bone marrow and interfere with normal blood cell production, leading to a shortage of red blood cells, platelets, and normal white blood cells.

CMML is considered a myelodysplastic/myeloproliferative neoplasm (MDS/MPN), which means it has features of both myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN). MDS are conditions in which the bone marrow does not produce enough healthy blood cells, while MPNs are conditions in which the bone marrow produces too many abnormal blood cells.

In CMML, the myelomonocytic cells may accumulate in various organs and tissues, leading to enlargement of the spleen (splenomegaly) and liver (hepatomegaly), as well as an increased risk of infections, bleeding, and anemia. The symptoms of CMML can vary widely depending on the severity of the disease and the specific organs affected.

CMML is typically a disease of older adults, with a median age at diagnosis of around 70 years. It is slightly more common in men than in women. The exact cause of CMML is not known, but it is thought to be related to genetic mutations that occur over time and are associated with aging. Treatment options for CMML depend on the stage and severity of the disease, as well as the patient's overall health and preferences.

Chromatography, supercritical fluid (SFC) is a type of chromatographic technique that uses supercritical fluids as the mobile phase to separate and analyze components of a mixture. A supercritical fluid is a substance that is maintained at temperatures and pressures above its critical point, where it exhibits properties of both a gas and a liquid, making it an ideal medium for separations due to its low viscosity, high diffusivity, and tuneable solvating strength.

In SFC, the supercritical fluid, typically carbon dioxide (CO2) due to its mild critical point conditions, is used to elute analytes from a stationary phase, such as a silica or polymer-based column. The interactions between the analytes and the stationary phase, along with the properties of the supercritical fluid, determine the separation efficiency and resolution of the technique.

SFC has several advantages over traditional liquid chromatography (LC) techniques, including faster analysis times, lower solvent consumption, and the ability to analyze a wider range of polar and nonpolar compounds. SFC is commonly used in the pharmaceutical industry for drug discovery and development, as well as in environmental, food, and chemical analyses.

Compassionate use trials, also known as expanded access or compassionate use programs, refer to the use of an experimental medical treatment outside of a clinical trial, typically for patients who have a serious or life-threatening condition and have exhausted all other available treatment options. These programs are designed to provide access to investigational therapies that have not yet been approved by regulatory authorities but have shown promising results in earlier stages of clinical development.

In compassionate use trials, patients receive the experimental therapy under a specific treatment protocol that outlines the dosage, administration, and monitoring requirements. The primary goal of these trials is to provide potential therapeutic benefits to patients who have no other alternatives, while also gathering additional safety and efficacy data on the investigational treatment.

Regulatory agencies such as the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) have guidelines and procedures in place for compassionate use trials to ensure that patients receive appropriate care, and that the safety and well-being of participants are protected throughout the process.

Acute myeloid leukemia (AML) is a type of cancer that originates in the bone marrow, the soft inner part of certain bones where new blood cells are made. In AML, the immature cells, called blasts, in the bone marrow fail to mature into normal blood cells. Instead, these blasts accumulate and interfere with the production of normal blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia).

AML is called "acute" because it can progress quickly and become severe within days or weeks without treatment. It is a type of myeloid leukemia, which means that it affects the myeloid cells in the bone marrow. Myeloid cells are a type of white blood cell that includes monocytes and granulocytes, which help fight infection and defend the body against foreign invaders.

In AML, the blasts can build up in the bone marrow and spread to other parts of the body, including the blood, lymph nodes, liver, spleen, and brain. This can cause a variety of symptoms, such as fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss.

AML is typically treated with a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the type and stage of the leukemia.

Subcutaneous injection is a route of administration where a medication or vaccine is delivered into the subcutaneous tissue, which lies between the skin and the muscle. This layer contains small blood vessels, nerves, and connective tissues that help to absorb the medication slowly and steadily over a period of time. Subcutaneous injections are typically administered using a short needle, at an angle of 45-90 degrees, and the dose is injected slowly to minimize discomfort and ensure proper absorption. Common sites for subcutaneous injections include the abdomen, thigh, or upper arm. Examples of medications that may be given via subcutaneous injection include insulin, heparin, and some vaccines.

Refractory anemia is a type of anemia that does not respond to typical treatments, such as iron supplements or hormonal therapy. It is often associated with various bone marrow disorders, including myelodysplastic syndromes (MDS), a group of conditions characterized by abnormal blood cell production in the bone marrow.

In refractory anemia, the bone marrow fails to produce enough healthy red blood cells, leading to symptoms such as fatigue, weakness, shortness of breath, and pale skin. The condition can be difficult to treat, and treatment options may include more aggressive therapies such as immunosuppressive drugs, chemotherapy, or stem cell transplantation.

It is important to note that the term "refractory" in this context refers specifically to the lack of response to initial treatments, rather than a specific severity or type of anemia.

Consolidation chemotherapy is a type of cancer treatment that is given after the initial or primary treatment, called induction therapy, to consolidate or strengthen the response and increase the chance of a cure. It typically involves the use of one or more anticancer drugs to target any remaining cancer cells in the body following remission. This approach is often used in the treatment of acute leukemias, such as acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), where the goal is to eliminate residual disease and reduce the risk of relapse. The specific drugs, doses, and schedules used in consolidation chemotherapy may vary depending on the type and stage of cancer being treated.

Induction chemotherapy is a type of cancer treatment that involves the use of cytotoxic drugs to reduce the size of tumors prior to administering other forms of therapy, such as radiation therapy or surgery. The goal of induction chemotherapy is to eliminate as many cancer cells as possible and shrink the tumor to improve the chances of a successful outcome with subsequent treatments.

This approach is often used in the treatment of certain types of cancer, including lymphoma, leukemia, and testicular cancer, among others. The specific drugs used and the duration of treatment may vary depending on the type and stage of cancer being treated.

It's important to note that induction chemotherapy is a complex medical procedure that should be administered under the close supervision of an experienced oncologist. Patients undergoing this treatment may experience side effects, such as nausea, vomiting, fatigue, and hair loss, among others. However, these side effects can often be managed with supportive care and medications.

Refractory anemia with excess blasts is a type of blood disorder that is characterized by the presence of increased numbers of immature blood cells, or "blasts," in the bone marrow and peripheral blood. This condition is considered a subtype of myelodysplastic syndrome (MDS), which is a group of disorders caused by abnormalities in the production of blood cells in the bone marrow.

In refractory anemia with excess blasts, the bone marrow fails to produce sufficient numbers of healthy red blood cells, white blood cells, and platelets. This results in anemia (low red blood cell count), neutropenia (low white blood cell count), and thrombocytopenia (low platelet count). Additionally, there is an increased number of blasts in the bone marrow and peripheral blood, which can indicate the development of acute myeloid leukemia (AML), a more aggressive form of blood cancer.

Refractory anemia with excess blasts is considered "refractory" because it does not respond well to treatment, including chemotherapy and stem cell transplantation. The prognosis for this condition varies depending on the severity of the disease and other individual factors, but it is generally poor, with many patients progressing to AML within a few years.

"Drug approval" is the process by which a regulatory agency, such as the US Food and Drug Administration (FDA), grants formal authorization for a pharmaceutical company to market and sell a drug for a specific medical condition. The approval process is based on rigorous evaluation of clinical trial data to ensure that the drug is safe and effective for its intended use.

The FDA's approval process typically involves several stages, including preclinical testing in the lab and animal studies, followed by three phases of clinical trials in human subjects. The first phase tests the safety of the drug in a small group of healthy volunteers, while the second and third phases test the drug's efficacy and side effects in larger groups of patients with the medical condition for which the drug is intended.

If the results of these studies demonstrate that the drug is safe and effective, the pharmaceutical company can submit a New Drug Application (NDA) or Biologics License Application (BLA) to the FDA for review. The application includes data from the clinical trials, as well as information about the manufacturing process, labeling, and proposed use of the drug.

The FDA reviews the application and may seek input from independent experts before making a decision on whether to approve the drug. If approved, the drug can be marketed and sold to patients with the medical condition for which it was approved. The FDA continues to monitor the safety and efficacy of approved drugs after they reach the market to ensure that they remain safe and effective for their intended use.

DNA methylation is a process by which methyl groups (-CH3) are added to the cytosine ring of DNA molecules, often at the 5' position of cytospine phosphate-deoxyguanosine (CpG) dinucleotides. This modification is catalyzed by DNA methyltransferase enzymes and results in the formation of 5-methylcytosine.

DNA methylation plays a crucial role in the regulation of gene expression, genomic imprinting, X chromosome inactivation, and suppression of transposable elements. Abnormal DNA methylation patterns have been associated with various diseases, including cancer, where tumor suppressor genes are often silenced by promoter methylation.

In summary, DNA methylation is a fundamental epigenetic modification that influences gene expression and genome stability, and its dysregulation has important implications for human health and disease.

DNA modification methylases are a type of enzyme that catalyze the transfer of methyl groups (-CH3) to specific nucleotides in DNA, usually cytosine or adenine residues. This process is known as DNA methylation and is an important epigenetic mechanism that regulates gene expression, genome stability, and other cellular processes.

There are several types of DNA modification methylases, including:

1. Cytosine-5 methyltransferases (CNMTs or DNMTs): These enzymes catalyze the transfer of a methyl group to the fifth carbon atom of cytosine residues in DNA, forming 5-methylcytosine (5mC). This is the most common type of DNA methylation and plays a crucial role in gene silencing, X-chromosome inactivation, and genomic imprinting.
2. N6-adenine methyltransferases (MTases): These enzymes catalyze the transfer of a methyl group to the sixth nitrogen atom of adenine residues in DNA, forming N6-methyladenine (6mA). This type of DNA methylation is less common than 5mC but has been found to be involved in various cellular processes, such as transcriptional regulation and DNA repair.
3. GpC methyltransferases: These enzymes catalyze the transfer of a methyl group to the second carbon atom of guanine residues in DNA, forming N4-methylcytosine (4mC). This type of DNA methylation is relatively rare and has been found mainly in prokaryotic genomes.

Dysregulation of DNA modification methylases has been implicated in various diseases, including cancer, neurological disorders, and immunological diseases. Therefore, understanding the function and regulation of these enzymes is essential for developing novel therapeutic strategies to treat these conditions.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

In a medical context, "survival" generally refers to the continuation of life following a serious illness, injury, or dangerous event. It is often used in research and clinical settings to describe the length and quality of life after a specific treatment or diagnosis. For example, survival rate might refer to the percentage of patients who are still alive after a certain period of time following a cancer diagnosis or surgery. Survival can also be used more broadly to describe an individual's ability to adapt and persist in the face of adversity or challenge, whether that's due to medical conditions or other life circumstances.

I'm sorry for any confusion, but "International Agencies" is not a medical term. It refers to organizations that operate on a global scale, often established by treaties between nations, to address issues that affect multiple countries. Examples include the United Nations (UN), World Health Organization (WHO), and International Committee of the Red Cross (ICRC).

However, if you're asking about international agencies related to healthcare or medicine, I can provide some examples:

1. World Health Organization (WHO): A specialized agency of the United Nations responsible for international public health.
2. Joint United Nations Programme on HIV/AIDS (UNAIDS): Leads and inspires the world to achieve its shared vision of zero new HIV infections, zero discrimination, and zero AIDS-related deaths.
3. Food and Agriculture Organization (FAO): A specialized agency of the United Nations that leads international efforts to defeat hunger.
4. United Nations Children's Fund (UNICEF): Works for children's rights, their survival, development, and protection.
5. World Trade Organization (WTO): Sets rules for trade between nations and tries to ensure that trade flows as smoothly, predictably, and freely as possible. It can impact access to medical goods and services.
6. World Intellectual Property Organization (WIPO): Promotes the protection of intellectual property throughout the world through cooperation among states and in collaboration with other international organizations. This can affect pharmaceutical patents and innovation.

These agencies play crucial roles in shaping health policy, providing guidelines, funding research, and coordinating responses to global health issues.

Epigenomics is the study of the epigenome, which refers to all of the chemical modifications and protein interactions that occur on top of a person's genetic material (DNA). These modifications do not change the underlying DNA sequence but can affect gene expression, or how much a particular gene is turned on or off.

Examples of epigenetic modifications include DNA methylation, histone modification, and non-coding RNA molecules. These modifications can be influenced by various factors such as age, environment, lifestyle, and disease state. Epigenomic changes have been implicated in the development and progression of many diseases, including cancer, and are an active area of research in molecular biology and genomics.

The United States Food and Drug Administration (FDA) is a federal government agency responsible for protecting public health by ensuring the safety, efficacy, and security of human and veterinary drugs, biological products, medical devices, our country's food supply, cosmetics, and products that emit radiation. The FDA also provides guidance on the proper use of these products, and enforces laws and regulations related to them. It is part of the Department of Health and Human Services (HHS).

Thalidomide is a pharmaceutical drug that was initially developed and marketed as a sedative and treatment for morning sickness in pregnant women. However, it was later found to cause severe birth defects when given during pregnancy, particularly damage to the limbs, ears, and eyes of the developing fetus. As a result, thalidomide was banned in many countries in the 1960s.

In recent years, thalidomide has been reintroduced as a treatment for certain medical conditions, including multiple myeloma (a type of cancer that affects plasma cells) and leprosy. It is also being studied as a potential treatment for other diseases, such as rheumatoid arthritis and Crohn's disease.

Thalidomide works by suppressing the immune system and inhibiting the formation of new blood vessels (angiogenesis). However, its use is tightly regulated due to its teratogenic effects, meaning it can cause birth defects if taken during pregnancy. Women who are pregnant or planning to become pregnant should not take thalidomide, and healthcare providers must follow strict guidelines when prescribing the drug to ensure that it is used safely and effectively.

A "Drug Administration Schedule" refers to the plan for when and how a medication should be given to a patient. It includes details such as the dose, frequency (how often it should be taken), route (how it should be administered, such as orally, intravenously, etc.), and duration (how long it should be taken) of the medication. This schedule is often created and prescribed by healthcare professionals, such as doctors or pharmacists, to ensure that the medication is taken safely and effectively. It may also include instructions for missed doses or changes in the dosage.

Antimetabolites are a class of drugs that interfere with the normal metabolic processes of cells, particularly those involved in DNA replication and cell division. They are commonly used as chemotherapeutic agents to treat various types of cancer because many cancer cells divide more rapidly than normal cells. Antimetabolites work by mimicking natural substances needed for cell growth and division, such as nucleotides or amino acids, and getting incorporated into the growing cells' DNA or protein structures, which ultimately leads to the termination of cell division and death of the cancer cells. Examples of antimetabolites include methotrexate, 5-fluorouracil, and capecitabine.

Remission induction is a treatment approach in medicine, particularly in the field of oncology and hematology. It refers to the initial phase of therapy aimed at reducing or eliminating the signs and symptoms of active disease, such as cancer or autoimmune disorders. The primary goal of remission induction is to achieve a complete response (disappearance of all detectable signs of the disease) or a partial response (a decrease in the measurable extent of the disease). This phase of treatment is often intensive and may involve the use of multiple drugs or therapies, including chemotherapy, immunotherapy, or targeted therapy. After remission induction, patients may receive additional treatments to maintain the remission and prevent relapse, known as consolidation or maintenance therapy.

Biological availability is a term used in pharmacology and toxicology that refers to the degree and rate at which a drug or other substance is absorbed into the bloodstream and becomes available at the site of action in the body. It is a measure of the amount of the substance that reaches the systemic circulation unchanged, after administration by any route (such as oral, intravenous, etc.).

The biological availability (F) of a drug can be calculated using the area under the curve (AUC) of the plasma concentration-time profile after extravascular and intravenous dosing, according to the following formula:

F = (AUCex/AUCiv) x (Doseiv/Doseex)

where AUCex is the AUC after extravascular dosing, AUCiv is the AUC after intravenous dosing, Doseiv is the intravenous dose, and Doseex is the extravascular dose.

Biological availability is an important consideration in drug development and therapy, as it can affect the drug's efficacy, safety, and dosage regimen. Drugs with low biological availability may require higher doses to achieve the desired therapeutic effect, while drugs with high biological availability may have a more rapid onset of action and require lower doses to avoid toxicity.

A blood transfusion is a medical procedure in which blood or its components are transferred from one individual (donor) to another (recipient) through a vein. The donated blood can be fresh whole blood, packed red blood cells, platelets, plasma, or cryoprecipitate, depending on the recipient's needs. Blood transfusions are performed to replace lost blood due to severe bleeding, treat anemia, support patients undergoing major surgeries, or manage various medical conditions such as hemophilia, thalassemia, and leukemia. The donated blood must be carefully cross-matched with the recipient's blood type to minimize the risk of transfusion reactions.

Leukemia, myeloid is a type of cancer that originates in the bone marrow, where blood cells are produced. Myeloid leukemia affects the myeloid cells, which include red blood cells, platelets, and most types of white blood cells. In this condition, the bone marrow produces abnormal myeloid cells that do not mature properly and accumulate in the bone marrow and blood. These abnormal cells hinder the production of normal blood cells, leading to various symptoms such as anemia, fatigue, increased risk of infections, and easy bruising or bleeding.

There are several types of myeloid leukemias, including acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). AML progresses rapidly and requires immediate treatment, while CML tends to progress more slowly. The exact causes of myeloid leukemia are not fully understood, but risk factors include exposure to radiation or certain chemicals, smoking, genetic disorders, and a history of chemotherapy or other cancer treatments.

Tetrazolium salts are a group of compounds that are commonly used as indicators of cell viability and metabolic activity. These salts are reduced by the action of dehydrogenase enzymes in living cells, resulting in the formation of formazan dyes, which are colored and can be measured spectrophotometrically.

The most commonly used tetrazolium salt is 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), which is reduced to a purple formazan product by mitochondrial dehydrogenases in viable cells. Other tetrazolium salts include 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT), which is reduced to a water-soluble formazan product, and 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS), which is reduced to a water-soluble formazan product by NAD(P)H-dependent dehydrogenases.

Tetrazolium salts are widely used in cell culture studies, toxicity testing, and drug development to assess cell viability, proliferation, and cytotoxicity. However, it is important to note that tetrazolium salt reduction can also occur in some non-viable cells or under certain experimental conditions, which may lead to false positive results. Therefore, these assays should be used with caution and validated for specific applications.

Cytarabine is a chemotherapeutic agent used in the treatment of various types of cancer, including leukemias and lymphomas. Its chemical name is cytosine arabinoside, and it works by interfering with the DNA synthesis of cancer cells, which ultimately leads to their death.

Cytarabine is often used in combination with other chemotherapy drugs and may be administered through various routes, such as intravenous (IV) or subcutaneous injection, or orally. The specific dosage and duration of treatment will depend on the type and stage of cancer being treated, as well as the patient's overall health status.

Like all chemotherapy drugs, cytarabine can cause a range of side effects, including nausea, vomiting, diarrhea, hair loss, and an increased risk of infection. It may also cause more serious side effects, such as damage to the liver, kidneys, or nervous system, and it is important for patients to be closely monitored during treatment to minimize these risks.

It's important to note that medical treatments should only be administered under the supervision of a qualified healthcare professional, and this information should not be used as a substitute for medical advice.

Antineoplastic combined chemotherapy protocols refer to a treatment plan for cancer that involves the use of more than one antineoplastic (chemotherapy) drug given in a specific sequence and schedule. The combination of drugs is used because they may work better together to destroy cancer cells compared to using a single agent alone. This approach can also help to reduce the likelihood of cancer cells becoming resistant to the treatment.

The choice of drugs, dose, duration, and frequency are determined by various factors such as the type and stage of cancer, patient's overall health, and potential side effects. Combination chemotherapy protocols can be used in various settings, including as a primary treatment, adjuvant therapy (given after surgery or radiation to kill any remaining cancer cells), neoadjuvant therapy (given before surgery or radiation to shrink the tumor), or palliative care (to alleviate symptoms and prolong survival).

It is important to note that while combined chemotherapy protocols can be effective in treating certain types of cancer, they can also cause significant side effects, including nausea, vomiting, hair loss, fatigue, and an increased risk of infection. Therefore, patients undergoing such treatment should be closely monitored and managed by a healthcare team experienced in administering chemotherapy.

The Maximum Tolerated Dose (MTD) is a term used in medical research, particularly in clinical trials of new drugs or treatments. It refers to the highest dose of a medication or treatment that can be given without causing unacceptable or severe side effects or toxicity to the patient.

Determining the MTD is an important step in developing new medications, as it helps researchers establish a safe and effective dosage range for future use. This process typically involves gradually increasing the dose in a group of subjects (often healthy volunteers in early phase trials) until intolerable side effects occur, at which point the previous dose is considered the MTD.

It's important to note that the MTD may vary between individuals and populations, depending on factors such as age, sex, genetic makeup, and overall health status. Therefore, individualized dosing strategies may be necessary to ensure safe and effective treatment with new medications.

Fatigue is a state of feeling very tired, weary, or exhausted, which can be physical, mental, or both. It is a common symptom that can be caused by various factors, including lack of sleep, poor nutrition, stress, medical conditions (such as anemia, diabetes, heart disease, or cancer), medications, and substance abuse. Fatigue can also be a symptom of depression or other mental health disorders. In medical terms, fatigue is often described as a subjective feeling of tiredness that is not proportional to recent activity levels and interferes with usual functioning. It is important to consult a healthcare professional if experiencing persistent or severe fatigue to determine the underlying cause and develop an appropriate treatment plan.

An acute disease is a medical condition that has a rapid onset, develops quickly, and tends to be short in duration. Acute diseases can range from minor illnesses such as a common cold or flu, to more severe conditions such as pneumonia, meningitis, or a heart attack. These types of diseases often have clear symptoms that are easy to identify, and they may require immediate medical attention or treatment.

Acute diseases are typically caused by an external agent or factor, such as a bacterial or viral infection, a toxin, or an injury. They can also be the result of a sudden worsening of an existing chronic condition. In general, acute diseases are distinct from chronic diseases, which are long-term medical conditions that develop slowly over time and may require ongoing management and treatment.

Examples of acute diseases include:

* Acute bronchitis: a sudden inflammation of the airways in the lungs, often caused by a viral infection.
* Appendicitis: an inflammation of the appendix that can cause severe pain and requires surgical removal.
* Gastroenteritis: an inflammation of the stomach and intestines, often caused by a viral or bacterial infection.
* Migraine headaches: intense headaches that can last for hours or days, and are often accompanied by nausea, vomiting, and sensitivity to light and sound.
* Myocardial infarction (heart attack): a sudden blockage of blood flow to the heart muscle, often caused by a buildup of plaque in the coronary arteries.
* Pneumonia: an infection of the lungs that can cause coughing, chest pain, and difficulty breathing.
* Sinusitis: an inflammation of the sinuses, often caused by a viral or bacterial infection.

It's important to note that while some acute diseases may resolve on their own with rest and supportive care, others may require medical intervention or treatment to prevent complications and promote recovery. If you are experiencing symptoms of an acute disease, it is always best to seek medical attention to ensure proper diagnosis and treatment.

Retrospective studies, also known as retrospective research or looking back studies, are a type of observational study that examines data from the past to draw conclusions about possible causal relationships between risk factors and outcomes. In these studies, researchers analyze existing records, medical charts, or previously collected data to test a hypothesis or answer a specific research question.

Retrospective studies can be useful for generating hypotheses and identifying trends, but they have limitations compared to prospective studies, which follow participants forward in time from exposure to outcome. Retrospective studies are subject to biases such as recall bias, selection bias, and information bias, which can affect the validity of the results. Therefore, retrospective studies should be interpreted with caution and used primarily to generate hypotheses for further testing in prospective studies.

Hematopoietic Stem Cell Transplantation (HSCT) is a medical procedure where hematopoietic stem cells (immature cells that give rise to all blood cell types) are transplanted into a patient. This procedure is often used to treat various malignant and non-malignant disorders affecting the hematopoietic system, such as leukemias, lymphomas, multiple myeloma, aplastic anemia, inherited immune deficiency diseases, and certain genetic metabolic disorders.

The transplantation can be autologous (using the patient's own stem cells), allogeneic (using stem cells from a genetically matched donor, usually a sibling or unrelated volunteer), or syngeneic (using stem cells from an identical twin).

The process involves collecting hematopoietic stem cells, most commonly from the peripheral blood or bone marrow. The collected cells are then infused into the patient after the recipient's own hematopoietic system has been ablated (or destroyed) using high-dose chemotherapy and/or radiation therapy. This allows the donor's stem cells to engraft, reconstitute, and restore the patient's hematopoietic system.

HSCT is a complex and potentially risky procedure with various complications, including graft-versus-host disease, infections, and organ damage. However, it offers the potential for cure or long-term remission in many patients with otherwise fatal diseases.

Recurrence, in a medical context, refers to the return of symptoms or signs of a disease after a period of improvement or remission. It indicates that the condition has not been fully eradicated and may require further treatment. Recurrence is often used to describe situations where a disease such as cancer comes back after initial treatment, but it can also apply to other medical conditions. The likelihood of recurrence varies depending on the type of disease and individual patient factors.

The combination of azacitidine and venetoclax is also approved for AML. Azacitidine is a chemical analogue of the nucleoside ... Azacitidine induces tumor regression on isocitrate dehydrogenase-1 mutant glioma xenografts in mice. In research, 5-azacitidine ... "Azacitidine (Vidaza) Use During Pregnancy". Drugs.com. 5 May 2020. Retrieved 12 August 2020. "Vidaza- azacitidine injection, ... since their levels of azacitidine may progressively increase. Based on animal studies and its mechanism of action, azacitidine ...
Azacitidine and decitabine are marketed as Vidaza and Dacogen respectively. Azacitidine is the first drug to be approved by FDA ... Azacitidine and decitabine are both frequently used demethylating agents while decitabine is significantly more potent in its ... The FDA initially rejected the use of azacitidine clinically due to negative side effects caused by elevated toxicity levels. ... Issa, J. P., Kantarjian, H. M. and Kirkpatrick, P. (2005). "Azacitidine". Nat Rev Drug Discov. 4 (4): 275-6. doi:10.1038/ ...
"Azacitidine, Decitabine". IOCB Prague. Retrieved 2022-08-05. "Dihydroxypropyladenine". IOCB Prague. Retrieved 2022-08-05. " ...
2010). "11 5-Azacytidine/Azacitidine". Small molecules in oncology. Recent Results in Cancer Research. Vol. 184. Heidelberg: ...
"Vidaza (azacitidine for injectable suspension) package insert" (PDF). Pharmion Corporation. U.S. Food and Drug Administration. ... March 2009). "Efficacy of azacitidine compared with that of conventional care regimens in the treatment of higher-risk ... FDA label information for Vidaza, a formulation of 5-azacitidine (an unmethylatable analog of cytidine that causes ... "A pilot pharmacokinetic study of oral azacitidine". Leukemia. 22 (9): 1680-1684. doi:10.1038/leu.2008.145. PMID 18548103. ...
... azacitidine DNA methylation is the modification of DNA nucleotides by addition of a methyl group. These methyl groups are ... azacitidine and decitabine, are FDA-approved for use in the United States in myelodysplastic syndrome and are being ... "A pilot pharmacokinetic study of oral azacitidine". Leukemia. 22 (9): 1680-4. doi:10.1038/leu.2008.145. PMID 18548103. Herman, ...
... azacitidine, decitabine) in previously untreated older AML patients. The drug is also being evaluated broadly across multiple ... Combined With Azacitidine or Decitabine in Older Patients With Newly Diagnosed Acute Myeloid Leukemia (CASCADE)" at ...
found methylation inhibitors known as azacitidine and decitabine. These compounds can actually help prevent cancer growth by ...
Wells RA, Leber B, Zhu NY, Storring JM (February 2014). "Optimizing outcomes with azacitidine: recommendations from Canadian ... February 2014). "Immune regulation by low doses of the DNA methyltransferase inhibitor 5-azacitidine in common human epithelial ...
5-azacitidine (5-AzaC) in mice reduced excessive ethanol consumption. 5-AzaC decreases DNA methylation by inhibiting the ...
May 2002). "Randomized controlled trial of azacitidine in patients with the myelodysplastic syndrome: a study of the cancer and ... Drug therapy may include the medications lenalidomide, antithymocyte globulin, and azacitidine. Some people can be cured by ... "Further analysis of trials with azacitidine in patients with myelodysplastic syndrome: studies 8421, 8921, and 9221 by the ...
Azacitidine is a drug approved by the U.S. Food and Drug Administration (FDA) for the treatment of CMML and by the European ... Decitabine is a similar drug to azacitidine and is approved by the FDA for treatments of all subtypes of MDS, including CMML. ... clinical utility of azacitidine". OncoTargets and Therapy. 3: 157-65. doi:10.2147/OTT.S5852. PMC 2939768. PMID 20856790. Robert ...
The deoxynucleoside analogues include cytarabine, gemcitabine, decitabine, azacitidine, fludarabine, nelarabine, cladribine, ...
"Phase I combination trial of lenalidomide and azacitidine in patients with higher-risk myelodysplastic syndromes". Journal of ...
Low doses of azacitidine and its analog decitabine have shown results against cancer through epigenetic demethylation. In ...
... sequential azacitidine and lenalidomide generate cancer testis antigen-specific cellular immunity". British Journal of ...
Azacitidine can be metabolized and incorporated into DNA and then recognized as a substrate for DNA methyltransferases, but ... Azacitidine and decitabine, which incorporate into the DNA and covalently trap the methyltransferases, have been approved by ... Various strategies such as using drugs like entinostat and azacitidine have been observed in clinical trials of non-small-cell ...
Clinical trial number NCT02719574 for "Open-label Study of FT-2102 With or Without Azacitidine or Cytarabine in Patients With ... November 2022). "Olutasidenib alone or with azacitidine in IDH1-mutated acute myeloid leukaemia and myelodysplastic syndrome: ...
... with subcutaneous 5-azacitidine and entinostat: a phase 2 consortium/stand up 2 cancer study". Oncotarget. 8 (21): 35326-35338 ... "Combination Epigenetic Therapy in Advanced Breast Cancer with 5-Azacitidine and Entinostat: A Phase II National Cancer ...
In combination with azacitidine, 25 participants achieved a CR (37%, 95% CI: 26, 50) with a median observed time in remission ... In November 2018, in the United States, venetoclax was approved in combination with azacitidine or decitabine or low-dose ... Study M14-358 (NCT02203773) was a non-randomized, open-label clinical trial of venetoclax in combination with azacitidine (n=67 ... In a phase 3 study of azacitidine and venetoclax in untreated acute myeloid leukemia not eligible for standard induction ...
It functions in a similar manner to azacitidine, although decitabine can only be incorporated into DNA strands while ... azacitidine can be incorporated into both DNA and RNA chains. It incorporates into DNA strands upon replication, and then when ...
The molecular formula C8H12N4O5 (molar mass: 244.205 g/mol) may refer to: Azacitidine Ribavirin, or tribavirin This set index ...
... an organic acid used for medical treatment of acne and as whitening agent Azacitidine ('AZA': drug and methylation inhibitor) ...
Intravenous Infusions in Patients with Myelodysplastic Syndrome with Excess Blasts Progressing on or After Azacitidine or ...
Cytarabine L01BC02 Fluorouracil L01BC03 Tegafur L01BC04 Carmofur L01BC05 Gemcitabine L01BC06 Capecitabine L01BC07 Azacitidine ...
... azacitidine) in phase III trials for myelodysplastic syndromes and AML Dacogen (decitabine) in phase III trials for AML and CML ...
Phase I trial of 5-azacitidine (5AC) and SNDX-275 in advanced lung cancer (NSCLC) Novel Sulphonylpyrroles as Inhibitors of Hdac ...
... with the average median survival overall for patients receiving classic azacitidine or decitabine is approximately 4.3-5.9 ...
... with a paper on induced XCR in somatic cell hybrid clones by 5-azacitidine treatment, and a paper on XCR in mouse oocytes. ...
... azacitidine (INN) azaclorzine (INN) azaconazole (INN) azacosterol (INN) Azactam azacyclonol (INN) azaftozine (INN) Azahexal ( ...
The combination of azacitidine and venetoclax is also approved for AML. Azacitidine is a chemical analogue of the nucleoside ... Azacitidine induces tumor regression on isocitrate dehydrogenase-1 mutant glioma xenografts in mice. In research, 5-azacitidine ... "Azacitidine (Vidaza) Use During Pregnancy". Drugs.com. 5 May 2020. Retrieved 12 August 2020. "Vidaza- azacitidine injection, ... since their levels of azacitidine may progressively increase. Based on animal studies and its mechanism of action, azacitidine ...
Azacitidine: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Before taking azacitidine,. *tell your doctor and pharmacist if you are allergic to azacitidine, any other medications, or any ... Talk to your doctor about the risks of taking azacitidine.. *you should know that azacitidine often causes diarrhea, which can ... If you or your partner become pregnant while taking azacitidine, call your doctor. Azacitidine may harm the fetus. ...
... about Azacitidine-Teva intended for persons living in Australia. ... What Azacitidine-Teva is used for. Azacitidine-Teva is an anti- ... Azacitidine-Teva contains a medicine called azacitidine which prevents the growth of cancer cells. Azacitidine-Teva has been ... After being given Azacitidine-Teva Storage Your doctor or pharmacist is responsible for storing Azacitidine-Teva. They are also ... What Azacitidine-Teva looks like Azacitidine-Teva is a white powder for suspension for injection and is supplied in a glass ...
Reviews and ratings for Azacitidine when used in the treatment of myelodysplastic syndrome. 19 reviews submitted with a 5.7 ... Azacitidine for Myelodysplastic Syndrome User Reviews. Brand names: Vidaza, Onureg Azacitidine has an average rating of 5.7 out ... Vidaza (azacitidine) I was diagnosed with CMML approx 3years ago and treatment of Azacitidine started 17mths ago... It has ... Vidaza (azacitidine) I have taken it for 4 months so far. It is now down to 5 days instead of 7 per month. The shots are ...
Azacitidine is a white to off-white solid. Azacitidine was found to be soluble in aqueous media across a pH range from 1.0 to ... Transporter Systems: Azacitidine is not a substrate of P-glycoprotein (P-gp). Azacitidine does not inhibit P-gp, breast cancer ... ONUREG (azacitidine) is supplied as film-coated tablets containing 200 mg or 300 mg of azacitidine for oral use. Each core ... Azacitidine was mutagenic in bacterial and mammalian cell systems. The clastogenic effect of azacitidine was shown by the ...
How does Azacitidine Accord work? The active substance in Azacitidine Accord, azacitidine, belongs to the group anti‑ ... Azacitidine Accord contains the active substance azacitidine.. Azacitidine Accord is a generic medicine. This means that ... Other information about Azacitidine Accord Azacitidine Accord received a marketing authorisation valid throughout the EU on 13 ... What are the benefits and risks of Azacitidine Accord? Because Azacitidine Accord is a generic medicine and is bioequivalent to ...
A Study of APG-115 Alone or Combined With Azacitidine in Patients With AML, CMML, or MDS Recruiting 18 years and older ... Azacitidine is approved by the U.S. Food and Drug Administration (FDA) for treating all myelodysplastic syndromes (MDS) ... A Study of APG-2575 in Combination With Azacitidine in Patients With Acute Myeloid Leukemia (AML) Recruiting 18 years and older ...
Aprea Therapeutics Presents Results From Phase Ib/II Clinical Study of APR-246 and Azacitidine (AZA) in Patients with TP53 ... Aprea Therapeutics Presents Results From Phase Ib/II Clinical Study of APR-246 and Azacitidine (AZA) in Patients with TP53 ... Aprea Therapeutics Presents Results From Phase Ib/II Clinical Study of APR-246 and Azacitidine (AZA) in Patients with TP53 ... Helsinn Group and MEI Pharma Announce First Patient Dosed in Pivotal Phase 3 Study of Pracinostat and Azacitidine in Acute ...
CanMED: NDC. The Cancer Medications Enquiry Database (CanMED) is a two-part resource for cancer drug treatment related studies.
On this page about Azacitidine (Teva) you will find information relating to side effects, age restrictions, food interactions, ... Other medicines containing the same active ingredients: azacitidine *Can I take Azacitidine (Teva) in sport? Find out on the ... Brand name: Azacitidine (Teva) TM. Your browser does not support the audio element. Listen to the Pronunciation: Play ... Azacitidine-Teva is indicated for the treatment of patients with: Intermediate-2 and High-risk Myelodysplastic Syndromes (MDS) ...
This custom health technology review will summarize evidence on the efficacy and safety of Azacitidine (intravenous and ...
The Phase 3 randomized, double-blind study evaluated the combination of magrolimab plus azacitidine as first-line treatments ... The study enrolled more than 500 patients who were randomized to receive magrolimab in combination with azacitidine or ... Gilead To Discontinue Phase 3 ENHANCE Study of Magrolimab Plus Azacitidine in Higher-Risk MDS .q4default .bwalignc { text-align ... azacitidine monotherapy. Primary endpoints were complete response and overall survival. Secondary endpoints included duration ...
"Azacitidine" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Azacitidine" by people in this website by year, and whether " ... Below are the most recent publications written about "Azacitidine" by people in Profiles. ... Potential clinical use of azacitidine and MEK inhibitor combination therapy in PTPN11-mutated juvenile myelomonocytic leukemia ...
FDA Approves Azacitidine for Newly Diagnosed Juvenile Myelomonocytic Leukemia. By The ASCO Post Staff. June 10, 2022. ... Patients were treated with intravenous azacitidine daily on days 1 to 7 of a 28-day cycle for a minimum of three cycles and a ... On May 20, the U.S. Food and Drug Administration approved azacitidine (Vidaza) for pediatric patients with newly diagnosed ... and activity of azacitidine prior to hematopoietic stem cell transplantation (HSCT) in 18 pediatric patients with juvenile ...
... we evaluated the effectiveness and safety of reduced-dose azacitidine (AZA) vs. decitabine (DAC) in adult MDS patients. ... Evaluation of Reduced-Dose Decitabine and Azacitidine for Treating Myelodysplastic Syndromes: A Retrospective Study Naibo Hu ... Keywords: Azacitidine, Dose-Response Relationship, Drug, Myelodysplastic syndromes, Aged, decitabine, Drug Tapering, Middle ... Sekeres MA, Othus M, List AF, Randomized phase II study of azacitidine alone or in combination with lenalidomide or with ...
GenPro presents azacitidine efficacy study to identify epigenetic predictors of Responder vs Non-Responder AML/MDS patients. ... GenPro presents azacitidine efficacy study to identify epigenetic predictors of Responder vs Non-Responder AML/MDS patients ...
REAL LIFE EXPERIENCE OF HOME CARE ADMINISTRATION OF 5-AZACITIDINE AND DOMICILIARY MANAGEMENT OF PATIENTS WITH MYELODYSPLASTIC ... REAL LIFE EXPERIENCE OF HOME CARE ADMINISTRATION OF 5-AZACITIDINE AND DOMICILIARY MANAGEMENT OF PATIENTS WITH MYELODYSPLASTIC ...
SAN DIEGO and CALGARY, AB: - Treatment with intravenous pelareorep plus azacitidine reduced tumor burden - Treatment with ... pelareorep and azacitidine dramatically upregulated multiple genes known to drive anti-cancer immune responses SAN DIEGO and ... Presentation of Preclinical Data Demonstrating the Synergistic Anti-Leukemic Effects of Pelareorep Combined with Azacitidine at ... Presentation of Preclinical Data Demonstrating the Synergistic Anti-Leukemic Effects of Pelareorep Combined with Azacitidine at ...
... azacitidine) is a small molecule pharmaceutical. Azacitidine was first approved as Vidaza on 2004-05-19. It is used to treat ... Onureg, Vidaza (azacitidine) is a small molecule pharmaceutical. Azacitidine was first approved as Vidaza on 2004-05-19. It is ...
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  • Azacitidine, sold under the brand name Vidaza among others, is a medication used for the treatment of myelodysplastic syndrome, myeloid leukemia, and juvenile myelomonocytic leukemia. (wikipedia.org)
  • Vidaza (azacitidine) 'My dad had MLS and then evolved into Leukemia (AML). (drugs.com)
  • Vidaza (azacitidine) 'My husband was diagnosed with MDS, no symptoms. (drugs.com)
  • Vidaza (azacitidine) 'I have just started my 2nd month of 7 days of injections. (drugs.com)
  • Vidaza (azacitidine) 'I have been on Vidaza treatment for eleven years now. (drugs.com)
  • Vidaza (azacitidine) 'I have taken it for 4 months so far. (drugs.com)
  • Vidaza (azacitidine) 'Injection site sore for weeks. (drugs.com)
  • Vidaza (azacitidine) 'I was diagnosed with myelodysplastic syndrome soon after having gone through a bout of Covid in 2022. (drugs.com)
  • This means that Azacitidine Accord contains the same active substance and works in the same way as a 'reference medicine' already authorised in the EU called Vidaza. (europa.eu)
  • Studies on the benefits and risks of the active substance in the authorised uses have already been carried out with the reference medicine, Vidaza, and do not need to be repeated for Azacitidine Accord. (europa.eu)
  • The European Medicines Agency concluded that, in accordance with EU requirements, Azacitidine Accord has been shown to be comparable to Vidaza. (europa.eu)
  • Therefore, the Agency's view was that, as for Vidaza, the benefits of Azacitidine Accord outweigh the identified risks and it can be authorised for use in the EU. (europa.eu)
  • On May 20, the U.S. Food and Drug Administration approved azacitidine (Vidaza) for pediatric patients with newly diagnosed juvenile myelomonocytic leukemia (JMML). (ascopost.com)
  • Onureg, Vidaza (azacitidine) is a small molecule pharmaceutical. (pharmakb.com)
  • Azacitidine was first approved as Vidaza on 2004-05-19. (pharmakb.com)
  • Our range of products include vidaza azacitidine 100mg injection, xylistin forte 2 miu injection, guficol plus 2 miu injection and bevatas 400 mg injection. (wellnessmedicalindia.com)
  • Vidaza (azacitidine for injection) is a cancer medication used to treat certain types of bone marrow cancers and blood cell disorders. (wellnessmedicalindia.com)
  • Azacitidine-Teva will be given to you as an injection under the skin (subcutaneously i.e. under the skin on your thigh, abdomen or upper arm) or as an intravenous infusion by a doctor or a nurse. (news-medical.net)
  • This is because the composition of Azacitidine Accord is the same as the reference medicine and when given by injection under the skin, the active substance in both products is expected to be absorbed in the same way. (europa.eu)
  • Leveraging the skills of our qualified team of professional, we are able to provide a wide array of 100mg Azacitidine Injection. (amohapharma.com)
  • 100mg Azacitidine Injection is able to kill the cancer cells and helps in normal maturation. (amohapharma.com)
  • Azacitidine 100 mg Injection is a medication used to treat myelodysplastic syndrome (a group of conditions in which the bone marrow produces blood cells that are misshapen and does not produce enough healthy blood cells). (totalpharmamed.com)
  • Providing you the best range of azacitidine for injection myaza with effective & timely delivery. (deephealthcare.co.in)
  • Azacitidine is indicated for the treatment of myelodysplastic syndrome, for which it received approval by the U.S. Food and Drug Administration (FDA) on May 19, 2004. (wikipedia.org)
  • In two randomized controlled trials comparing azacitidine to supportive treatment, 16% of subjects with myelodysplastic syndrome who were randomized to receive azacitidine had a complete or partial normalization of blood cell counts and bone marrow morphology, compared to none who received supportive care, and about two-thirds of patients who required blood transfusions no longer needed them after receiving azacitidine. (wikipedia.org)
  • Kidney toxicity, ranging from elevated serum creatinine to kidney failure and death, have been reported in patients treated with intravenous azacitidine in combination with other chemotherapeutic agents for conditions other than myelodysplastic syndrome. (wikipedia.org)
  • Azacitidine-Teva has been prescribed by your doctor for the treatment of myelodysplastic syndrome (MDS). (news-medical.net)
  • Azacitidine has an average rating of 5.7 out of 10 from a total of 17 reviews for the treatment of Myelodysplastic Syndrome. (drugs.com)
  • The Phase 3 randomized, double-blind study evaluated the combination of magrolimab plus azacitidine as first-line treatments for higher-risk myelodysplastic syndromes (HR-MDS), a disease without a new class of treatments approved in almost 20 years. (gilead.com)
  • A phase 1b study of venetoclax and azacitidine combination in patients with relapsed or refractory myelodysplastic syndromes. (uchicago.edu)
  • For the treatment of myelodysplastic syndromes, azacitidine is given subcutaneously or intravenously in a dose of 75 mg/m daily for 7 days, in 4-week cycles. (pocketdrugguide.com)
  • Azacitidine and its deoxy derivative, decitabine (also known as 5-aza-2′deoxycytidine) are used in the treatment of myelodysplastic syndrome. (junuvcp.com)
  • Previous first-line treatment for intermediate, high, very high risk myelodysplastic syndromes (based on IPSS-R) or CMML with any antineoplastic agents including for example chemotherapy, lenalidomide and hypomethylating agents (HMAs) such as decitibine and azacitidine. (who.int)
  • The combination of azacitidine and venetoclax is also approved for AML. (wikipedia.org)
  • Eprenetapopt combined with venetoclax and azacitidine in TP53-mutated acute myeloid leukaemia: a phase 1, dose-finding and expansion study. (uchicago.edu)
  • Impact of FLT3 Mutation on Outcomes after Venetoclax and Azacitidine for Patients with Treatment-Naïve Acute Myeloid Leukemia. (uchicago.edu)
  • Measurable Residual Disease Response and Prognosis in Treatment-Naïve Acute Myeloid Leukemia With Venetoclax and Azacitidine. (uchicago.edu)
  • During anamnesis, lower urinary tract and gynecological cycles of decitabine, it was decided to switch AML therapy to surgeries, obstetrical history, neurological disorders, diabetes, azacitidine associated with venetoclax, without new reports and trauma were excluded as possible causes of urinary of urinary retention (Figure 1 ). (bvsalud.org)
  • medical citation needed] Azacitidine and its deoxy derivative, decitabine (also known as 5-aza-2′-deoxycytidine) were first synthesized in Czechoslovakia as potential chemotherapeutic agents for cancer. (wikipedia.org)
  • After azanucleosides such as azacitidine have been metabolized to 5-aza-2′-deoxycytidine-triphosphate (aka, decitabine-triphosphate), they can be incorporated into DNA and azacytosine can be substituted for cytosine. (wikipedia.org)
  • However, as the efficacy and safety of rational dosing regimens are lacking, we evaluated the effectiveness and safety of reduced-dose azacitidine (AZA) vs. decitabine (DAC) in adult MDS patients. (medscimonit.com)
  • Currently, there are limited FDA-approved therapies for MDS, which include hypomethylating agents such as azacitidine and decitabine, iron chelators such as deferasirox, and lenalidomide. (medscape.com)
  • Do not substitute ONUREG for intravenous or subcutaneous azacitidine. (nih.gov)
  • The indications and dosing regimen for ONUREG differ from that of intravenous or subcutaneous azacitidine ( 2.1 , 5.1 ). (nih.gov)
  • This custom health technology review will summarize evidence on the efficacy and safety of Azacitidine (intravenous and subcutaneous) as maintenance therapy for patients with Acute Myeloid Leukemia. (cadth.ca)
  • Due to substantial differences in the pharmacokinetic parameters, the recommended dose and schedule for ONUREG ® are different from those for the intravenous or subcutaneous azacitidine products. (onuregpro.com)
  • Treatment of patients using intravenous or subcutaneous azacitidine at the recommended dosage of ONUREG ® may result in a fatal adverse reaction. (onuregpro.com)
  • Treatment with ONUREG ® at the doses recommended for intravenous or subcutaneous azacitidine may not be effective. (onuregpro.com)
  • SAN DIEGO and CALGARY, AB: - Treatment with intravenous pelareorep plus azacitidine reduced tumor burden - Treatment with pelareorep and azacitidine dramatically upregulated multiple genes known to drive anti-cancer immune responses SAN DIEGO and CALGARY, AB, Dec. 15, 2021 /PRNewswire/ - Oncolytics Biotech® Inc. (NASDAQ: ONCY) (TSX: ONC) announced preclinical data demonstrating the synergistic anti-leukemic effects of pelareorep combined with the chemotherapeutic agent azacitidine. (sdbn.org)
  • Patients were treated with intravenous azacitidine daily on days 1 to 7 of a 28-day cycle for a minimum of three cycles and a maximum of six cycles, provided patients did not have disease progression or were ready for HSCT between cycles 4 and 6. (ascopost.com)
  • The adverse effects of azacitidine are generally similar to those seen with cytarabine. (pocketdrugguide.com)
  • Azacitidine is an antimetabolite antineoplastic with general properties similar to those of cytarabine. (pocketdrugguide.com)
  • Here, we describe somatic biallelic TET2 mutations in an elderly patient with acute myeloid leukemia (AML) that was chemoresistant to anthracycline and cytarabine but acutely sensitive to 5′-azacitidine (5′-Aza) hypomethylating monotherapy, resulting in long-term morphological remission. (jci.org)
  • ONUREG ® is contraindicated in patients with known severe hypersensitivity to azacitidine or its components. (onuregpro.com)
  • tell your doctor and pharmacist if you are allergic to azacitidine, any other medications, or any of the ingredients in azacitidine tablets. (medlineplus.gov)
  • If you are allergic to azacitidine or any of the other ingredients of Azacitidine-Teva listed at the end of this leaflet. (news-medical.net)
  • If you are allergic to azacitidine, mannitol (Osmitrol, Resectisol), or any other medications, tell your doctor and pharmacist. (totalpharmamed.com)
  • Cellular Composition and 5hmC Signature Predict the Treatment Response of AML Patients to Azacitidine Combined with Chemotherapy. (uchicago.edu)
  • The study enrolled more than 500 patients who were randomized to receive magrolimab in combination with azacitidine or azacitidine monotherapy. (gilead.com)
  • Azacitidine is also indicated for the treatment of myeloid leukemia and juvenile myelomonocytic leukemia. (wikipedia.org)
  • Oral azacitidine modulates the immune microenvironment in acute myeloid leukemia (AML) patients in remission: A subanalysis from the QUAZAR AML-001 Trial. (ox.ac.uk)
  • Cytogenetics and gene mutations influence survival in older patients with acute myeloid leukemia treated with azacitidine or conventional care. (ox.ac.uk)
  • Azacitidine in 302 patients with WHO-defined acute myeloid leukemia: results from the Austrian Azacitidine Registry of the AGMT-Study Group. (agmt.at)
  • Your dose will be calculated based on your body surface area, with the usual dose of 75 mg Azacitidine-Teva per metre squared of body surface area. (news-medical.net)
  • Azacitidine is a chemical analogue of the nucleoside cytidine, which is present in DNA and RNA. (wikipedia.org)
  • Azacitidine is an analogue of cytidine, which means that it is incorporated into the genetic material of cells (RNA and DNA). (europa.eu)
  • Azacitidine API is a chemical analog of cytidine, a nucleoside present in DNA and RNA. (junuvcp.com)
  • It can also be hepatotoxic in patients with severe liver impairment, and patients with extensive liver tumors due to metastatic disease have developed progressive hepatic coma and death during azacitidine treatment, especially when their albumin levels are less than 30 g/L. It is contraindicated in patients with advanced malignant hepatic tumors. (wikipedia.org)
  • Sexually active women of reproductive potential should use contraception during while receiving azacitidine and for one week after the last dose, and sexually active men with female partners of reproductive potential should use contraception during treatment and for three months following the last dose. (wikipedia.org)
  • Be sure to tell your doctor how you are feeling during your treatment with azacitidine. (medlineplus.gov)
  • Your doctor will probably tell you to take an anti-diarrhea medication to prevent dehydration (loss of too much water from your body) during your treatment with azacitidine. (medlineplus.gov)
  • Use an effective method of contraception during treatment with Azacitidine-Teva and for up to six (6) months after discontinuation of Azacitidine-Teva. (news-medical.net)
  • Do not father a child while receiving treatment with Azacitidine-Teva. (news-medical.net)
  • Use barrier methods of contraception (e.g. condoms) during treatment and for up to three (3) months after discontinuation of Azacitidine-Teva, if your partner is of childbearing potential. (news-medical.net)
  • Azacitidine Accord treatment should be started and monitored under the supervision of a doctor experienced in the use of cancer medicines. (europa.eu)
  • Multicenter phase 2 study of oral azacitidine (CC-486) plus CHOP as initial treatment for PTCL. (uchicago.edu)
  • If there are rises in serum concentrations of urea or creatinine, the next cycle of azacitidine should be delayed until these return to normal or baseline, and the dose should be halved on the next treatment course. (pocketdrugguide.com)
  • During your azacitidine treatment, you should use birth control to prevent pregnancy in yourself or your partner. (totalpharmamed.com)
  • Azacitidine may be a preferred treatment for older patients with AML with Adverse-risk cytogenetics, particularly those with chromosome 5, 7, and/or 17 abnormalities and complex or monosomal karyotypes. (ox.ac.uk)
  • Azacitidine and its metabolites are primarily excreted by the kidneys, so patients with chronic kidney disease should be closely monitored for other side effects, since their levels of azacitidine may progressively increase. (wikipedia.org)
  • 320-67-2 Azacitidine is available as a powder. (chemicalbull.com)
  • Azacitidine is available as a powder that must be mixed with water before being injected subcutaneously (under the skin) or intravenously (into a vein) by a doctor or nurse in a medical office or hospital outpatient department. (totalpharmamed.com)
  • For more information about using Azacitidine Accord, see the package leaflet or contact your doctor or pharmacist. (europa.eu)
  • Recommendations and precautions to be followed by healthcare professionals and patients for the safe and effective use of Azacitidine Accord have been included in the summary of product characteristics and the package leaflet . (europa.eu)
  • Renal tubular acidosis developed in five patients with chronic myelogenous leukemia (an unapproved use) treated with azacitidine and etoposide, and patients with renal impairment may be at increased risk for renal toxicity. (wikipedia.org)
  • You or your partner should not become pregnant while you are taking azacitidine. (medlineplus.gov)
  • If you or your partner become pregnant while taking azacitidine, call your doctor. (medlineplus.gov)
  • Avoid becoming pregnant while receiving Azacitidine-Teva but if you do, tell. (news-medical.net)
  • While taking azacitidine, neither you nor your partner should become pregnant. (totalpharmamed.com)
  • Efficacy was evaluated in AZA-JMML-001 (ClinicalTrials.gov identifier NCT02447666 ), an international, multicenter, open-label study to evaluate the pharmacokinetics, pharmacodynamics, safety, and activity of azacitidine prior to hematopoietic stem cell transplantation (HSCT) in 18 pediatric patients with juvenile myelomonocytic leukemia. (ascopost.com)
  • Talk to your doctor about the risks of taking azacitidine. (medlineplus.gov)
  • Your doctor has weighed the risks of you taking Azacitidine-Teva against the benefits they expect it will have for you. (news-medical.net)
  • What are the benefits and risks of Azacitidine Accord? (europa.eu)
  • Because Azacitidine Accord is a generic medicine and is bioequivalent to the reference medicine, its benefits and risks are taken as being the same as the reference medicine's. (europa.eu)
  • Azacitidine should be used with caution in renal impairment and doses adjusted accordingly (see below). (pocketdrugguide.com)
  • Based on animal studies and its mechanism of action, azacitidine can cause severe fetal damage. (wikipedia.org)
  • you should know that azacitidine often causes diarrhea, which can be severe. (medlineplus.gov)
  • History of severe hypersensitivity to azacitidine or its components ( 4 ). (nih.gov)
  • Compared with wild-type, OS was significantly reduced among CCR-treated patients with TP53 or NRAS mutations and azacitidine-treated patients with FLT3 or TET2 mutations. (ox.ac.uk)
  • Azacitidine" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • Your doctor will give you medication to prevent nausea and vomiting 30 minutes before you receive each dose of azacitidine for the first two cycles. (medlineplus.gov)
  • Other product types may be available that contain the medication azacitidine. (chemocare.com)
  • The influence of gene mutations in azacitidine-treated patients warrants further study. (ox.ac.uk)
  • Azacitidine-Teva is an anti-cancer agent. (news-medical.net)
  • Azacitidine-Teva contains a medicine called azacitidine which prevents the growth of cancer cells. (news-medical.net)
  • Azacitidine is in a class of medications called demethylation agents. (medlineplus.gov)
  • Azacitidine belongs to a class of drugs known as demethylation agents. (totalpharmamed.com)
  • Pevonedistat with azacitidine in older patients with TP53-mutated AML: a phase 2 study with laboratory correlates. (uchicago.edu)
  • Adverse renal effects of azacitidine include abnormalities in renal-function tests, renal tubular acidosis, renal failure, and death. (pocketdrugguide.com)
  • AZACITIDINE (ay za SITE i deen) treats blood and bone marrow cancers. (chemocare.com)
  • This leaflet answers some common questions about Azacitidine-Teva. (news-medical.net)
  • Other side effects of Azacitidine include rash, itching, and difficulty breathing or swallowing. (totalpharmamed.com)
  • Ask your doctor if you have any questions about how Azacitidine-Teva works or why this medicine has been prescribed for you. (news-medical.net)
  • As for every medicine, the company provided studies on the quality of Azacitidine Accord. (europa.eu)
  • There was no need for ' bioequivalence ' studies to investigate whether Azacitidine Accord is absorbed similarly to the reference medicine to produce the same level of the active substance in the blood. (europa.eu)