Leukemia, Myelomonocytic, Chronic
Chromatography, Supercritical Fluid
Compassionate Use Trials
Leukemia, Myeloid, Acute
Anemia, Refractory, with Excess of Blasts
DNA Modification Methylases
United States Food and Drug Administration
Drug Administration Schedule
Antineoplastic Combined Chemotherapy Protocols
Maximum Tolerated Dose
Hematopoietic Stem Cell Transplantation
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)
There are several subtypes of MDS, each with distinct clinical features and prognosis. The most common subtype is refractory anemia with excess blasts (RAEB), followed by chronic myelomonocytic leukemia (CMMoL) and acute myeloid leukemia (AML).
The exact cause of MDS is not fully understood, but it is believed to result from a combination of genetic mutations and environmental factors. Risk factors for developing MDS include exposure to certain chemicals or radiation, age over 60, and a history of previous cancer treatment.
Symptoms of MDS can vary depending on the specific subtype and severity of the disorder, but may include fatigue, weakness, shortness of breath, infection, bleeding, and easy bruising. Diagnosis is typically made through a combination of physical examination, medical history, blood tests, and bone marrow biopsy.
Treatment for MDS depends on the specific subtype and severity of the disorder, as well as the patient's overall health and preferences. Options may include supportive care, such as blood transfusions and antibiotics, or more intensive therapies like chemotherapy, bone marrow transplantation, or gene therapy.
Overall, myelodysplastic syndromes are a complex and heterogeneous group of disorders that can have a significant impact on quality of life and survival. Ongoing research is focused on improving diagnostic accuracy, developing more effective treatments, and exploring novel therapeutic approaches to improve outcomes for patients with MDS.
The term "chronic" refers to the fact that this type of leukemia progresses slowly over time, often taking years or even decades to develop. It is most commonly seen in adults over the age of 60, and men are more likely to be affected than women.
CMML can be divided into two subtypes:
* CMML-1: This subtype is characterized by a higher number of immature cells in the blood and bone marrow, and a better prognosis.
* CMML-2: This subtype is characterized by a lower number of immature cells in the blood and bone marrow, and a poorer prognosis.
Treatment options for CMML include chemotherapy, targeted therapy, and stem cell transplantation. The specific treatment plan will depend on the subtype of the disease, the patient's overall health, and other factors.
Overall, myelomonocytic leukemia is a rare but potentially aggressive form of cancer that requires careful monitoring and management to improve outcomes for patients.
AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.
There are several subtypes of AML, including:
1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.
The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Confusion or seizures
AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.
Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:
1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.
It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.
There are several subtypes of refractory anemia, including:
1. Refractory anemia with excess blasts (RAEB): This type of anemia is characterized by a high number of immature red blood cells in the bone marrow.
2. Refractory anemia with ringed sideroblasts (RARS): This type of anemia is characterized by the presence of abnormal red blood cells that have a "ring-like" appearance under a microscope.
3. Refractory anemia with multilineage dysplasia (RARMD): This type of anemia is characterized by abnormal cell development in the bone marrow, including immature red blood cells, white blood cells, and platelets.
Refractory anemia can be caused by a variety of factors, including genetic mutations, exposure to certain chemicals or toxins, and certain medical conditions such as chronic kidney disease or rheumatoid arthritis. Treatment for refractory anemia typically involves blood transfusions and supportive care, such as folic acid supplements and antibiotics to prevent infection. In some cases, bone marrow transplantation may be recommended.
The term "refractory" refers to the fact that this type of anemia does not respond well to standard treatments, such as blood transfusions or medications. The term "excess blasts" refers to the presence of a large number of immature cells in the bone marrow.
RAEB is a serious and potentially life-threatening condition that can develop into acute myeloid leukemia (AML), a type of cancer that affects the blood and bone marrow. AML is characterized by the rapid growth of abnormal white blood cells, which can crowd out normal cells in the bone marrow and lead to a variety of symptoms, including fatigue, fever, night sweats, and weight loss.
RAEB is usually diagnosed in adults over the age of 60, although it can occur at any age. The condition is often associated with other health problems, such as myelodysplastic syndrome (MDS), a group of disorders that affect the bone marrow and blood cells.
Treatment for RAEB typically involves chemotherapy and/or bone marrow transplantation. The goal of treatment is to slow the progression of the disease, reduce symptoms, and improve quality of life. In some cases, RAEB may be managed with supportive care, such as blood transfusions and antibiotics, to help manage symptoms and prevent complications.
Overall, refractory anemia with excess blasts is a serious and complex condition that requires careful management by a healthcare team of hematologists, oncologists, and other specialists. With appropriate treatment, many people with RAEB are able to achieve long-term remission and improve their quality of life.
Myeloid leukemia can be classified into several subtypes based on the type of cell involved and the degree of maturity of the abnormal cells. The most common types of myeloid leukemia include:
1. Acute Myeloid Leukemia (AML): This is the most aggressive form of myeloid leukemia, characterized by a rapid progression of immature cells that do not mature or differentiate into normal cells. AML can be further divided into several subtypes based on the presence of certain genetic mutations or chromosomal abnormalities.
2. Chronic Myeloid Leukemia (CML): This is a slower-growing form of myeloid leukemia, characterized by the presence of a genetic abnormality known as the Philadelphia chromosome. CML is typically treated with targeted therapies or bone marrow transplantation.
3. Myelodysplastic Syndrome (MDS): This is a group of disorders characterized by the impaired development of immature blood cells in the bone marrow. MDS can progress to AML if left untreated.
4. Chronic Myelomonocytic Leukemia (CMML): This is a rare form of myeloid leukemia that is characterized by the accumulation of immature monocytes in the blood and bone marrow. CMML can be treated with chemotherapy or bone marrow transplantation.
The symptoms of myeloid leukemia can vary depending on the subtype and severity of the disease. Common symptoms include fatigue, weakness, fever, night sweats, and weight loss. Diagnosis is typically made through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment options for myeloid leukemia can include chemotherapy, targeted therapies, bone marrow transplantation, and supportive care to manage symptoms and prevent complications. The prognosis for myeloid leukemia varies depending on the subtype of the disease and the patient's overall health. With current treatments, many patients with myeloid leukemia can achieve long-term remission or even be cured.
In the medical field, fatigue is often evaluated using a combination of physical examination, medical history, and laboratory tests to determine its underlying cause. Treatment for fatigue depends on the underlying cause, but may include rest, exercise, stress management techniques, and medication.
Some common causes of fatigue in the medical field include:
1. Sleep disorders, such as insomnia or sleep apnea
2. Chronic illnesses, such as diabetes, heart disease, or arthritis
3. Infections, such as the flu or a urinary tract infection
4. Medication side effects
5. Poor nutrition or hydration
6. Substance abuse
7. Chronic stress
8. Depression or anxiety
9. Hormonal imbalances
10. Autoimmune disorders, such as thyroiditis or lupus.
Fatigue can also be a symptom of other medical conditions, such as:
2. Hypoglycemia (low blood sugar)
3. Hypothyroidism (underactive thyroid)
4. Hyperthyroidism (overactive thyroid)
5. Chronic fatigue syndrome
9. Heart failure
10. Liver or kidney disease.
It is important to seek medical attention if fatigue is severe, persistent, or accompanied by other symptoms such as fever, pain, or difficulty breathing. A healthcare professional can diagnose and treat the underlying cause of fatigue, improving overall quality of life.
Examples of acute diseases include:
1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.
Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.
Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.
In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.
Institute of Organic Chemistry and Biochemistry
List of antineoplastic agents
Tumor suppressor gene
Molecular and epigenetic mechanisms of alcoholism
Chronic myelomonocytic leukemia
Thomas P. Loughran Jr.
ATC code L01
List of drugs: As-Az
Index of oncology articles
Azacitidine - NCI
DailyMed - Search Results for Azacitidine
Azacitidine: MedlinePlus Drug Information
MedlinePlus - Search Results for: Azacitidine
Azacitidine - PubMed
Azacitidine - PubMed
Azacitidine - Drugs and Lactation Database (LactMed®) - NCBI Bookshelf
Oral Form of Azacitidine Improves Overall Survival in Patients with AML in Remission
Case Study: Adding Venetoclax to Azacitidine for Patients with AML - Dana-Farber Cancer Institute | Boston, MA
Is enasidenib plus azacitidine better than with azacitidine alone for AML patients? - ecancer
A Study of APG-115 Alone or Combined With Azacitidine in Patients With AML, CMML, or MDS | Aplastic Anemia & MDS International...
Older Patients With Previously Untreated AML May Benefit from Azacitidine, Venetoclax - Cancer Therapy Advisor
Impact of azacitidine before allogeneic stem-cell transplantation for myelodysplastic syndromes: a study by the Société...
Myelodysplastic Syndrome Clinical Trial: Study of Efficacy and Safety of MBG453 in Combination With Azacitidine in Subjects...
ONUREG® (azacitidine) Sitemap | for HCPs
DailyMed - AZACITIDINE injection, powder, lyophilized, for solution
Azacitidine (Onureg) | Canadian Journal of Health Technologies
Haute Autorité de Santé - Résultat de recherche
Azacitidine Oral Tablet 200 mg, 300 mg - Community Health Net
Visi Vaistai - Azacitidine Mylan 25mg/ml milteliai injekcinei suspensijai N1
Combination of azacitidine, venetoclax and ruxolitinib in blast phase myeloproliferative neoplasms. | Br J Haematol;202(2):...
Oncolytics Biotech® Announces the Presentation of Preclinical Data Demonstrating the Synergistic Anti-Leukemic Effects of...
Detailed Study on Global and United States Azacitidine Market 2019 by Size, Applications, Type, Manufacturers, Region and 2024...
Maintenance therapy: Oral azacitidine in patients with AML improves long-term overall survival
Pharmaceutical Benefits Scheme (PBS)
DLI after haploidentical BMT with post-transplant CY
Clinical Outcomes Similar With 5- or 7-Day Azacitidine in Lower-Risk Myelodysplastic Syndrome - Hematology Advisor
Table 2 - Analysis of MarketScan Data for Immunosuppressive Conditions and Hospitalizations for Acute Respiratory Illness,...
- This use is approved for the Onureg brand of azacitidine. (cancer.gov)
- ONUREG ® is contraindicated in patients with known severe hypersensitivity to azacitidine or its components. (onuregpro.com)
- 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)
- Do not substitute ONUREG ® for intravenous or subcutaneous azacitidine. (onuregpro.com)
- An oral formulation of azacitidine improved overall survival in patients with acute myeloid leukemia in first remission. (pharmacytimes.com)
- An oral formulation of azacitidine (CC-486) improved overall survival (OS) and relapse-free survival (RFS) in patients with acute myeloid leukemia (AML) in first remission following induction chemotherapy, according to late-breaking data presented on Tuesday at the 61st American Society of Hematology Annual Meeting and Exposition. (pharmacytimes.com)
- Among older patients with acute myeloid leukemia (AML) who have not received any previous therapy and were ineligible for standard induction chemotherapy, those treated with azacitidine and venetoclax had superior overall survival and incidence of remission compared with patients who were treated with azacitidine alone, according to study results published in The New England Journal of Medicine . (cancertherapyadvisor.com)
- Azacitidine and venetoclax in previously untreated acute myeloid leukemia. (cancertherapyadvisor.com)
- Preclinical studies featured in the poster evaluated pelareorep in combination with azacitidine in acute myeloid leukemia (AML) cells in vitro and in a leukemia xenograft mouse model. (financialnewsmedia.com)
- The phase-III trial QUAZAR AML-001 investigates the effects of treatment with oral azacitidine as maintenance therapy on long-term overall survival (OS) in patients with acute myeloid leukemia. (bpno.dk)
- This is an open-label Phase 1b/2 clinical study of BI 836858 given in combination with azacitidine, followed by BI 836858 plus azacitidine maintenance, in newly diagnosed acute myeloid leukemia. (clinicaltrials.gov)
- Mutant Isocitrate Dehydrogenase 1 Inhibitor Ivosidenib in Combination With Azacitidine for Newly Diagnosed Acute Myeloid Leukemia. (ox.ac.uk)
- BACKGROUND: In the AZA-001 trial, azacitidine (75 mg/m 2 /d subcutaneously for Days 1-7 of every 28-day cycle) demonstrated improved survival compared with conventional care regimens in patients with International Prognostic Scoring System-defined intermediate-2- or high-risk myelodysplastic syndrome and World Health Organization-defined acute myeloid leukemia with 20% to 30% bone marrow blasts. (johnshopkins.edu)
- 9. Mutational analysis in serial marrow samples during azacitidine treatment in patients with post-transplant relapse of acute myeloid leukemia or myelodysplastic syndromes. (nih.gov)
- Results from the dose escalation cohort of the trial combining azacitidine or decitabine plus venetoclax were recently published ( Lancet Oncology , 2018) with 61% achieving a CR or CR with incomplete marrow recovery, considerably higher than would be expected with azacitidine or decitabine alone. (dana-farber.org)
- One of the next steps would be figuring out whether there is a role to actually add a third agent into this combination because right now azacitidine and venetoclax, which is a BCL2 inhibitor, is an FDA approved standard for newly diagnosed and we now know azacitidine with enasidenib is also effective in that newly diagnosed population. (ecancer.org)
- NCT02993523 ) to determine the efficacy and safety of combination azacitidine and venetoclax therapy compared with azacitidine and placebo in patients with AML who were not eligible to receive intensive induction chemotherapy due to coexisting conditions, age, or both. (cancertherapyadvisor.com)
- Participants included in the study were randomly assigned to receive either azacitidine-venetoclax treatment or azacitidine-placebo. (cancertherapyadvisor.com)
- A total of 431 participants were included in the study (286 in the azacitidine-venetoclax group and 145 in the azacitidine-placebo group). (cancertherapyadvisor.com)
- Nausea of any grade was reported in 44% of patients in the azacitidine-venetoclax arm and in 35% of patients in the placebo arm. (cancertherapyadvisor.com)
- Among azacitidine-venetoclax and placebo groups, other adverse events included grade 3 or greater thrombocytopenia (45% and 38%, respectively), neutropenia (42% and 29%, respectively), and febrile neutropenia (42% and 19%, respectively). (cancertherapyadvisor.com)
- In addition, 85% of azacitidine-venetoclax group members and 67% of control group members had infections of any grade. (cancertherapyadvisor.com)
- The safety profile of azacitidine plus venetoclax was consistent with the known side effect profiles of both agents, and adverse events were consistent with expectations for an older AML population," the authors noted. (cancertherapyadvisor.com)
- The combination of azacitidine plus venetoclax in this challenging patient population in this trial was an effective treatment regimen that led to significant improvements in the incidence of composite complete remission and overall survival. (cancertherapyadvisor.com)
- Combination of azacitidine, venetoclax and ruxolitinib in blast phase myeloproliferative neoplasms. (bvsalud.org)
Hypersensitivity to azacitidine1
- Hypersensitivity to Azacitidine or Mannitol ( 4.2 ). (nih.gov)
- This is a Phase III multi-center, randomized, two-arm parallel-group, double-blind, placebo controlled study of MBG453 or placebo added to azacitidine in adult subjects with intermediate, high or very high risk myelodysplastic syndrome (MDS) as per IPSS-R, or Chronic Myelomonocytic Leukemia-2 (CMML-2). (survivornet.com)
- MDS: The recommended starting dosage for the first treatment cycle, for all patients regardless of baseline hematology values, is azacitidine for injection 75 mg/m 2 daily for 7 days to be administered by subcutaneous injection or intravenous infusion. (nih.gov)
- These highlights do not include all the information needed to use AZACITIDINE FOR INJECTION safely and effectively. (nih.gov)
- See full prescribing information for AZACITIDINE FOR INJECTION. (nih.gov)
- Do not substitute azacitidine for injection for oral azacitidine. (nih.gov)
- The indications and dosing regimen for azacitidine for injection differ from that of oral azacitidine ( 2.1 , 5.1 ). (nih.gov)
- Dr Courtney DiNardo speaks to ecancer at the ASH 2019 meeting in Orlando about enasidenib plus azacitidine when treating older patients with AML. (ecancer.org)
- The global Azacitidine market size is expected to gain market growth in the forecast period of 2020 to 2025, with a CAGR of xx% in the forecast period of 2020 to 2025 and will expected to reach USD xx million by 2025, from USD xx million in 2019. (amplemarketreports.com)
- Patients with RAS pathway mutations were assigned to receive azacitidine delivered subcutaneously 75 mg/m 2 for 7 days, plus intravenous lenzilumab 552 mg on days 1 and 15 of cycle 1 and on day 1 only of all subsequent cycles. (medscape.com)
- Unlike monitoring of patients who receive azacitidine alone, ongoing attentiveness to the monitoring and management of myelosuppression is key for patient safety with this combination therapy," the investigators concluded. (cancertherapyadvisor.com)
- The purpose of the current study is to assess clinical effects of MBG453 in combination with azacitidine in adult subjects with IPSS-R intermediate, high, very high risk MDS and CMML-2. (survivornet.com)
- To test if the combination of romidepsin, CC-486 (5-azacitidine), dexamethasone, and lenalidomide (RAdR) can be given safely to participants with relapsed or treatment refractory TCM. (nih.gov)
- Thomas is a co-investigator of the ongoing phase 2/3 PREACH-M trial, which is testing a novel strategy of treating CMML with mutations in the RAS pathway with a combination of azacitidine and the investigational antibody lenzilumab, which is a targeted inhibitor of granulocyte-macrophage colony-stimulating factor (GM-CSF). (medscape.com)
- SAN DIEGO, CA and CALGARY, AB - December 15, 2021 - Oncolytics Biotech ® Inc. (NASDAQ: ONCY) (TSX: ONC) announced preclinical data demonstrating the synergistic anti-leukemic effects of pelareorep combined with the chemotherapeutic agent azacitidine. (financialnewsmedia.com)
- The primary objective of this study is to compare overall survival (OS) in the MBG453 plus azacitidine arm versus placebo plus azacitidine arm where OS is the time from randomization until death due to any cause. (survivornet.com)
- Subjects will be randomized in a 1:1 ratio to treatment arms as follow: MBG453 800 mg IV Q4W plus azacytidine, Placebo IV Q4W plus azacitidine The randomization will be stratified into 4 groups: intermediate risk MDS, high risk MDS, very high risk MDS and CMML-2. (survivornet.com)
- The authors concluded that "the 5-day azacitidine in lower-risk MDS showed comparable efficacy to a 7-day regimen in terms of similar overall response and other outcomes, despite significantly higher rates of CyR in the 7-day regimen. (hematologyadvisor.com)
- Azacitidine is also being studied in the treatment of other conditions and types of cancer . (cancer.gov)
- 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)
- Tony continued on treatment and remained in a CR for over 15 months, longer than is typical for azacitidine alone in this setting. (dana-farber.org)
- METHODS: This secondary analysis of the AZA-001 phase 3 study evaluated the time to first response and the potential benefit of continued azacitidine treatment beyond first response in responders. (johnshopkins.edu)
- Although 7-day uninterrupted dosing of azacitidine is used for patients with lower-risk MDS, its efficacy and safety compared with 5-day dosing has been confirmed. (hematologyadvisor.com)
- Azacitidine may cause fatal or serious tumor lysis syndrome, including in patients with MDS. (nih.gov)
- Patients with TET2 mutations only were assigned to receive azacitidine on the same schedule, plus IV sodium ascorbate (ASC) 30 g for 7 days, with the first dose 15 g, and subsequent doses 30 g if there is no evidence of tumor lysis syndrome. (medscape.com)
- 8. Azacitidine induces profound genome-wide hypomethylation in primary myelodysplastic bone marrow cultures but may also reduce histone acetylation. (nih.gov)
- Patients in both arms received standard doses of azacitidine (75 mg per square meter of body surface area). (cancertherapyadvisor.com)
- 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)
- If you vomit after taking azacitidine, do not take another dose. (medlineplus.gov)
- do not breastfeed while you are taking azacitidine and for 1 week after your final dose. (medlineplus.gov)
- Azacitidine caused fetal death and anomalies in pregnant rats via a single intraperitoneal dose less than the recommended human daily dose of oral azacitidine on a mg/m 2 basis. (onuregpro.com)
- Impact of azacitidine before allogeneic stem-cell transplantation for myelodysplastic syndromes: a study by the Société Française de Greffe de Moelle et de Thérapie-Cellulaire and the Groupe-Francophone des Myélodysplasies. (inserm.fr)
- Regional analysis is another highly comprehensive part of the research and analysis study of the global Azacitidine market presented in the report. (amplemarketreports.com)
- For the period 2015-2020, this study provides the Azacitidine sales, revenue and market share for each player covered in this report. (amplemarketreports.com)
- This page contains brief information about azacitidine and a collection of links to more information about the use of this drug, research results, and ongoing clinical trials. (cancer.gov)
- Find Clinical Trials for Azacitidine - Check for trials from NCI's list of cancer clinical trials now accepting patients. (cancer.gov)
- A copy of the ASH poster titled, " The Clinical Oncolytic Reovirus Formulation Reolysin Synergistically Augments the Anti-Leukemic Activity of Azacitidine , " is available on the Posters & Publications page of Oncolytics' website ( LINK ). (financialnewsmedia.com)
- CONCLUSIONS: Continued azacitidine therapy in responders was associated with a quantitative increase in response to a higher response category in 48% of patients, and therefore may enhance clinical benefit in patients with higher-risk MDS. (johnshopkins.edu)
- Talk to your doctor about the risks of taking azacitidine. (medlineplus.gov)
- Azacitidine comes as a tablet to take by mouth. (medlineplus.gov)
- Azacitidine is associated with a low rate of transient serum enzyme elevations during therapy and has not been convincingly implicated in cases of clinically apparent acute liver injury with jaundice. (nih.gov)
- Although 91% of first responses occurred by 6 cycles, continued azacitidine improved response category in 48% of patients. (johnshopkins.edu)
- you should know that azacitidine often causes diarrhea, which can be severe. (medlineplus.gov)
- The multicenter, phase 2 trial randomly assigned 55 patients with low or intermediate-1 risk MDS as determined by the International Prognostic Scoring System (IPSS) to receive either 5- or 7-day dosing of azacitidine. (hematologyadvisor.com)
- Take azacitidine at around the same time every day. (medlineplus.gov)
- There are no data regarding the presence of azacitidine in human milk or the effects on the breastfed child or milk production. (onuregpro.com)