Dactinomycin
A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)
Gestational Trophoblastic Disease
A group of diseases arising from pregnancy that are commonly associated with hyperplasia of trophoblasts (TROPHOBLAST) and markedly elevated human CHORIONIC GONADOTROPIN. They include HYDATIDIFORM MOLE, invasive mole (HYDATIDIFORM MOLE, INVASIVE), placental-site trophoblastic tumor (TROPHOBLASTIC TUMOR, PLACENTAL SITE), and CHORIOCARCINOMA. These neoplasms have varying propensities for invasion and spread.
Wilms Tumor
A malignant kidney tumor, caused by the uncontrolled multiplication of renal stem (blastemal), stromal (STROMAL CELLS), and epithelial (EPITHELIAL CELLS) elements. However, not all three are present in every case. Several genes or chromosomal areas have been associated with Wilms tumor which is usually found in childhood as a firm lump in a child's side or ABDOMEN.
Leukocyte Disorders
Rhabdomyosarcoma
A malignant solid tumor arising from mesenchymal tissues which normally differentiate to form striated muscle. It can occur in a wide variety of sites. It is divided into four distinct types: pleomorphic, predominantly in male adults; alveolar (RHABDOMYOSARCOMA, ALVEOLAR), mainly in adolescents and young adults; embryonal (RHABDOMYOSARCOMA, EMBRYONAL), predominantly in infants and children; and botryoidal, also in young children. It is one of the most frequently occurring soft tissue sarcomas and the most common in children under 15. (From Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p2186; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, pp1647-9)
Trophoblastic Neoplasms
Trophoblastic growth, which may be gestational or nongestational in origin. Trophoblastic neoplasia resulting from pregnancy is often described as gestational trophoblastic disease to distinguish it from germ cell tumors which frequently show trophoblastic elements, and from the trophoblastic differentiation which sometimes occurs in a wide variety of epithelial cancers. Gestational trophoblastic growth has several forms, including HYDATIDIFORM MOLE and CHORIOCARCINOMA. (From Holland et al., Cancer Medicine, 3d ed, p1691)
Ifosfamide
Etoposide
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
Sarcoma, Ewing
Antineoplastic Combined Chemotherapy Protocols
Cyclophosphamide
Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.
Neoplasms, Germ Cell and Embryonal
Combined Modality Therapy
Doxorubicin
Bleomycin
Methotrexate
Drug Administration Schedule
Neoplasm Recurrence, Local
Disease-Free Survival
Neoplasm Staging
Treatment Outcome
Survival Rate
Drug Information Services
Universal Precautions
Self-Help Groups
Feminism
Neoplasms
Internet
Names
Personal names, given or surname, as cultural characteristics, as ethnological or religious patterns, as indications of the geographic distribution of families and inbreeding, etc. Analysis of isonymy, the quality of having the same or similar names, is useful in the study of population genetics. NAMES is used also for the history of names or name changes of corporate bodies, such as medical societies, universities, hospitals, government agencies, etc.
Therapeutic Equivalency
Rhabdomyosarcoma, Embryonal
A form of RHABDOMYOSARCOMA arising primarily in the head and neck, especially the orbit, of children below the age of 10. The cells are smaller than those of other rhabdomyosarcomas and are of two basic cell types: spindle cells and round cells. This cancer is highly sensitive to chemotherapy and has a high cure rate with multi-modality therapy. (From Holland et al., Cancer Medicine, 3d ed, p2188)
Rhabdomyosarcoma, Alveolar
A form of RHABDOMYOSARCOMA occurring mainly in adolescents and young adults, affecting muscles of the extremities, trunk, orbital region, etc. It is extremely malignant, metastasizing widely at an early stage. Few cures have been achieved and the prognosis is poor. "Alveolar" refers to its microscopic appearance simulating the cells of the respiratory alveolus. (Holland et al., Cancer Medicine, 3d ed, p2188)
Sertoli-Leydig Cell Tumor
A sex cord-gonadal stromal tumor consists of LEYDIG CELLS; SERTOLI CELLS; and FIBROBLASTS in varying proportions and degree of differentiation. Most such tumors produce ANDROGENS in the Leydig cells, formerly known as androblastoma or arrhenoblastoma. Androblastomas occur in the TESTIS or the OVARY causing precocious masculinization in the males, and defeminization, or virilization (VIRILISM) in the females. In some cases, the Sertoli cells produce ESTROGENS.
Hydatidiform Mole
Trophoblastic hyperplasia associated with normal gestation, or molar pregnancy. It is characterized by the swelling of the CHORIONIC VILLI and elevated human CHORIONIC GONADOTROPIN. Hydatidiform moles or molar pregnancy may be categorized as complete or partial based on their gross morphology, histopathology, and karyotype.
Choriocarcinoma
A malignant metastatic form of trophoblastic tumors. Unlike the HYDATIDIFORM MOLE, choriocarcinoma contains no CHORIONIC VILLI but rather sheets of undifferentiated cytotrophoblasts and syncytiotrophoblasts (TROPHOBLASTS). It is characterized by the large amounts of CHORIONIC GONADOTROPIN produced. Tissue origins can be determined by DNA analyses: placental (fetal) origin or non-placental origin (CHORIOCARCINOMA, NON-GESTATIONAL).
Pulmonary Blastoma
Aspirin
The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
Platelet Aggregation Inhibitors
Salicylates
Anti-Inflammatory Agents, Non-Steroidal
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
Prostanoic Acids
Effect of hepatocarcinogens on the binding of glucocorticoid-receptor complex in rat liver nuclei. (1/3633)
The effects of a number of carcinogens and hepatotoxins on the binding kinetics of the interactions of glucocorticoidcytosol receptor complex with nuclear acceptor sites in rat liver were investigated. Both the apparent sites in rat liver were investigated. Both the apparent concentration of nuclear binding sites and the Kd were significantly diminished following treatment of rats with sublethal doses of the carcinogens aflatoxin B1, diethylnitrosamine, dimethylnitrosamine, thioacetamide, 3'-methyl-4-dimethylaminoazobenzene, 4-dimethylaminoazobenzene, and 3-methylcholanthrene. Treatment with actinomycin D resulted in a slight reduction in the apparent concentration of nuclear acceptor sites but had no effect on the nuclear binding Kd. The hepatotoxic but noncarcinogenic analgesic, acetaminophen, as well as the weakly toxic aflatoxin B1 cognate, aflatoxin B2, were without effect on the kinetics or binding capacity of glucocorticoid-nuclear acceptor site interaction. These experiments suggest that chemically induced alteration of functional glucocorticoid binding sites on chromatin may be involved in the biochemical effects produced in liver by carcinogens of several chemical types. This experimental model may provide a useful approach for further elucidation of early events in carcinogenesis. (+info)The stability and fate of a spliced intron from vertebrate cells. (2/3633)
Introns constitute most of the length of typical pre-mRNAs in vertebrate cells. Thus, the turnover rate of introns may significantly influence the availability of ribonucleotides and splicing factors for further rounds of transcription and RNA splicing, respectively. Given the importance of intron turnover, it is surprising that there have been no reports on the half-life of introns from higher eukaryotic cells. Here, we determined the stability of IVS1Cbeta1, the first intron from the constant region of the mouse T-cell receptor-beta, (TCR-beta) gene. Using a tetracycline (tet)-regulated promoter, we demonstrate that spliced IVS1Cbeta1 and its pre-mRNA had half-lives of 6.0+/-1.4 min and 3.7+/-1.0 min, respectively. We also examined the half-lives of these transcripts by using actinomycin D (Act.D). Act.D significantly stabilized IVS1Cbeta1 and its pre-mRNA, suggesting that Act.D not only blocks transcription but exerts rapid and direct posttranscriptional effects in the nucleus. We observed that in vivo spliced IVS1Cbeta1 accumulated predominantly as lariat molecules that use a consensus branchpoint nucleotide. The accumulation of IVS1Cbeta1 as a lariat did not result from an intrinsic inability to be debranched, as it could be debranched in vitro, albeit somewhat less efficiently than an adenovirus intron. Subcellular-fractionation and sucrose-gradient analyses showed that most spliced IVS1Cbeta1 lariats cofractionated with pre-mRNA, but not always with mRNA in the nucleus. Some IVS1Cbeta1 also appeared to be selectively exported to the cytoplasm, whereas TCR-beta pre-mRNA remained in the nucleus. This study constitutes the first detailed analysis of the stability and fate of a spliced nuclear intron in vivo. (+info)Retinoic acid stimulates the expression of 11beta-hydroxysteroid dehydrogenase type 2 in human choriocarcinoma JEG-3 cells. (3/3633)
The syncytiotrophoblasts of the human placenta express high levels of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the enzyme responsible for the inactivation of glucocorticoids. It has been proposed that the placental 11beta-HSD2 serves as a barrier to protect the fetus from high levels of maternal cortisol. To examine the hypothesis that nutritional signals regulate the expression of 11beta-HSD2 in placental syncytiotrophoblasts, we investigated the effects of retinoic acids (RAs), the major metabolites of vitamin A, on the expression of 11beta-HSD2 using human choriocarcinoma JEG-3 cells as a model. This trophoblast-like cell line displays a number of functional similarities to the syncytiotrophoblast. Treatment for 24 h with all-trans RA (1-1000 nM) resulted in a dose-dependent increase in 11beta-HSD2 activity with a maximal effect (increase to 3-fold) at 100 nM. The effect of all-trans RA (100 nM) was also time-dependent in that the effect was detectable at 6 h and reached its maximum by 48 h. Similar increases in 11beta-HSD2 activity were observed when the cells were treated with 9-cis RA. Results from semi-quantitative reverse transcription-polymerase chain reaction demonstrated that there was a corresponding increase in 11beta-HSD2 mRNA after RA treatment. Moreover, treatment with actinomycin D (100 ng/ml) abrogated the increase in 11beta-HSD2 mRNA induced by RA, indicating an effect on transcription. In conclusion, the present study has demonstrated for the first time that RA, at physiological concentrations, induces 11beta-HSD2 gene expression and enzyme activity in JEG-3 cells. If this occurs in vivo, the present finding suggests that high expression of 11beta-HSD2 in the human placenta may be maintained, at least in part, by dietary intake of vitamin A. (+info)Inhibition of Pichinde virus replication by actinomycin D. (4/3633)
The yields of Pichinde virus, a member of the arenavirus group, were markedly inhibited when infected BHK 21 cells were incubated in the presence of 0.4 to 4 mug/ml of actinomycin D. Maximal inhibition was observed when actinomycin D was added after the adsorption of virus to cultures; however, addition of drug as late as 12 h after infection reduced the 24 h yield by 50%. Virus antigen synthesis, as measured by complement fixation and immunodiffusion, was not dramatically reduced by actinomycin D. The expression of virus antigens on the surface of infected cells was greater on cells treated with actinomycin D than on untreated cells. Putative defective particles with a density of Pichinde virus were not detected in fluids of cultures incubated with actinomycin D and 3H-amino acids. Actinomycin D appears to inhibit Pichinde virus late in the replicative cycle. The observations raise the possibility that the drug inhibits the synthesis of proteins of the host cell membrane which are required for virus maturation. (+info)Regulation of interleukin-8 expression by reduced oxygen pressure in human glioblastoma. (5/3633)
Oxygen deprivation is an important biological feature of tumor growth. We previously showed that in glioma, anoxia increases expression of IL-8, a chemokine and angiogenic factor. Here, we analysed for the first time the biochemical mechanisms inducing the IL-8 gene upon anoxia in glioma cells, and showed that they differ from those inducing the VEGF gene. Both genes are induced in biologically and genetically heterogenous glioblastoma cell lines (LN-229, LN-Z308, U87MG, T98G), whereas, in gliosarcoma cells (D247MG), only the VEGF gene is induced. The kinetics of IL-8 and VEGF mRNA inductions differ in these cells and reoxygenation experiments showed that the induction is due to the anoxic stress per se. Furthermore, in LN-229 and LN-Z308 cell lines actinomycin D, DRB and nuclear run-on experiments showed that anoxia stimulates increased transcription of both genes. Electromobility shift assays show increased protein binding to the AP-1 site on the IL-8 promoter following anoxia treatment. Finally, in situ hybridization on glioblastoma sections shows that the in vivo expression patterns of IL-8 and VEGF genes overlap, but are not identical. Since intratumoral augmentation of IL-8 and VEGF secretion, following microenvironmental decreases in oxygen pressure, may promote angiogenesis, further definition of these pathways is essential to appropriately target them for antitumoral therapy. (+info)Nuclear foci of mammalian recombination proteins are located at single-stranded DNA regions formed after DNA damage. (6/3633)
A sensitive and rapid in situ method was developed to visualize sites of single-stranded (ss) DNA in cultured cells and in experimental test animals. Anti-bromodeoxyuridine antibody recognizes the halogenated base analog incorporated into chromosomal DNA only when substituted DNA is in the single strand form. After treatment of cells with DNA-damaging agents or gamma irradiation, ssDNA molecules form nuclear foci in a dose-dependent manner within 60 min. The mammalian recombination protein Rad51 and the replication protein A then accumulate at sites of ssDNA and form foci, suggesting that these are sites of recombinational DNA repair. (+info)Interaction of asparagine and EGF in the regulation of ornithine decarboxylase in IEC-6 cells. (7/3633)
Our laboratory has shown that asparagine (ASN) stimulates both ornithine decarboxylase (ODC) activity and gene expression in an intestinal epithelial cell line (IEC-6). The effect of ASN is specific, and other A- and N-system amino acids are almost as effective as ASN when added alone. In the present study, epidermal growth factor (EGF) was unable to increase ODC activity in cells maintained in a salt-glucose solution (Earle's balanced salt solution). However, the addition of ASN (10 mM) in the presence of EGF (30 ng/ml) increased the activity of ODC 0.5- to 4-fold over that stimulated by ASN alone. EGF also showed induction of ODC with glutamine and alpha-aminoisobutyric acid, but ODC induction was maximum with ASN and EGF. Thus the mechanism of the interaction between ASN and EGF is important for understanding the regulation of ODC under physiological conditions. Therefore, we examined the expression of the ODC gene and those for several protooncogenes under the same conditions. Increased expression of the genes for c-Jun and c-Fos but not for ODC occurred with EGF alone. The addition of ASN did not further increase the expression of the protooncogenes, but the combination of EGF and ASN further increased the expression of ODC over that of ASN alone. Western analysis showed no significant difference in the level of ODC protein in Earle's balanced salt solution, ASN, EGF, or EGF plus ASN. Addition of cycloheximide during ASN and ASN plus EGF treatment completely inhibited ODC activity without affecting the level of ODC protein. These results indicated that 1) the increased expression of protooncogenes in response to EGF is independent of increases in ODC activity and 2) potentiation between EGF and ASN on ODC activity may not be due to increased gene transcription but to posttranslational regulation and the requirement of ongoing protein synthesis involving a specific factor dependent on ASN. (+info)Stochastic and nonstochastic post-transcriptional silencing of chitinase and beta-1,3-glucanase genes involves increased RNA turnover-possible role for ribosome-independent RNA degradation. (8/3633)
Stochastic and nonstochastic post-transcriptional gene silencing (PTGS) in Nicotiana sylvestris plants carrying tobacco class I chitinase (CHN) and beta-1,3-glucanase transgenes differs in incidence, stability, and pattern of expression. Measurements with inhibitors of RNA synthesis (cordycepin, actinomycin D, and alpha-amanitin) showed that both forms of PTGS are associated with increased sequence-specific degradation of transcripts, suggesting that increased RNA turnover may be a general feature of PTGS. The protein synthesis inhibitors cycloheximide and verrucarin A did not inhibit degradation of CHN RNA targeted for PTGS, confirming that PTGS-related RNA degradation does not depend on ongoing protein synthesis. Because verrucarin A, unlike cycloheximide, dissociates mRNA from ribosomes, our results also suggest that ribosome-associated RNA degradation pathways may not be involved in CHN PTGS. (+info)
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Dactinomycin: MedlinePlus Drug Information
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Dactinomycin
Literature References: Antibiotic substance belonging to the actinomycin complex, produced by several Streptomyces spp. Historical background of actinomycins and chemistry, toxicology, pharmacology of actinomycin D: Ann. N.Y. Acad. Sci. 89, 285-485 (1960). Isoln from broth cultures of S. parvulus: Manaker et al., Antibiot. Ann. 1954/55, 853. Structure: Bullock, Johnson, J. Chem. Soc. 1957, 3280. Synthesis: Brockmann, Manegold, Naturwissenschaften 51, 383 (1964); Brockmann, Lackner, ibid. 384, 435 (1964); Brockmann et al., DE 1172680 (1964 to Bayer); eidem, Ber. 101, 1312 (1968); Meienhofer, J. Am. Chem. Soc. 92, 3771 (1970); T. Tanaka et al., Bull. Chem. Soc. Jpn. 53, 1352 (1980); K. Nakajima et al., Pept. Chem. 19, 143-148 (1981). Conformation from NMR: Conti, DeSantis, Nature 227, 1239 (1970); Lackner, Ber. 104, 3653 (1971). Toxicity data: F. S. Philips et al., Ann. N.Y. Acad. Sci. 89, 348 (1960). Review and evaluation of studies of carcinogenic action in laboratory animals: IARC Monographs ...
dactinomycin Intravenous - patient information, description, dosage and directions.
Description of the drug dactinomycin Intravenous. - patient information, description, dosage and directions. What is ... Uses For dactinomycin. Dactinomycin belongs to the group of medicines known as antineoplastics. It is used to treat some kinds ... After treatment with dactinomycin has ended, normal hair growth should return.. After you stop using dactinomycin, it may still ... Infection-Dactinomycin can decrease your bodys ability to fight infection. *Liver disease-Effects of dactinomycin may be ...
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Dactinomycin Side Effects - DrugInformer
Source: Dactinomycin. View full report on Dactinomycin related vomiting Did the author experience vomiting while taking ... Dactinomycin Side Effects. Filter Table by Serious Outcome. ×. Filter by Serious Outcome. ... For more details, please use our Workbench for research on individual brands like Dactinomycin. ... The following are comments from users that experienced side effects while taking Dactinomycin ...
CyclophosphamideReceive dactinomycinIntravenousSide effects of dactinomycinStarting dactinomycin treatmentCytotoxicVialVincristine and dactinomycinAntineoplasticAntibioticInterferes with the growthGestationalOrphan Drug DesignationSarcomaMedicationInterventionWilmsToxicityActive IngredientTreatmentTumorsAntineoplasticsPatientsVeinInhibitsChlorambucilDrugPhaseAllergicCancerHarmToxic propertiesMedicinesSeverityPregnant
Cyclophosphamide10
- RATIONALE: Drugs used in chemotherapy, such as vincristine, dactinomycin, and cyclophosphamide, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. (clinicaltrials.gov)
- PURPOSE: This phase II trial is studying how well giving vincristine, dactinomycin, and cyclophosphamide together works in treating patients with embryonal rhabdomyosarcoma. (clinicaltrials.gov)
- Determine the progression-free survival rate in patients with low-risk embryonal rhabdomyosarcoma treated with intensive chemotherapy comprising vincristine, dactinomycin, and cyclophosphamide followed by vincristine and dactinomycin. (clinicaltrials.gov)
- OUTLINE: Patients receive vincristine IV, dactinomycin IV, and cyclophosphamide IV on day 1. (clinicaltrials.gov)
- OBJECTIVES: - Determine the progression-free survival rate in patients with low-risk embryonal rhadomyosarcoma treated with a shortened treatment schedule of vincristine, dactinomycin, and cyclophosphamide with or without radiotherapy. (centerwatch.com)
- Alternating weekly chemotherapy with etoposide-methotrexate-dactinomycin/cyclophosphamide-vincristine for high-risk gestational trophoblastic disease. (duke.edu)
- OBJECTIVE: To evaluate the response rate and toxicity of alternating weekly therapy with etoposide-methotrexate-dactinomycin/cyclophosphamide-vincristine for women with high-risk gestational trophoblastic disease. (duke.edu)
- CONCLUSION: The regimen of alternating weekly etoposide-methotrexate-dactinomycin/cyclophosphamide-vincristine is effective and well-tolerated chemotherapy for patients with high-risk gestational trophoblastic disease. (duke.edu)
- Determine the toxic effects of this regimen when given in alternating courses with vincristine, dactinomycin, and cyclophosphamide (VAC) as continuation therapy in patients with partial or complete response. (bioportfolio.com)
- This randomized phase III trial studies how well combination chemotherapy (vincristine sulfate, dactinomycin, cyclophosphamide) alternated with vincristine sulfate and irinotecan hydrochlo. (bioportfolio.com)
Receive dactinomycin5
- Your doctor will probably not want you to receive dactinomycin injection. (medlineplus.gov)
- You should not receive dactinomycin if you have recently had chickenpox or herpes zoster (shingles). (wellspan.org)
- You should not receive dactinomycin if you are allergic to it, or if you have recently had chickenpox or herpes zoster (shingles). (wellspan.org)
- ARM I: Patients receive dactinomycin intravenously (IV) over 15 minutes on day 1. (clinicaltrials.gov)
- Patients receive dactinomycin IV over 15 minutes on day 1. (clinicaltrials.gov)
Intravenous1
- Dactinomycin is given via intravenous injection. (medicalrealm.net)
Side effects of dactinomycin1
- What are the possible side effects of dactinomycin? (wellspan.org)
Starting dactinomycin treatment1
- Before starting dactinomycin treatment, make sure you tell your doctor about any other medications you are taking (including prescription, over-the-counter, vitamins, herbal remedies, etc. (chemocare.com)
Cytotoxic4
- Dactinomycin is in the cytotoxic antibiotic family of medications. (wikipedia.org)
- Dactinomycin is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy drug. (chemocare.com)
- Dactinomycin is believed to produce its cytotoxic effects by binding DNA and inhibiting RNA synthesis. (drugbank.ca)
- Dactinomycin is a cytotoxic chemotherapy, prescribed for Wilm's tumor, Ewing s sarcoma and testicular cancer. (medindia.net)
Vial2
Vincristine and dactinomycin2
- A 16-month-old girl was receiving chemotherapy with vincristine and dactinomycin (Regimen EE-4A) for a left-sided Wilms tumor, clinicopathologic stage II with favorable histology, after nephrectomy. (jcancer.org)
- To determine the two-year second event-free survival percentage for children who relapse following initial therapy with nephrectomy only following treatment with vincristine and dactinomycin, with or without doxorubicin, depending upon the site of relapse and presence or absence of microscopic residual disease. (clinicaltrials.gov)
Antineoplastic2
- Dactinomycin is an antineoplastic. (oncologydrugs.co.in)
- According to the NCI dactinomycin is a chromopeptide antineoplastic antibiotic isolated from the bacterium Streptomyces parvulus. (oncoletter.ch)
Antibiotic3
- Dactinomycin is a type of antibiotic that is only used in cancer chemotherapy. (medlineplus.gov)
- Actinomycin D (Dactinomycin) is a significant polypeptide antibiotic isolated from soil bacteria of the genus Streptomyces. (selleckchem.com)
- Dactinomycin is also a form of antibiotic which is useful in treating children related / pediatric forms of cancer. (medicalrealm.net)
Interferes with the growth2
- Dactinomycin is a cancer medication that interferes with the growth and spread of cancer cells in the body. (wellspan.org)
- Dactinomycin interferes with the growth of cancer cells, which are eventually destroyed. (drugster.info)
Gestational7
- Dactinomycin is also used alone or in combination with other medications to treat gestational trophoblastic tumors (a type of tumor that forms inside a woman's uterus while she is pregnant). (medlineplus.gov)
- This randomized phase III trial studies how well methotrexate works compared to dactinomycin in treating patients with low-risk gestational trophoblastic neoplasia. (clinicaltrials.gov)
- It is not yet known whether methotrexate is more effective than dactinomycin in treating gestational trophoblastic disease. (clinicaltrials.gov)
- I. To test the hypothesis that treatment with multi-day methotrexate is inferior to treatment with pulse actinomycin-D (dactinomycin) in patients with low-risk gestational trophoblastic disease with respect to complete response. (clinicaltrials.gov)
- Dactinomycin is used to treat Wilms' tumor, Childhood Rhabdomyosarcoma, Ovarian (germ cell) cancer, Gestational trophoblastic neoplasm, Ewing's sarcoma, Metastatic testicular tumors (nonseminoatous), Gestational trophoblastic neoplasm, Locally recurrent or locoregional solid tumors (sarcomas, carcinomas and adenocarcinomas), Soft tissue sarcoma and Osteosarcoma. (oddwayinternational.com)
- Buy Dacilon Injection generic drug of Dactinomycin online at a low price from the most trusted pharmacy for Testicular cancer, Wilms' tumor, Gestational trophoblastic neoplasia. (safegenericpharmacy.net)
- To evaluate the combination chemotherapy regimen with floxuridine , dactinomycin , etoposide , and vincristine (FAEV) as primary treatment for gestational trophoblastic neoplasia (GTN). (bvsalud.org)
Orphan Drug Designation2
- The U.S. Food and Drug Administration (FDA) has granted Orphan Drug designation to NanoSmart Pharmaceuticals' novel formulation of dactinomycin for the treatment of Ewing sarcoma, a rare type of childhood bone cancer. (ascopost.com)
- The Food and Drug Administration (FDA) has granted Orphan Drug designation to dactinomycin nanoparticle formulation (NanoSmart) for the treatment of Ewing's sarcoma. (empr.com)
Sarcoma1
- Dactinomycin is also used in combination with other medications to treat certain types of testicular cancer and Ewing's sarcoma (a type of cancer in bones or muscles). (medlineplus.gov)
Medication3
- Dactinomycin, also known as actinomycin D, is a chemotherapy medication used to treat a number of types of cancer. (wikipedia.org)
- Dactinomycin is classified as a vesicant medication, meaning it can cause damage to tissue that comes in direct contact with the drug. (chemocare.com)
- Dactinomycin may also be used for purposes not listed in this medication guide. (wellspan.org)
Intervention1
- While treatment with antithrombotic or fibrinolytic agents and other agents has been attempted with variable success in hepatic SOS after stem cell transplantation [ 5 , 6 ], the efficacy of pharmacological intervention has not been systematically studied in dactinomycin-induced SOS. (jcancer.org)
Wilms5
- Dactinomycin is used in combination with other medications, surgery, and/or radiation therapy to treat Wilms' tumor (a type of kidney cancer that occurs in children) and rhabdomyosarcoma (cancer that forms in muscles) in children. (medlineplus.gov)
- Dactinomycin is a trade name for actinomycin D. It is a chemotherapy drug that is given as a treatment for some types of cancer, most commonly some cancers that occur in children such as Wilms' tumor and germ cell tumors, although it may sometimes be used for adults. (springer.com)
- To make sure you can safely take dactinomycin, tell your doctor if you have recently received radiation treatment for Wilms tumor. (wellspan.org)
- A 16-month-old girl with stage II Wilms tumor receiving post-nephrectomy chemotherapy with dactinomycin and vincristine developed hepatic sinusoidal obstruction syndrome with painful hepatomegaly, ascites with significant weight gain, grossly deranged liver function, severe thrombocytopenia, and reversal of blood flow in the portal vein on Doppler sonography. (jcancer.org)
- stage I focal anaplastic (FA) or diffuse anaplastic (DA) Wilms' tumor: Patients receive regimen EE-4A comprising dactinomycin (DACT) IV weekly on weeks 0, 3, 6, 9, 12, 15, and 18 and vincristine sulfate (VCR) IV weekly on weeks 1-10, 12, 15, and 18. (clinicaltrials.gov)
Toxicity1
- Because of increased toxicity, use of dactinomycin in infants less than 6 to 12 months of age is not recommended. (drugster.info)
Active Ingredient1
- It contains a generic drug of Dactinomycin as an active ingredient. (safegenericpharmacy.net)
Treatment6
- However, the toxic properties of the actinomycins (including dactinomycin) in relation to antibacterial activity are such as to preclude their use as antibiotics in the treatment of infectious diseases. (drugbank.ca)
- Dactinomycin is usually given only on certain days during a treatment cycle. (wellspan.org)
- N-acetylcysteine is a safe and probably an effective treatment for dactinomycin-induced hepatic sinusoidal obstructive syndrome. (jcancer.org)
- It is uncommon in the setting of conventional chemotherapy but tends to happen in children receiving dactinomycin treatment [ 3 , 4 ]. (jcancer.org)
- Before you begin treatment with dactinomycin, you and your doctor should talk about the good dactinomycin will do as well as the risks of using it. (drugster.info)
- Background: Dactinomycin (AMD) and vincristine (VCR) have been used for the treatment of childhood cancer over the past 40 years but evidence-based dosing guidance is lacking. (elsevier.com)
Tumors2
- Dactinomycin may also be used to treat certain types of cancerous tumors that are located in a specific area of the body. (medlineplus.gov)
- Dactinomycin is also used to treat solid tumors. (wellspan.org)
Antineoplastics1
- Dactinomycin belongs to the group of medicines known as antineoplastics. (drugster.info)
Patients2
- Patients then receive vincristine IV and dactinomycin IV on day 1. (clinicaltrials.gov)
- Results of a study in patients with malignant melanoma indicate that dactinomycin ( 3 H actinomycin D) is minimally metabolized, is concentrated in nucleated cells, and does not penetrate the blood-brain barrier. (drugs.com)
Vein3
- Dactinomycin should be administered only into a vein. (medlineplus.gov)
- Dactinomycin comes as a powder to be mixed with liquid to be injected intravenously (into a vein) by a doctor or nurse in a medical facility. (medlineplus.gov)
- Dactinomycin is injected into a vein through an IV. (wellspan.org)
Inhibits1
- Actinomycin D (Dactinomycin) inhibits DNA repair and rests the cell cycle at G1 phase with IC50 of 0.42 μM and 0.4 nM, respectively. (selleckchem.com)
Chlorambucil1
- Pioneers in the industry, we offer pharmaceutical drop shipping, drop shipping service singapore post, clokeran 5mg (chlorambucil tablets), cytax 260 mg (paclitaxel injection), dacilon 0.5mg (dactinomycin injection) and epithra 100 mg (epirubicin injection) from India. (medicineonlineshop.com)
Drug5
- If you have an allergy to dactinomycin or any other part of this drug. (mskcc.org)
- In some cases, health care professionals may use the trade name Cosmegen or other name Actinomycin-D when referring to the generic drug name dactinomycin. (chemocare.com)
- DACTINOMYCIN (dak ti noe MYE sin) is a chemotherapy drug. (cvs.com)
- Significantly better results have been obtained by giving local anesthesia injections of acetylsalicylic acid, dactinomycin and by chymotrypsin together than with by single drug alone. (todaysparentusa.com)
- Dactinomycin is an anti cancer drug. (medicalrealm.net)
Phase1
- In polytheism the next phase of the experiment, linagliptin and dactinomycin were immediately given to the second younger generation mice after a training session. (todaysparentusa.com)
Allergic2
- tell your doctor and pharmacist if you are allergic to dactinomycin, any other medications, or any of the ingredients in dactinomycin injection. (medlineplus.gov)
- Tell your doctor if you have ever had any unusual or allergic reaction to dactinomycin or any other medicines. (drugster.info)
Cancer6
- Dactinomycin injection must be given in a hospital or medical facility under the supervision of a doctor who is experienced in giving chemotherapy medications for cancer. (medlineplus.gov)
- Dactinomycin is also sometimes used to treat a type of cancer of the ovaries (a cancer that begins in the female reproductive organs where eggs are formed). (medlineplus.gov)
- The amount of dactinomycin that you will receive depends on many factors, including your height and weight, your general health or other health problems, and the type of cancer or condition being treated. (chemocare.com)
- There is a slight risk of developing a secondary cancer months to years after taking dactinomycin. (chemocare.com)
- Using dactinomycin may increase your risk of developing other types of cancer, such as leukemia. (wellspan.org)
- Dactinomycin for injection should be administered only under the supervision of a physician who is experienced in the use of cancer chemotherapeutic agents. (drugster.info)
Harm2
- Dactinomycin may harm the fetus. (medlineplus.gov)
- It is not known whether dactinomycin passes into breast milk or if it could harm a nursing baby. (wellspan.org)
Toxic properties1
- Due to the toxic properties of dactinomycin (e.g., corrosivity, carcinogenicity, mutagenicity, teratogenicity), special handling procedures should be reviewed prior to handling and followed diligently. (drugster.info)
Medicines1
- Using dactinomycin with any of the following medicines is not recommended. (drugster.info)
Severity4
- Dactinomycin side effects are often predictable in terms of their onset, duration and severity. (chemocare.com)
- The risk or severity of bleeding can be increased when (R)-warfarin is combined with Dactinomycin. (drugbank.ca)
- The risk or severity of adverse effects can be increased when Dactinomycin is combined with 2-Methoxyethanol. (drugbank.ca)
- The risk or severity of adverse effects can be increased when Dactinomycin is combined with 9-(N-methyl-L-isoleucine)-cyclosporin A. (drugbank.ca)
Pregnant3
- You should not become pregnant or breast-feed while you are receiving dactinomycin. (medlineplus.gov)
- If you become pregnant while receiving dactinomycin, call your doctor. (medlineplus.gov)
- Do not use dactinomycin if you are pregnant. (wellspan.org)