Amsacrine
Aminoacridines
DNA Topoisomerases, Type II
Topoisomerase II Inhibitors
Teniposide
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Teniposide 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 cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle.
Intercalating Agents
Dipodomys
Aminacrine
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.
Cytarabine
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)
Daunorubicin
Asparaginase
Drug Resistance
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
Effect of cellular ATP depletion on topoisomerase II poisons. Abrogation Of cleavable-complex formation by etoposide but not by amsacrine. (1/246)
Topoisomerase (topo) II poisons have been categorized into ATP-independent and -dependent drugs based on in vitro studies. We investigated drug-induced topoII-DNA complexes in intact cells almost completely depleted of ATP. Virtually no DNA single-strand breaks (SSBs), as measured by alkaline elution, were detected in energy-depleted cells treated with the topoII poisons etoposide, teniposide, daunorubicin, doxorubicin, mitoxantrone, or clerocidin. This inhibition was reversible; subsequent incubation with glucose restored the level of DNA SSBs. The effect of ATP depletion was specific for topoII, because topoI-mediated cleavable complexes induced by camptothecin were unaffected by ATP depletion. Furthermore, etoposide-induced DNA-protein complexes and DNA double-strand breaks, as measured by filter elution techniques, and topoIIalpha and -beta trapping, as measured by a band depletion assay, were completely inhibited by energy depletion. Differences in drug transport could not explain the effect of ATP depletion. The topoII poison amsacrine (m-AMSA) was unique with respect to ATP dependence. In ATP-depleted cells, m-AMSA-induced DNA SSBs, DNA double-strand breaks, DNA-protein complexes, topoIIalpha and -beta trapping were only modestly reduced. The accumulation of m-AMSA was reduced in ATP-depleted cells, which indicates that drug transport could contribute to the modest decrease in m-AMSA-induced cleavable complexes. In conclusion, drug-induced topoII-DNA complexes were completely antagonized in ATP-depleted cells, except in the case of m-AMSA. One possible interpretation is that m-AMSA mainly produces prestrand passage DNA lesions, whereas the other topoII poisons tested exclusively stabilize poststrand passage DNA lesions in intact cells. (+info)Human small cell lung cancer NYH cells selected for resistance to the bisdioxopiperazine topoisomerase II catalytic inhibitor ICRF-187 demonstrate a functional R162Q mutation in the Walker A consensus ATP binding domain of the alpha isoform. (2/246)
Bisdioxopiperazine drugs such as ICRF-187 are catalytic inhibitors of DNA topoisomerase II, with at least two effects on the enzyme: namely, locking it in a closed-clamp form and inhibiting its ATPase activity. This is in contrast to topoisomerase II poisons as etoposide and amsacrine (m-AMSA), which act by stabilizing enzyme-DNA-drug complexes at a stage in which the DNA gate strand is cleaved and the protein is covalently attached to DNA. Human small cell lung cancer NYH cells selected for resistance to ICRF-187 (NYH/187) showed a 25% increase in topoisomerase IIalpha level and no change in expression of the beta isoform. Sequencing of the entire topoisomerase IIalpha cDNA from NYH/187 cells demonstrated a homozygous G-->A point mutation at nucleotide 485, leading to a R162Q conversion in the Walker A consensus ATP binding site (residues 161-165 in the alpha isoform), this being the first drug-selected mutation described at this site. Western blotting after incubation with ICRF-187 showed no depletion of the alpha isoform in NYH/187 cells in contrast to wild-type (wt) cells, whereas equal depletion of the beta isoform was observed in the two sublines. Alkaline elution assay demonstrated a lack of inhibition of etoposide-induced DNA single-stranded breaks in NYH/187 cells, whereas this inhibition was readily apparent in NYH cells. Site-directed mutagenesis in human topoisomerase IIalpha introduced into a yeast Saccharomyces cerevisiae strain with a temperature-conditional yeast TOP2 mutant demonstrated that R162Q conferred resistance to the bisdioxopiperazines ICRF-187 and -193 but not to etoposide or m-AMSA. Both etoposide and m-AMSA induced more DNA cleavage with purified R162Q enzyme than with the wt. The R162Q enzyme has a 20-25% decreased catalytic capacity compared to the wt and was almost inactive at <0.25 mM ATP compared to the wt. Kinetoplast DNA decatenation by the R162Q enzyme at 1 mM ATP was not resistant to ICRF-187 compared to wt, whereas it was clearly less sensitive than wt to ICRF-187 at low ATP concentrations. This suggests that it is a shift in the equilibrium to an open-clamp state in the enzyme's catalytic cycle caused by a decreased ATP binding by the mutated enzyme that is responsible for bisdioxopiperazine resistance. (+info)Enhanced amsacrine-induced mutagenesis in plateau-phase Chinese hamster ovary cells, with targeting of +1 frameshifts to free 3' ends of topoisomerase II cleavable complexes. (3/246)
Previous work showed that the DNA double-strand cleaving agents bleomycin and neocarzinostatin were more mutagenic in plateau-phase than in log-phase cells. To determine whether topoisomerase II poisons that produce double-strand breaks by trapping of cleavable complexes would, likewise, induce mutations specific to plateau-phase cells, aprt mutations induced by amsacrine in both log-phase and plateau-phase CHO cells were analyzed. The maximum aprt mutant frequencies obtained were 7 x 10(-6) after treatment with 0.02 microM amsacrine in log phase and 27 x 10(-6) after treatment with 1 microM amsacrine in plateau phase, compared with a spontaneous frequency of < 1 x 10(-6). Base substitutions dominated the spectrum of mutations in log-phase cells, but were much less prevalent in plateau-phase cells. Both spectra also included small deletions, insertions and duplications, as well as few large-scale deletions or rearrangements. About 5% of the log-phase mutants and 16% of the plateau-phase mutants were +1 frameshifts, and all but one of these were targeted to potential free 3' termini of cleavable complexes, as determined by mapping of cleavage sites in DNA treated with topoisomerase II plus amsacrine in vitro. Thus, these insertions may arise from templated extension of the exposed 3' terminus by a DNA polymerase, followed by resealing of the strand, as shown previously for acridine-induced frameshifts in T4 phage. (+info)Autologous bone marrow transplantation in non-Hodgkin's lymphoma patients: effect of a brief course of G-CSF on harvest and recovery. (4/246)
This study compares harvest and hematological recovery data of 100 lymphoma patients who underwent BM harvest either after a short course of G-CSF (16 microg/kg for 3 days) (n = 57) or in steady-state conditions (n = 43). G-CSF allowed the attainment of a significantly higher median number of total nucleated cells x 10(8)/kg (4.4, range 1.4-17, vs 2.1, range 0.6-4.2; P < 0.0001), mononuclear cells x 10(8)/kg (0.55, range 0.20-1.4, vs 0.41, range 0.15-0.76, P < 0.0001) and CFU-GM/ml (310, range 10-5500, vs 80, range 10-3800, P = 0.008), with lower volumes of blood collected (17.5 ml/kg, range 8-31 vs 21.0, range 15-30, P = 0.0001). Hematological recovery was faster in patients who received pre-treated BM (median time to PMN >0.5 x 10(9)/l and to platelets >20 x 10(9)/l was 12, range 10-14, and 13, range 10-18, days, respectively) than in those autotransplanted with steady-state BM (median time to PMN >0.5 x 10(9)/l and to platelets >20 x 10(9)/l 13, range 10-18 and 14, range 10-20 days, respectively, P = 0.004 and P = 0.01). Transfusional requirement was significantly different and patients of the G-CSF group needed shorter hospitalization (17 days, range 12-24, vs 20 days, range 14-32; P = 0.02). These data suggest that treating patients with G-CSF before BM harvest improves the quality of the harvest and accelerates engraftment and hematological recovery. (+info)Transfection of 9-hydroxyellipticine-resistant Chinese hamster fibroblasts with human topoisomerase IIalpha cDNA: selective restoration of the sensitivity to DNA religation inhibitors. (5/246)
In the Chinese hamster lung cell line DC-3F/9-OH-E, selected for resistance to 9-OH-ellipticine and cross-resistant to other topoisomerase II inhibitors, the amount of topoisomerase IIalpha is 4-5-fold lower than in the parental DC-3F cells, whereas topoisomerase IIbeta is undetectable. Cloning and sequencing of topoisomerase IIalpha cDNAs from DC-3F and DC-3F/9-OH-E cells revealed an allele polymorphism, one allele differing from the other by the presence of seven silent mutations and three mutations in the noncoding region. In addition, the mutated allele contains three missense mutations located close to the ATP binding site (Thr371Ser) or to the catalytic site (Ala751Gly; Ile863Thr). To analyze the contribution of these topoisomerase IIalpha alterations to their resistance phenotype, DC-3F/9-OH-E cells were transfected with an eukaryotic expression vector containing the human topoisomerase IIalpha cDNA. In one transfected clone, the amount of topoisomerase IIalpha isoform and the catalytic activity were similar to that in the parental DC-3F cells. These cells, which contain only topoisomerase IIalpha, are then a unique mammalian cell line to analyze the physiological and pharmacological properties of this enzyme. However, the restoration of a nearly normal topoisomerase IIalpha activity in the DC-3F/9-OH-E cells did not have the same effect on their sensitivity to different enzyme inhibitors; a 75% reversion of the resistance, associated with a 2-3-fold increased stabilization of the cleavable complex, was observed with both etoposide and m-AMSA, two drugs that inhibit the DNA religation step in the enzyme catalytic cycle; in contrast, the transfected cells remained fully resistant to ellipticine derivatives that did not induce the stabilization of the cleavable complex. We hypothesized that a trans-acting factor, inhibiting the induction of cleavable complex formation by drugs that are not religation inhibitors, might be present in the resistant cells. However, such a factor was not detected in in vitro experiments, and other hypotheses are discussed. (+info)Murine transgenic cells lacking DNA topoisomerase IIbeta are resistant to acridines and mitoxantrone: analysis of cytotoxicity and cleavable complex formation. (6/246)
Murine transgenic cell lines lacking DNA topoisomerase II (topo II)beta have been used to assess the importance of topo IIbeta as a drug target. Western blot analysis confirmed that the topo IIbeta -/- cell lines did not contain topo IIbeta protein. In addition, both the topo IIbeta +/+ and topo IIbeta -/- cell lines contained similar levels of topo IIalpha protein. The trapped in agarose DNA immunostaining assay (TARDIS) was used to detect topo IIalpha and beta cleavable complexes in topo IIbeta -/- and topo IIbeta +/+ cells. These results show that both topo IIalpha and beta are in vivo targets for etoposide, mitoxantrone, and amsacrine (mAMSA) in topo IIbeta +/+ cells. As expected, only the alpha-isoform was targeted in topo IIbeta -/- cells. Clonogenic assays comparing the survival of topo IIbeta -/- and topo IIbeta +/+ cells were carried out to establish whether the absence of topo IIbeta caused drug resistance. Increased survival of topo IIbeta -/- cells compared with topo IIbeta +/+ cells was observed after treatment with amsacrine (mAMSA), methyl N-(4'-[9-acridinylamino]-2-methoxyphenyl) carbamate hydrochloride (AMCA), methyl N-(4'-[9-acridinylamino]-2-methoxyphenyl)carbamate hydrochloride (mAMCA), mitoxantrone, and etoposide. These studies showed that topo IIbeta -/- cells were significantly more resistant to mAMSA, AMCA, mAMCA, and mitoxantrone, than topo IIbeta +/+ cells, indicating that topo IIbeta is an important target for the cytotoxic effects of these compounds. (+info)Altered drug interaction and regulation of topoisomerase IIbeta: potential mechanisms governing sensitivity of HL-60 cells to amsacrine and etoposide. (7/246)
Topoisomerase II (topo II), an enzyme essential for cell viability, is present in mammalian cells as the alpha- and beta-isoforms. In human leukemia HL-60/S or HL-60/doxorubicin (DOX)0.05 cells, the levels of topo IIalpha- or beta-protein were similar in either asynchronous exponential or synchronized cultures. Although topo IIalpha was hypophosphorylated in HL-60/DOX0.05 compared with HL-60/S cells, both overall and site-specific hyperphosphorylation of topo IIbeta was apparent in HL-60/DOX0.05 compared with HL-60/S cells. The phosphorylation of topo IIalpha and not beta was enhanced in the S and G(2) + M phases of HL-60/S cells. In contrast, an increase in the phosphorylation of topo IIbeta compared with alpha was apparent in the G(1) and S phases of HL-60/DOX0.05 cells. The cytotoxicity and depletion of topo IIalpha or beta in cells treated with drug for 1 h revealed that mole-for-mole, amsacrine was 2-fold more effective than etoposide in killing HL-60/S or HL-60/DOX0.05 cells and in depleting the beta versus alpha topo II protein. Present results demonstrate that: 1) hyperphosphorylation of topo IIbeta in HL-60/DOX0.05 cells may be a compensatory consequence of the hypophosphorylation of topo IIalpha to maintain normal topo II function during proliferation, and 2) enhanced sensitivity of HL-60/S or HL-60/DOX0.05 cells to amsacrine may be due to the preferential interaction and depletion of topo IIbeta. (+info)An antitumor drug-induced topoisomerase cleavage complex blocks a bacteriophage T4 replication fork in vivo. (8/246)
Many antitumor and antibacterial drugs inhibit DNA topoisomerases by trapping covalent enzyme-DNA cleavage complexes. Formation of cleavage complexes is important for cytotoxicity, but evidence suggests that cleavage complexes themselves are not sufficient to cause cell death. Rather, active cellular processes such as transcription and/or replication are probably necessary to transform cleavage complexes into cytotoxic lesions. Using defined plasmid substrates and two-dimensional agarose gel analysis, we examined the collision of an active replication fork with an antitumor drug-trapped cleavage complex. Discrete DNA molecules accumulated on the simple Y arc, with branch points very close to the topoisomerase cleavage site. Accumulation of the Y-form DNA required the presence of a topoisomerase cleavage site, the antitumor drug, the type II topoisomerase, and a T4 replication origin on the plasmid. Furthermore, all three arms of the Y-form DNA were replicated, arguing strongly that these are trapped replication intermediates. The Y-form DNA appeared even in the absence of two important phage recombination proteins, implying that Y-form DNA is the result of replication rather than recombination. This is the first direct evidence that a drug-induced topoisomerase cleavage complex blocks the replication fork in vivo. Surprisingly, these blocked replication forks do not contain DNA breaks at the topoisomerase cleavage site, implying that the replication complex was inactivated (at least temporarily) and that topoisomerase resealed the drug-induced DNA breaks. The replication fork may behave similarly at other types of DNA lesions, and thus cleavage complexes could represent a useful (site-specific) model for chemical- and radiation-induced DNA damage. (+info)
Amsacrine (Intravenous route)
Abdul Mamsa, MD Neurologist in Kissimmee, FL 34741
Topoisomerase II-mediated DNA cleavage by amonafide and its structural analogs<...
Pilot study of adriamycin and amsacrine (m-AMSA) in patients with advanced breast cancer<...
mAMSA resistant human topoisomerase IIbeta mutation G465D has reduced ATP hydrolysis activity - Northumbria Research Link
Plus it
Amsacrine - DrugBank
Tumor penetration of AMSA in man<...
IJMS | Free Full-Text | DNA Self-Assembly: From Chirality to Evolution | Notes
Compound having antitumor properties - Patent # 4366318 - PatentGenius
Standardization of the alkaline elution procedure using X-ray-damaged nuclear DNA<...
Bill Stumpf
The capture of a DNA double helix by an ATP-dependent protein clamp: a key step in DNA transport by type II DNA topoisomerases
Topoisomerase II Alpha - Product: Leica Biosystems
Human Topoisomerase II Assay Kit, Topo II Assay, kDNA, Topoisomerase II, Measure Topo II Activity in a Crude Extract
Human Topoisomerase II Assay Kit, Topo II Assay, kDNA, Topoisomerase II, Measure Topo II Activity in a Crude Extract
Plus it
DIGITAL.CSIC: Mitotic arrest induced by a novel family of DNA topoisomerase II inhibitors
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Teniposide (By injection)
Lycobetaine acts as a selective topoisomerase IIβ poison and inhibits the growth of human tumour cells | British Journal of...
Mdm2 inhibitors synergize with topoisomerase II inhibitors to induce p53-independent pancreatic cancer cell death
Neoamphimedine circumvents metnase-enhanced DNA topoisomerase IIα activity through ATP-competitive inhibition<...
NK314 | CAS#208237-49-4 | Chk1 inhibitor | topoisomerase II inhibitor | MedKoo Biosciences
Identifying new topoisomerase II poison scafolds by combining publicly available toxicity data and 2D/3D-based virtual...
A phase 1 trial of XK469: toxicity profile of a selective topoisomerase IIbeta inhibitor. - PubMed - NCBI
Teniposide - DrugBank
Geneclean II DNA纯化试剂盒
Cushings with Moxie: Fighting The Worst Disease Youve Never Heard Of: 2012
Global Ceramic Injection Molding Industry 2016 Deep Market Research Report
2-2-chloroethyl-piperidine-1-carboxylic-acidethyl-ester | VWR
Cell cycle phase-specific phosphorylation of human topoisomerase II alpha. Evidence of a role for protein kinase C. - Oxford...
COMPOSITIONS AND METHODS FOR TREATING NEPHROPATHY - Patent application
Maternal exposure to potential inhibitors of DNA topoisomerase II and infant leukemia (United States): a report from the...
Data on benzocaine together with perrigo co. being its main component
Plus it
Mitotic chromosomes are compacted laterally by KIF4 and condensin and axially by topoisomerase II alpha - Murdoch Childrens...
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RCSB PDB
- 3RAF: Quinazolinedione-DNA cleavage complex of type IV topoisomerase from S. pneumoniae Structure Summary...
Optical-Tweezers Study of Topoisomerase Inhibition
Prognostic Values of Filamin-A Status for Topoisomerase II Poison Chemotherapy [Abstract]
METHODS FOR TREATMENT OF MULTIPLE MYELOMA USING 3-(4-AMINO-1-OXO-1,3-DIHYDROISOINDOL-2-YL)-PIPERIDINE-2,6-DIONE IN COMBINATION...
Natural Compounds as Anticancer Agents Targeting DNA Topoisomerases | Bentham Science
Etoposide | CAS#33419-42-0 | Topoisomerase II Inhibitor | MedKoo Biosciences
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Fundamental and Basic Research in Homeopathy - Initiative to Promote Research in Homeopathy
Topoisomerase Inhibitors | MedChemExpress
Search
Amsacrine
... (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. It has been used in acute lymphoblastic leukemia ... Ketron AC, Denny WA, Graves DE, Osheroff N (February 2012). "Amsacrine as a Topoisomerase II Poison: Importance of Drug-DNA ... Horstmann MA, Hassenpflug WA, zur Stadt U, Escherich G, Janka G, Kabisch H (December 2005). "Amsacrine combined with etoposide ... Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II. In contrast, the ...
FLAG (chemotherapy)
FLAMSA adds amsacrine ("AMSA") to the standard FLAG regimen. (G-CSF is still included, even though the "G" is taken out of the ... December 2009). "Fludarabine, amsacrine, high-dose cytarabine and 12 Gy total body irradiation followed by allogeneic ... October 2013). "Combination of fludarabine, amsacrine, and cytarabine followed by reduced-intensity conditioning and allogeneic ... acronym.) Amsacrine is an alkylating antineoplastic agent that is highly active toward AML, unlike more conventional alkylators ...
Aldehyde oxidase
Others include amsacrine, 6,6'-azopurine, chlorpromazine, cimetidine, cyanide, diethylstilbestrol, genestein, isovanillin, and ...
Acridine
... and related derivatives (such as amsacrine) bind to DNA and RNA due to their abilities to intercalate. Acridine orange ...
Dimethylacetamide
... amsacrine). Dimethylacetamide, like most simple alkyl amides, is of low acute toxicity. Chronic exposure can cause ...
Topoisomerase inhibitor
showed an incidence of mutation and deletion in TopIIα mRNA of etoposide and m-amsacrine (mAMSA)-resistant cell lines. TopIIα ...
List of MeSH codes (D03)
... amsacrine MeSH D03.494.046.250.450 - ethacridine MeSH D03.494.046.250.650 - nitracrine MeSH D03.494.046.250.720 - proflavine ...
ATC code L01
L01XK01 Olaparib L01XK02 Niraparib L01XK03 Rucaparib L01XK04 Talazoparib L01XK05 Veliparib L01XK06 Pamiparib L01XX01 Amsacrine ...
IARC group 2B
4-thiadiazole Amsacrine ortho-Anisidine Anthraquinone Antimony trioxide Aramite Auramine Azaserine Aziridine Benz[j] ...
Index of oncology articles
... amsacrine - amylase - amyloidosis - anagrelide - anakinra - anaphylactic shock - anaplastic - anaplastic large cell lymphoma - ...
List of drugs: Am
... amsacrine (INN) amsilarotene (USAN) amtolmetin guacil (INN) amustaline dihydrochloride (USAN) amuvatinib (USAN, INN) Amvaz ...
Extravasation (intravenous)
List of vesicant and irritant medications: Amsacrine Cisplatin Dactinomycin Daunorubicin Docetaxel Doxorubicin Epirubicin ...
Amsacrine C03190
Amsacrine Intravenous Advanced Patient Information - Drugs.com
Detailed drug Information for amsacrine Intravenous. Includes common brand names, drug descriptions, warnings, side effects and ... Uses for amsacrine. Amsacrine belongs to the general group of medicines known as antineoplastics. It is used to treat acute ... Studies on amsacrine have been done only in adult patients, and there is no specific information comparing use of amsacrine in ... Proper use of amsacrine. Amsacrine often causes nausea and vomiting. However, it is very important that you continue to receive ...
Proposition-65-List - 51264-14-3 Amsacrine - CAS Analytical Genprice Lab
Amsacrine - OEL Fastrac with ADE - Affygility Solutions
... for Amsacrine. Available for instant download from Affygility Solutions. ... Amsacrine appears to cleave DNA by inducing double stranded breaks. Amsacrine also targets and inhibits topoisomerase II. ... Amsacrine is an antineoplastic agent indicated for the treatment of leukemia, particularly acute myeloid leukemia (AML). ... To order an OEL/ADE monograph for Amsacrine, just click the ADD TO CART button. ...
Intensified double induction therapy with high dose mitoxantrone, etoposide, m-amsacrine and high dose ara-C for elderly acute...
Intensified double induction therapy with high dose mitoxantrone, etoposide, m-amsacrine and high dose ara-C for elderly acute ... Intensified double induction therapy with high dose mitoxantrone, etoposide, m-amsacrine and high dose ara-C for elderly acute ... in the first course and m-amsacrine together with high dose ara-C (MAMAC) in the second course. Treatment results were compared ...
Amsacrine - Drug Monograph - DrugInfoSys.com
Amsacrine : Venkatasai Life Sciences
Intensified double induction therapy with high dose mitoxantrone, etoposide, m-amsacrine and high dose ara-C for elderly acute...
Intensified double induction therapy with high dose mitoxantrone, etoposide, m-amsacrine and high dose ara-C for elderly acute ... Intensified double induction therapy with high dose mitoxantrone, etoposide, m-amsacrine and high dose ara-C for elderly acute ... in the first course and m-amsacrine together with high dose ara-C (MAMAC) in the second course. Treatment results were compared ...
Amsacrine (54301-15-4) | Chemical Effects in Biological Systems
Amsacrine (54301-15-4). Citation Information. NTP. Amsacrine (54301-15-4). Chemical Effects in Biological Systems (CEBS). ... Evaluation of the Chronic Toxicity and Carcinogenicity of Amsacrine (54301-15-4) in Male B6C3F1 Mice Exposed via ... Evaluation of the Chronic Toxicity and Carcinogenicity of Amsacrine (54301-15-4) in Female B6C3F1 Mice Exposed via ...
DailyMed - CEFTRIAXONE- ceftriaxone sodium injection, powder, for solution
7.1 Vancomycin, Amsacrine, Aminoglycosides, and Fluconazole. Vancomycin, amsacrine, aminoglycosides, and fluconazole are ... 7.1 Vancomycin, Amsacrine, Aminoglycosides, and Fluconazole 7.2 Calcium-containing Products 8 USE IN SPECIFIC POPULATIONS 8.1 ... Vancomycin, amsacrine, aminoglycosides and fluconazole are physically incompatible with ceftriaxone in admixtures. When any of ... Vancomycin, amsacrine, aminoglycosides and fluconazole are physically incompatible. (7.1). *Calcium-containing products: ...
Analysis of yeast DNA topoisomerase II mutants resistant to the antitumor drug amsacrine | fatcat!
The causality between amsacrine resistance and the presence of these mutations in yeast DNA topoisomerase II has been firmly ... Analysis of yeast DNA topoisomerase II mutants resistant to the antitumor drug amsacrine release_5ly7zuydmbb5vk5n7esdtl3m7m by ... By selecting transformants that grow in the presence of the antitumor drug amsacrine at 35 degrees C, a nonpermissive ... DNA topoisomerase II is the only significant cellular target of amsacrine. Three classes of such mutants have been identified: ...
Chemotherapy-Induced Hair Loss
Dexamethasone (Systemic) Monograph for Professionals - Drugs.com
Pediatric Dilated Cardiomyopathy: Practice Essentials, Background, Pathophysiology
Idiopathic dilated cardiomyopathy (DCM) refers to congestive cardiac failure secondary to dilatation and systolic dysfunction (with or without diastolic dysfunction) of the ventricles (predominantly the left ventricle) in the absence of congenital, valvular, or coronary artery disease or any systemic disease known to cause myocardial dysfunct...
Journals on the Web
DailyMed - CEFTRIAXONE injection, powder, for solution
Anti-mullerian inhibiting substance type II receptor (MISIIR) immunoconjugates to detect and treat cancer - Adams, Gregory P.
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Novel Use of a Nicotinic Receptor Agonist 156 - AstraZeneca AB
Biomarkers Search
Activated Toxicity of Diesel Particulate Extract by Ultraviolet A Radiation in Mammalian Cells: Role of Singlet Oxygen |...
AZITHROMYCIN DERIVATIVES CONTAINING A PHOSPHONIUM ION AS ANTICANCER AGENTS - NOVINTUM BIOTECHNOLOGY GMBH
Actinomycin
Influenza B virus B/Brisbane/60/2008 antigen (formaldehyde inactivated): Uses, Interactions, Mechanism of Action | DrugBank...
C74167|Sulmepride|modify|27-JUN-08|(null)|(null
Mitoxantrone4
- Here, we have characterized 2 non-synonymous single nucleotide polymorphisms (nsSNPs) including rs762022284 and rs764177670 in TOP2A gene, which could affect its response to Amsacrine and Mitoxantrone as important inhibitors of the enzyme. (brieflands.com)
- The data suggested that the presence of rs762022284 and rs764177670 nsSNPs could affect Top2-α response to Amsacrine and Mitoxantrone, indicating the necessity of consideration of population-dependent genotypes in cancer chemotherapy, using these drugs. (brieflands.com)
- Recently, we computationally examined the mechanisms, by which nsSNP variations in Top2-α could affect its response to Amsacrine and Mitoxantrone as important inhibitors of the enzyme. (brieflands.com)
- In the present study, the allele frequency of two novel SNPs altering human DNA Top2-α interaction with Amsacrine and Mitoxantrone ( 11 ) was surveyed in the Iranian population. (brieflands.com)
Altretamine1
- And lys undergo facile oxidation of drugs with a threshold mode of amsacrine for altretamine is hydroxylation pars: To the protein target of cd28b8 signaling. (themauimiracle.org)
Belongs1
- Amsacrine belongs to the group of cancer-fighting medications called antineoplastics . (pharmachoice.com)
Acute1
- Amsacrine is used to treat acute adult leukemia (cancer of the white blood cells) in people who have been treated previously with other cancer medications. (pharmachoice.com)
Dose2
- The recommended dose and dosing schedule of amsacrine varies according to body size. (pharmachoice.com)
- While in remission, the dose of amsacrine is usually reduced and given every 4 to 8 weeks, depending on the number of white blood cells in the blood. (pharmachoice.com)
Cancer2
- Amsacrine kills cancer cells by interfering with their growth and reproduction. (pharmachoice.com)
- As well as interfering with the growth and reproduction of cancer cells, amsacrine can interfere with some of your normal cells. (pharmachoice.com)
Etoposide6
- In a multicenter trial 33 patients aged 61-65 years with de novo or secondary AML were treated with double induction therapy including high dose mitoxantrone, etoposide and ara-C (MAV) in the first course and m-amsacrine together with high dose ara-C (MAMAC) in the second course. (nih.gov)
- Abrogation Of cleavable-complex formation by etoposide but not by amsacrine. (nih.gov)
- She underwent four cycles of chemotherapy with DA (daunorubicin, cytarabine) 2MACE (amsacrine, cytarabine, etoposide) and MidAC (mitoxantrone, cytarabine). (handselfdn.org)
- His treatment was commenced on 23 Feb 2007 according to Medical Research Council (MRC)-AML-15 protocol and consisted of 2 courses of induction with ADE chemotherapy (Ara-C + Daunorubicin + Etoposide) and consolidation with MACE (Amsacrine + Cytosine + Etoposide) and MIDAC (Mitoxantrone+ high dose Cytarabine). (org.pk)
- Following remission, 1,017 patients were randomly assigned to a third course, MACE (amsacrine, etoposide, and Ara-C), plus a fourth course of MidAc (mitoxantrone and Ara-C) and following an amendment to one or two courses of high-dose Ara-C. Primary end points were cumulative incidence of relapse (CIR), relapse-free survival (RFS), and overall survival (OS). (regionh.dk)
- We found that sensitivity to amsacrine showed a correlation with the level of expression of topoisomerase II alpha protein, and that sensitivity to etoposide showed a similar correlation with the level of expression of topoisomerase II beta protein. (ox.ac.uk)
Mitoxantrone1
- Including mitoxantrone and amsacrine. (themauimiracle.org)
Antineoplastic1
- Amsacrine is an antineoplastic agent indicated for the treatment of leukemia, particularly acute myeloid leukemia (AML). (affygility.com)
Topoisomerase3
- Amsacrine also targets and inhibits topoisomerase II. (affygility.com)
- By selecting transformants that grow in the presence of the antitumor drug amsacrine at 35 degrees C, a nonpermissive temperature for the top2-4 allele, plasmid-borne top2 mutants expressing amsacrine-resistant and physiologically functional DNA topoisomerase II were readily obtained. (fatcat.wiki)
- The causality between amsacrine resistance and the presence of these mutations in yeast DNA topoisomerase II has been firmly established, and this causality in turn shows that, in yeast at least, DNA topoisomerase II is the only significant cellular target of amsacrine. (fatcat.wiki)
Antineoplastics1
- Amsacrine belongs to the general group of medicines known as antineoplastics. (drugs.com)
Cells3
- Amsacrine interferes with the growth of cancer cells, which are then eventually destroyed by the body. (drugs.com)
- Since the growth of normal body cells may also be affected by amsacrine, other effects will also occur. (drugs.com)
- Rapidly dividing cells are two to four times more sensitive to amsacrine than are resting cells. (affygility.com)
Data2
- No data regarding the Paedriatic dosage details of Amsacrine is available. (druginfosys.com)
- No data regarding the neonatal dosage details of Amsacrine is available. (druginfosys.com)
Double1
- Amsacrine appears to cleave DNA by inducing double stranded breaks. (affygility.com)
Studies1
- Studies on amsacrine have been done only in adult patients, and there is no specific information comparing use of amsacrine in children with use in other age groups. (drugs.com)
Treatment1
- Before you begin treatment with amsacrine, you and your doctor should talk about the good amsacrine will do as well as the risks of using it. (drugs.com)