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.
Cardiotoxins
Agents that have a damaging effect on the HEART. Such damage can occur from ALKYLATING AGENTS; FREE RADICALS; or metabolites from OXIDATIVE STRESS and in some cases is countered by CARDIOTONIC AGENTS. Induction of LONG QT SYNDROME or TORSADES DE POINTES has been the reason for viewing some drugs as cardiotoxins.
Antineoplastic Combined Chemotherapy Protocols
Leukemia, Erythroblastic, Acute
Friend murine leukemia virus
Leukemia, Experimental
Chlorophyllides
Neuropeptides
Pharmacopoeias as Topic
Authoritative treatises on drugs and preparations, their description, formulation, analytic composition, physical constants, main chemical properties used in identification, standards for strength, purity, and dosage, chemical tests for determining identity and purity, etc. They are usually published under governmental jurisdiction (e.g., USP, the United States Pharmacopoeia; BP, British Pharmacopoeia; P. Helv., the Swiss Pharmacopoeia). They differ from FORMULARIES in that they are far more complete: formularies tend to be mere listings of formulas and prescriptions.
Preservatives, Pharmaceutical
Food Preservatives
Xylitol
Biofuels
Body Composition
Tablets
Excipients
Foramen Ovale, Patent
Leukemia, Myeloid, Acute
Leukemia, Myeloid
Remission Induction
Hematopoietic Stem Cell Transplantation
Transfer of HEMATOPOIETIC STEM CELLS from BONE MARROW or BLOOD between individuals within the same species (TRANSPLANTATION, HOMOLOGOUS) or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). Hematopoietic stem cell transplantation has been used as an alternative to BONE MARROW TRANSPLANTATION in the treatment of a variety of neoplasms.
Nuclear Reprogramming
The process that reverts CELL NUCLEI of fully differentiated somatic cells to a pluripotent or totipotent state. This process can be achieved to a certain extent by NUCLEAR TRANSFER TECHNIQUES, such as fusing somatic cell nuclei with enucleated pluripotent embryonic stem cells or enucleated totipotent oocytes. GENE EXPRESSION PROFILING of the fused hybrid cells is used to determine the degree of reprogramming. Dramatic results of nuclear reprogramming include the generation of cloned mammals, such as Dolly the sheep in 1997.
Epigenesis, Genetic
A genetic process by which the adult organism is realized via mechanisms that lead to the restriction in the possible fates of cells, eventually leading to their differentiated state. Mechanisms involved cause heritable changes to cells without changes to DNA sequence such as DNA METHYLATION; HISTONE modification; DNA REPLICATION TIMING; NUCLEOSOME positioning; and heterochromatization which result in selective gene expression or repression.
Inventions
Lower Gastrointestinal Tract
Phenotype
Fibrocystic Breast Disease
A common and benign breast disease characterized by varying degree of fibrocystic changes in the breast tissue. There are three major patterns of morphological changes, including FIBROSIS, formation of CYSTS, and proliferation of glandular tissue (adenosis). The fibrocystic breast has a dense irregular, lumpy, bumpy consistency.
Calcium Phosphates
Bone Substitutes
Synthetic or natural materials for the replacement of bones or bone tissue. They include hard tissue replacement polymers, natural coral, hydroxyapatite, beta-tricalcium phosphate, and various other biomaterials. The bone substitutes as inert materials can be incorporated into surrounding tissue or gradually replaced by original tissue.
Porosity
Bone and Bones
Minerals
Native, inorganic or fossilized organic substances having a definite chemical composition and formed by inorganic reactions. They may occur as individual crystals or may be disseminated in some other mineral or rock. (Grant & Hackh's Chemical Dictionary, 5th ed; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Bone Cements
Adhesives used to fix prosthetic devices to bones and to cement bone to bone in difficult fractures. Synthetic resins are commonly used as cements. A mixture of monocalcium phosphate, monohydrate, alpha-tricalcium phosphate, and calcium carbonate with a sodium phosphate solution is also a useful bone paste.
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<...
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
Mamsa Dhatu: A Closer Look at the Muscles from the Ayurvedic Perspective
Real-Politik Ditto: Did science really cure the first case of HIV (aka AIDS...
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...
Teniposide Injection Wholesaler,Teniposide Injection Supplier
Mitoxantrone cancer drug molecule - Stock Image F012/9242 - Science Photo Library
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
AID 211293 - Tested for inhibitory activity against Topoisomerase II isolated from HeLa cells by using SDS-K+ precipitation...
Anti-Topoisomerase II beta/TOP2B antibody (ab52769) | Abcam
Fundamental and Basic Research in Homeopathy - Initiative to Promote Research in Homeopathy
Topoisomerase Inhibitors | MedChemExpress
Search
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 ...
Amsakrin - Википедија
Amsacrine. Molimo Vas, obratite pažnju na važno upozorenje. u vezi sa temama iz oblasti medicine (zdravlja). ...
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
L01XJ03 Glasdegib L01XK01 Olaparib L01XK02 Niraparib L01XK03 Rucaparib L01XK04 Talazoparib L01XK05 Veliparib L01XX01 Amsacrine ...
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 ...
Amsacrine
... (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. It has been used in acute lymphoblastic leukemia ... Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better ... Horstmann MA, Hassenpflug WA, zur Stadt U, Escherich G, Janka G, Kabisch H (December 2005). "Amsacrine combined with etoposide ...
Bleomycin
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
Ribociclib
Cyclin-dependent kinases (CDKs) 4 and 6 are enzymes that have been shown to promote cell division and multiplication in both normal and cancer cells. Many cancer cells have shown abnormalities that increase the activity of CDK, leading to the inactivation of certain tumor suppressor genes.[3][10] When used in combination with other drugs such as an ALK or an MEK inhibitor, ribociclib has been shown to have a synergistic effect, resulting in improved responses.[11][12] Again, this is likely a result of "crosstalk" between signaling pathways. Simply blocking one pathway in cancer tumorigenesis can sometimes result in "tumor compensation", where the tumor compensates for the blocked signaling pathway by utilizing other pathways to survive. By blocking several pathways at once, it is thought that the tumor is less able to compensate, and a greater anti-tumor response is often observed. Utilizing ribociclib in combination with other agents has been shown to reduce the development of resistance to ...
Cladribine
In the mid-1990s Beutler, in collaboration with Jack Sipe, a neurologist at Scripps, ran several clinical trials exploring the utility of cladribine in multiple sclerosis, based on the drug's immunosuppressive effects. Sipe's insight into MS, and Beutler's interest in MS due to his sister having it, led a very productive collaboration.[18]:17[22] Ortho-Clinical, a subsidiary of J&J, filed an NDA for cladribine for MS in 1997 but withdrew it in the late 1990s after discussion with the FDA proved that more clinical data would be needed.[23][24] Ivax acquired the rights for oral administration of cladribine to treat MS from Scripps in 2000,[25] and partnered with Serono in 2002.[24] Ivax was acquired by Teva in 2006,[26][27] and Merck KGaA acquired control of Serono's drug business in 2006.[28] An oral formulation of the drug with cyclodextrin was developed[29]:16 and Ivax and Serono, and then Merck KGaA conducted several clinical studies. Merck KGaA submitted an application to the European ...
Intercalation (biochemistry)
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
Amrubicin
... (INN; previously known as SM-5887) is an anthracycline used in the treatment of lung cancer.[1] It is marketed in Japan since 2002 by Sumitomo under the brand name Calsed.[2] Amrubicin acts by inhibiting topoisomerase II, and has been compared in clinical trials with topotecan, a Topoisomerase I inhibitor.[3][4] It has also been studied for the treatment of bladder carcinoma[5] and gastric cancer.[6] Amrubicin was the first anthracycline derivative created by de novo synthesis and was first published in 1989 by scientists from Sumitomo.[7] ...
Docetaxel
where CL is total body clearance (L/h), BSA is total body surface area (m2), AAG and ALB represent alpha1 acid glycoprotein and albumin plasma concentrations (g/L) respectively, and AGE is the patients age (years).[13] HEP12 represents a measure of hepatic dysfunction, affecting clearance of docetaxel. This final model accounted for a modest proportion of patients and identified most of the patients varying from the model (population median of CL = 35.6 L/h) as having hepatic dysfunction, indicating hepatic function as the most unpredictable factor with regards to clearance variability.[13] Patients with significant hepatic dysfunction had an approximately 30% decrease in clearance of docetaxel and were also at a higher risk of toxicity poisoning from docetaxel treatment.[13] Clearance has been shown from population pharmacokinetic studies to decrease significantly with age, increased alpha1 acid glycoprotein and albumin concentrations and decreased body surface area.[13] Renal impairment is ...
Photodynamic therapy
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
Talazoparib
... acts as an inhibitor of poly ADP ribose polymerase (PARP) which aids in single strand DNA repair. Cells that have BRCA1/2 mutations are susceptible to the cytotoxic effects of PARP inhibitors because of an accumulation of DNA damage.[2] Talazoparib is theorized to have a higher potency than olaparib due to the additional mechanism of action called PARP trapping. PARP trapping is the mechanism of action where the PARP molecule is trapped on the DNA, which interferes with the cells ability to replicate. Talazoparib is found to be ~100 fold more efficient in PARP trapping than olaparib.[9] However, this increased potency may not translate directly to clinical effectiveness as many other factors must be considered.[4][9] ...
Crosslinking of DNA
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
mTOR inhibitors
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
Chemotherapy regimen
fludarabine, cytarabine, amsacrine myelodysplastic syndrome, acute myeloid leukemia FLAMSA-BU or FLAMSA-Bu fludarabine, ... fludarabine, cytarabine, amsacrine, melphalan myelodysplastic syndrome, acute myeloid leukemia FOLFIRI fluorouracil (5-FU), ... cytarabine, amsacrine, busulfan myelodysplastic syndrome, acute myeloid leukemia FLAMSA-MEL or FLAMSA-Mel ...
ഹൈഡ്രോക്സി കാർബാമൈഡ് - വിക്കിപീഡിയ
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
Amsacrine - Wikipedia
Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. It has been used in acute lymphoblastic leukemia ... Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better ... Horstmann MA, Hassenpflug WA, zur Stadt U, Escherich G, Janka G, Kabisch H (December 2005). "Amsacrine combined with etoposide ...
Amsacrine - DrugBank
Amsacrine gluconate. M4P91439UZ. 80277-07-2. XXNAQBNJPZNRSZ-IFWQJVLJSA-N. Amsacrine hydrochloride. U66HX4K4CO. 54301-15-4. ... Amsacrine appears to cleave DNA by inducing double stranded breaks. Amsacrine also targets and inhibits topoisomerase II. ... Gitoformate may decrease the cardiotoxic activities of Amsacrine.. Experimental. Haloperidol. The metabolism of Amsacrine can ... Metildigoxin may decrease the cardiotoxic activities of Amsacrine.. Experimental. Metoprolol. The metabolism of Amsacrine can ...
Structural Biochemistry/Amsacrine - Wikibooks, open books for an open world
Amsacrine kills cancerous cells by inhibiting the Topo II enzyme. It stabilizes the enzyme with the broken DNA strand complex ... Amsacrine is a potent intercalating antineoplastic agent. It is effective in the treatment of adult acute leukemias and ... "Amsacrine." Scott Hamilton CARES Initiative. N.p.. Web. 07 Dec 2012. ,http://chemocare.com/chemotherapy/drug-info/Amsacrine. ... Retrieved from "https://en.wikibooks.org/w/index.php?title=Structural_Biochemistry/Amsacrine&oldid=3117334" ...
Amsacrine (Amsidine) Drug Information - Indications, Dosage, Side Effects and Precautions
Amsacrine(Amsidine) generic is an antineoplastic agent, prescribed for malignant lymphoma and acute adult lymphoblastic ... General Information on Amsacrine. Generic Name : Amsacrine Latest prescription information about Amsacrine. Learn how to ... How should Amsacrine be taken? It comes as a red colored solution for injection to be administered by a healthcare provider ... What are the side effects of Amsacrine? Most Common : Fatigue (tiredness), sore mouth and throat, loss of fertility, absence of ...
Amsacrine | definition of amsacrine by Medical dictionary
... amsacrine explanation free. What is amsacrine? Meaning of amsacrine medical term. What does amsacrine mean? ... Looking for online definition of amsacrine in the Medical Dictionary? ... amsacrine. Also found in: Wikipedia. amsacrine. /am·sa·crine/ (am´sah-krēn) an antineoplastic that inhibits DNA synthesis; used ... Amsacrine , definition of amsacrine by Medical dictionary https://medical-dictionary.thefreedictionary.com/amsacrine ...
Human Metabolome Database: Showing metabocard for Amsacrine (HMDB0014421)
Showing metabocard for Amsacrine (HMDB0014421). IdentificationTaxonomyOntologyPhysical propertiesSpectraBiological properties ... Amsacrine. Description. Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the ... Finlay GJ, Atwell GJ, Baguley BC: Inhibition of the action of the topoisomerase II poison amsacrine by simple aniline ... Lee MS, Wang JC, Beran M: Two independent amsacrine-resistant human myeloid leukemia cell lines share an identical point ...
Human Metabolome Database: Showing metabocard for Amsacrine (HMDB0014421)
Amsacrine is a very strong basic compound (based on its pKa). Amsacrine is formally rated as a possible carcinogen (by IARC 2B ... Amsacrine. Description. Amsacrine, also known as MAMSA or amsacrinum, belongs to the class of organic compounds known as ... Showing metabocard for Amsacrine (HMDB0014421). Jump To Section: IdentificationTaxonomyOntologyPhysical propertiesSpectra ... Amsacrine is a drug which is used for treatment of acute myeloid leukaemia. It is frequently used in combination with other ...
Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on...
Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on ... Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on ... Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on ... Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on ...
Amsacrine (Intravenous route)
If amsacrine accidentally leaks out of the vein into which it is injected, it may damage some tissues and cause scarring. Tell ... Amsacrine may lower your bodys resistance, and there is a chance you might get the infection the immunization is meant to ... After treatment with amsacrine has ended, normal hair growth should return. Other side effects not listed may also occur in ... Amsacrine interferes with the growth of cancer cells, which are then eventually destroyed by the body. Since the growth of ...
Amsacrine - wikidoc
Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. It has been used in acute lymphoblastic leukemia. ... retinoids (Alitretinoin, Tretinoin), Fusion protein (Aflibercept) - Altretamine, Amsacrine, Anagrelide, Arsenic trioxide, ... "Amsacrine combined with etoposide and high-dose methylprednisolone as salvage therapy in acute lymphoblastic leukemia in ... Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better ...
Chemotherapy drugs and combination regimens - Information and support - Macmillan Cancer Support
Amsacrine - Antineoplastic agents - Pocket Drug Guide
Amsacrine is poorly absorbed after oral doses. When given intravenously it has a reported terminal half-life of about 5 to 8 ... Amsacrine is an antineoplastic agent that appears to act by intercalation with DNA and inhibition of nucleic acid synthesis. It ... Amsacrine is prepared as a solution in lactic acid and dimethylacetamide, and is given, diluted in glucose 5%, by intravenous ... Amsacrine reacts with certain plastics.. Adverse Effects, Treatment, and Precautions. For a general outline see Antineoplastics ...
Drug Information
Ceftriaxone and Dextrose - FDA prescribing information, side effects and uses
DailyMed - CEFTRIAXONE AND DEXTROSE- ceftriaxone injection, 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. (7.1). *Calcium-containing products: ... Vancomycin, amsacrine, aminoglycosides, and fluconazole are physically incompatible with ceftriaxone in admixtures. When any of ...
Amsacrine evokes permanent discussion of a few viewers, and potentially because of acetyldigitoxin
Patent US5840334 - Self-binding shearform compositions - Google Patents
AML2003 - Standard-Therapy vs Intensified Therapy for Adult Acute Myeloid Leukemia Patients |= 60 Years - Full Text View -...
Cytarabine+Amsacrine+Mitoxantrone Procedure: early allogeneic PBSCT within induction therapy Procedure: autologous PBSCT Phase ... Amsacrine. Antimetabolites, Antineoplastic. Antimetabolites. Molecular Mechanisms of Pharmacological Action. Antineoplastic ... High-dose cytarabine consolidation with or without additional amsacrine and mitoxantrone in acute myeloid leukemia: results of ...
Patente WO2011099007A1 - Pharmaceutical compositions and methods for the treatment and prevention of ... - Google Patentes
Use of Cxcr4 Protein Expression on the Surface of Stem Cells as a Marker for Tumor Tropic Potential - CEDARS-SINAI MEDICAL...
Extracorporeal Removal of Microvesicular Particles - AETHLON MEDICAL, INC.
4 Doubling Up: How the Genetic Code Replicates Itself | A Positron Named Priscilla: Scientific Discovery at the Frontier |...
such as the acridines (e.g., Amsacrine); anthracyclines (e.g., Adriamycin); anthraquinones (e.g., Mitoxantrone); and the ... Amsacrine. So now there is a search for factors that could inhibit, or enhance, the impact of topoisomerase poisons. "The hope ... VP-16 and Amsacrine. The end result is the increased killing of cancer cells. This therapeutic strategy will soon begin ...
Cimetidine Hydrochloride Monograph for Professionals - Drugs.com
Patente US20070128245 - Porous calcium phosphate bone material - Google Patentes
Search of: 'Acute Promyelocytic Leukemia' | 'Antibiotics, Antitubercular' - List Results - ClinicalTrials.gov
Topoisomerase Inhibitors
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Topoisomerase<...
"Divergent activity of derivatives of amsacrine (m-amsa) towards lewis " by B C. Baguley, A R. Kernohan et al.
Cytarabine1
- Fludarabine (30 mg/m2), cytarabine (2 g/m2), and amsacrine (100 mg/m2) for 4 days were used for cytoreduction. (uptodate.com)
Etoposide3
- Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better known agent etoposide). (wikipedia.org)
- Topoisomerase II inhibitors are Amsacrine and Etoposide. (thefreedictionary.com)
- Semisynthetic Topo II poisons, amsacrine (m-AMSA) and etoposide, stabilise the covalent Topo II-DNA cleavage complex on both DNA strands. (thefreedictionary.com)
Synonyms1
- Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. (wikipedia.org)
AMSA6
- 2] (n = 44) Amsacrine 6 (of 19) adults Systemic clearance (AMSA) with disseminated (CLs) of cancer given 30 [sup. (thefreedictionary.com)
- Divergent activity of derivatives of amsacrine (m-amsa) towards lewis " by B C. Baguley, A R. Kernohan et al. (jax.org)
- Divergent activity of derivatives of amsacrine (m-amsa) towards lewis lung carcinoma and p388 leukaemia in mice. (jax.org)
- Twelve patients with recurrent and metastatic breast cancer were treated with a combination of adriamycin and amsacrine (m-AMSA) to evaluate its efficacy and toxicity. (elsevier.com)
- Amsacrine ( AMSA ) exhibits positive cooperativity in their equilibrium binding to DNA as indicated by the positive slope in the initial region of the binding isotherms (Scatchard plots) under conditions simulating physiological ionic strengths . (bvsalud.org)
- FLAMSA adds amsacrine ("AMSA") to the standard FLAG regimen. (wikipedia.org)
Antineoplastic agent4
- Amsacrine is an aminoacridine derivative that is a potent intercalating antineoplastic agent. (drugbank.ca)
- Amsacrine is a potent intercalating antineoplastic agent. (wikibooks.org)
- Amsacrine is an antineoplastic agent that appears to act by intercalation with DNA and inhibition of nucleic acid synthesis. (pocketdrugguide.com)
- Amsacrine is an alkylating antineoplastic agent that is highly active toward AML, unlike more conventional alkylators like cyclophosphamide. (wikipedia.org)
Chemotherapy1
- Amsacrine and sulfonylhydrazines, sulphonamide derivatives, are antineoplastic agents that are frequently used in cancer chemotherapy [5, 6]. (thefreedictionary.com)
Remission1
- For the induction of remission, amsacrine may be given at a dose of 90 mg/m daily for 5 to 8 days, depending on clinical response. (pocketdrugguide.com)
Camptothecin2
- The present study was designed to determine and compare the clastogenicity of amsacrine and camptothecin in vivo in mouse bone marrow and peripheral blood lymphocytes and in vitro in mouse lymphoma L5178Y cells. (epa.gov)
- It was expected that amsacrine, which interferes with topoisomerase II to induce double-strand DNA breaks, and camptothecin, which interferes with topoisomerase I to induce single-strand DNA breaks, would induce different types of chromosomal aberrations. (epa.gov)
Topo II1
- Amsacrine kills cancerous cells by inhibiting the Topo II enzyme. (wikibooks.org)
Topoisomerase II1
- Amsacrine also targets and inhibits topoisomerase II. (drugbank.ca)
Binds2
- Amsacrine binds to DNA through intercalation and external binding. (drugbank.ca)
- Amsacrine binds in a cooperative manner to deoxyribonucleic acid. (bvsalud.org)
High-dose1
- Amsacrine and continuous-infusion high-dose cytosine arabinoside as induction therapy for patients with newly-diagnosed acute myelogenous leukemia. (nih.gov)
Interferes1
- Amsacrine interferes with the growth of cancer cells, which are then eventually destroyed by the body. (allinahealth.org)
Adriamycin1
- We conclude that the combination of adriamycin and amsacrine at the dose and schedule used in our trial has little antitumor effect in the treatment of advanced breast cancer. (elsevier.com)
Acetyldigitoxin2
- Acetyldigitoxin may decrease the cardiotoxic activities of Amsacrine. (drugbank.ca)
- Although amsacrine and acetyldigitoxin are frequently combined together, their effects seized may be additive measure on lowering your blood and pressure. (elkmeadownursery.com)
Leukemia1
- Judd, Multiple Patterns of Resistance of Human Leukemia Cell Sublines to Amsacrine Analogues, J. (thefreedictionary.com)
Drugs1
- Use with diuretics or nephrotoxic drugs such as the aminoglycosides may theoretically increase the risk of cardiotoxicity with amsacrine by precipitating hypokalaemia. (pocketdrugguide.com)
Adult1
- Studies on this medicine 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. (allinahealth.org)
Caution1
- Amsacrine should be given with caution to patients with liver or kidney disease, who may require dosage adjustments. (pocketdrugguide.com)
Combination1
- The therapeutic efficacy of BCG vaccine can be decreased when used in combination with Amsacrine. (drugbank.ca)
Dosage1
- What is the dosage of Amsacrine? (medindia.net)
Cells3
- Rapidly dividing cells are two to four times more sensitive to amsacrine than are resting cells. (drugbank.ca)
- NSC 343499), a lipophilic and water-soluble derivative of amsacrine (NSC 249992), on cell viability, growth, clonogenicity, and progression through the cell cycle were investigated in suspension cultures of Friend erythroleukemic cells and in adherent cultures of Chinese hamster ovary cells. (aacrjournals.org)
- Since the growth of normal body cells may also be affected by amsacrine, other effects will also occur. (allinahealth.org)
Effects2
- The risk or severity of adverse effects can be increased when Cabazitaxel is combined with Amsacrine. (drugbank.ca)
- What are the side effects of Amsacrine? (medindia.net)
Treatment2
- Amsacrine is a drug which is used for treatment of acute myeloid leukaemia. (hmdb.ca)
- Before you begin treatment with amsacrine, you and your doctor should talk about the good this medicine will do as well as the risks of using it. (allinahealth.org)
Solution2
- Amsacrine is incompatible with sodium chloride 0.9% injection and with other chloride-containing solutions, apparently because of the poor solubility of the hydrochloride salt in aqueous solution. (pocketdrugguide.com)
- Amsacrine is prepared as a solution in lactic acid and dimethylacetamide, and is given, diluted in glucose 5%, by intravenous infusion over 60 to 90 minutes. (pocketdrugguide.com)
Appears1
- Amsacrine appears to cleave DNA by inducing double stranded breaks. (drugbank.ca)