An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.
Acridines which are substituted in any position by one or more amino groups or substituted amino groups.
DNA TOPOISOMERASES that catalyze ATP-dependent breakage of both strands of DNA, passage of the unbroken strands through the breaks, and rejoining of the broken strands. These enzymes bring about relaxation of the supercoiled DNA and resolution of a knotted circular DNA duplex.
Compounds that inhibit the activity of DNA TOPOISOMERASE II. Included in this category are a variety of ANTINEOPLASTIC AGENTS which target the eukaryotic form of topoisomerase II and ANTIBACTERIAL AGENTS which target the prokaryotic form of topoisomerase II.
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.
Agents that are capable of inserting themselves between the successive bases in DNA, thus kinking, uncoiling or otherwise deforming it and therefore preventing its proper functioning. They are used in the study of DNA.
A genus of the family Heteromyidae which contains 22 species. Their physiology is adapted for the conservation of water, and they seldom drink water. They are found in arid or desert habitats and travel by hopping on their hind limbs.
A highly fluorescent anti-infective dye used clinically as a topical antiseptic and experimentally as a mutagen, due to its interaction with DNA. It is also used as an intracellular pH indicator.
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.
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)
An antimitotic agent with immunosuppressive properties.
Vomiting caused by expectation of discomfort or unpleasantness.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
An anthracenedione-derived antineoplastic agent.
Compounds that inhibit the activity of DNA TOPOISOMERASE I.
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
A hydrolase enzyme that converts L-asparagine and water to L-aspartate and NH3. EC 3.5.1.1.
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)

In deciding to use a medicine, the risks of taking the medicine must be weighed against the good it will do. This is a decision you and your doctor will make. For this medicine, the following should be considered: Allergies Tell your doctor if you have ever had any unusual or allergic reaction to this medicine or any other medicines. Also tell your health care professional if you have any other types of allergies, such as to foods, dyes, preservatives, or animals. For non-prescription products, read the label or package ingredients carefully. Children 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. Older adults Many medicines have not been studied specifically in older people. Therefore, it may not be known whether they work exactly the same way they do in younger adults or if they cause different side effects or problems in older people. There is no specific information ...
Abdul Mamsa, MD is a Neurologist at 820 W Oak St, Kissimmee, FL 34741. Wellness.com provides reviews, contact information, driving directions and the phone number for Abdul Mamsa, MD in Kissimmee, FL.
TY - JOUR. T1 - Topoisomerase II-mediated DNA cleavage by amonafide and its structural analogs. AU - Hsiang, W. H.. AU - Jiang, J. B.. AU - Liu, L. F.. N1 - Copyright: Copyright 2004 Elsevier B.V., All rights reserved.. PY - 1989. Y1 - 1989. N2 - Treatment of SV40-infected monkey cells with amonafide (benzisoquinolinedione), an intercalative antitumor drug, resulted in rapid accumulation of linearized intracellular SV40 DNA molecules that were protein linked. Studies using purified mammalian DNA topoisomerase II have shown that amonafide and its structural analogs interfere with the breakage-rejoining reaction of the enzyme by stabilizing a reversible enzyme-DNA cleavable complex. Denaturation of the cleavable complex with sodium dodecyl sulfate resulted in DNA cleavage and the covalent association of topoisomerase II polypeptides with the cleaved DNA. Unwinding measurements indicate that amonafide is a DNA intercalator. These results suggest that amonafide and its structural analogs (e.g., ...
TY - JOUR. T1 - Pilot study of adriamycin and amsacrine (m-AMSA) in patients with advanced breast cancer. AU - Chang, A. Y.C.. AU - Solan, A.. AU - Kaplan, B. H.. AU - Vogl, S. E.. AU - Camacho, F. J.. AU - Taylor IV, S. G.. N1 - Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 1988. Y1 - 1988. N2 - 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. Adriamycin was given at 40 mg/m2 i.v. and m-AMSA at 50 mg/m2 i.v. every 3 weeks. No response was observed. One patient received an escalated m-AMSA dose at 70 mg/m2 and the same dose of adriamycin. She died of treatment-related leukopenia and infection. 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.. AB - Twelve patients with recurrent and metastatic breast cancer were treated with a ...
Type II Human DNA Topoisomerases (topos II) play an essential role in DNA replication and transcription and are important targets for cancer chemotherapeutic drugs. Topoisomerase II causes transient double-strand breaks in DNA, forming a gate through which another double helix is passed, and acts as a DNA dependent ATPase. Mutations in topoII have been linked to atypical multi-drug resistance. Both human Topoisomerase II isoforms, alpha and beta, are targeted by amsacrine. We have used a forced molecular evolution approach to identify mutations conferring resistance to acridines. Here we report mutation betaG465D, which was selected with mAMSA and DACA and is cross-resistant to etoposide, ellipticine and doxorubicin. Resistance to mAMSA appears to decrease over time indicating a previously unreported resistance mechanism. G465D lies within the B domain in the region that contacts the cleaved gate helix. There is a 3-fold decrease in ATP affinity and ATP hydrolysis and an altered requirement for ...
A human breast cancer cell line (MCF7/WT) was selected for resistance to etoposide (VP-16) by stepwise exposure to 2-fold increasing concentrations of this agent. The resulting cell line (MCF7/VP) was 28-, 21-, and 9-fold resistant to VP-16, VM-26, and doxorubicin, respectively. MCF7/VP cells also exhibited low-level cross-resistance to 4′-(9-acridinylamino)-methanesulfon-m-anisidide, mitoxantrone, and vincristine and no cross-resistance to genistein and camptothecin. Furthermore, these cells were collaterally sensitive to the alkylating agents melphalan and chlorambucil. DNA topoisomerase II levels were similar in both wild-type MCF7/WT and drug-resistant MCF7/VP cells. In contrast, topoisomerase II from MCF7/VP cells appeared to be 7-fold less sensitive to drug-induced cleavable complex formation in whole cells and 3-fold less sensitive in nuclear extracts than topoisomerase II from MCF7/WT cells. Although this suggested that the resistant cells may contain a qualitatively altered ...
Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects. [PubChem]
TY - JOUR. T1 - Tumor penetration of AMSA in man. AU - Zhengang, Guo. AU - Savaraj, Niramol. AU - Feun, Lynn G.. AU - Lu, Katherine. AU - Stewart, David J.. AU - Luna, Mario. AU - Benjamin, Robert S.. AU - Loo, Ti Li. N1 - Funding Information: Supported in part by NCI Contract No. CM-87185 and Grant No. CA-14528.. PY - 1983. Y1 - 1983. N2 - 4)9-Acridinylamino)-methanesulfon-m-anisidide [AMSA) has shown significant antitumor activity against several murine tumors and leukemias. During its Phase I and II clinical trial, we were able to obtain tumors, plasma, and CSF specimens from patients who received varying doses of AMSA, as well as patients who received high doses and had autologous bone marrow rescue. The drug was analyzed chromatographically. The tumor to plasma drug concentration ratios ranged from 200% to 486% apparently independent of dose and sampling time. Because AMSA was not detected in the CSF, the drug may not be effective in the treatment of meningeal metastasis. High-dose AMSA ...
Transient or long-term DNA self-assembly participates in essential genetic functions. The present review focuses on tight DNA-DNA interactions that have recently been found to play important roles in both controlling DNA higher-order structures and their topology. Due to their chirality, double helices are tightly packed into stable right-handed crossovers. Simple packing rules that are imposed by DNA geometry and sequence dictate the overall architecture of higher order DNA structures. Close DNA-DNA interactions also provide the missing link between local interactions and DNA topology, thus explaining how type II DNA topoisomerases may sense locally the global topology. Finally this paper proposes that through its influence on DNA self-assembled structures, DNA chirality played a critical role during the early steps of evolution.
The compound 4-(9-[4-[N-methyl-carboxamido]-5-methyl]acridinylamino)methanesulphon-m-a nisidide and acid addition salts thereof have antitumor properties.
TY - JOUR. T1 - Standardization of the alkaline elution procedure using X-ray-damaged nuclear DNA. AU - Bolognesi, C.. AU - Cesarone, C. F.. AU - Santi, L.. PY - 1979. Y1 - 1979. UR - http://www.scopus.com/inward/record.url?scp=0018600110&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0018600110&partnerID=8YFLogxK. M3 - Article. C2 - 42176. AN - SCOPUS:0018600110. VL - 65. SP - 511. EP - 516. JO - Tumori. JF - Tumori. SN - 0300-8916. IS - 5. ER - ...
Learn about the designer Bill Stumpf, inventor of the first ergonomic work chair and winner of the 2006 National Design Award in Product Design.
The binding of linear and circular forms of DNA to yeast DNA topoisomerase II or its complex with AMPPNP, the nonhydrolyzable beta,gamma-imido analog of ATP, was carried out to probe the ATP analog-induced conformational change of the enzyme. Binding of the ATP analog is shown to convert the enzyme …
Antigen Background Topoisomerase II alpha is an essential nuclear enzyme involved in DNA replication and is a target for many anti-cancer drugs used for cancer therapy. Decreased expression of topoisomerase II alpha is the predominant mechanism of resistance to several chemotherapeutic agents. A significant variation in the range of expression of this protein has been reported in many different tumors. Reports of the analysis of primary breast tumors have indicated that topoisomerase II beta is more widely expressed than topoisomerase II alpha. Topoisomerase II alpha expression and activity is linked to the cell cycle and is associated with the proliferation status of cells.. ...
Human Topoisomerase II Assay Kit available from TopoGEN - measure topo II activity in a crude extract. Highly specific and quantifiable.
Human Topoisomerase II Assay Kit available from TopoGEN - measure topo II activity in a crude extract. Highly specific and quantifiable.
A drug-resistant human small cell lung cancer cell line, H209/V6, selected in the presence of increasing concentrations of 9-(4,6-O-ethylidene-β-d-glucopyranosyl)-4′-demethylepipodophyllotoxin (VP-16) from parental H209 cells, is 22-, 9-, and 4-fold resistant to VP-16, 4′-(9-acridinylamino)methanesulfon-m-anisidide, and doxorubicin, respectively, but not cross-resistant to 1,4-dihydroxy-5,8-bis({2-[(2-hydroxyethyl)amino]ethyl}-amino)-9,10-anthracenedione. These cells do not overexpress P-glycoprotein or the multidrug resistance-associated protein. Immunoblotting demonstrates that H209 cells contain the Mr 170,000 isoform of topoisomerase II (topo II), while H209/V6 cells have a Mr 160,000 enzyme but none of the Mr 170,000 isoform. The cell lines have equal amounts of topo IIβ. The H209/V6 cells have a 5-fold decrease in total immunoreactive topo IIα. The catalytic and VP-16-induced DNA cleavage activities of the topo II present in 0.35 m NaCl nuclear extracts are decreased 2- to 3-fold in ...
A small structure-focused library of propargylic enol ethers was prepared by means of a modular and efficient chemodifferentiating organocatalyzed multicomponent reaction. The most active compound (GI50 0.25 μM) against solid tumor cells was selected as lead. Cell cycle analysis and immunoblotting demonstrated arrest at the metaphase, pointing out human topoisomerase II as plausible molecular target. In vitro assays were carried out, showing that the lead behaves as a catalytic inhibitor of the enzyme ...
The amount of muscle and the thickness of the skin and ligaments depend upon a persons constitution. People with a vata prakruti have minimal amounts of muscle and thin skin and ligaments even when healthy and balanced. Those with a pitta nature have moderate muscular formation along with a moderate thickness of the skin and ligaments. Individuals with a kapha nature have larger muscle mass with thicker skin and ligaments. Regardless of the dosha, the tissues are healthy if they are consistent in formation with the doshic balance of the individual and are tone and supple.. Vitiation of kapha dosha in the mamsavaha srota (channel that carries posaka rakta dhatu) results in low mamsagni. This results in excessive mamsa dhatu formation but the tissue formed is hard and inflexible. In addition, the upadhatus (secondary tissues) are similarly affected. Thus, the skin and ligaments of the body become thicker, harder, and tighter. Psychologically, self-confidence is quiet and strong but the motivation ...
In the Subjects, Materials, and Methods Subjects section of this paper one reads: In February 2007, an HIV-infected patient underwent stem cell transplantation (SCT) due to a relapse of AML with a graft consisting of CCR5A32/A32 donor cells. The pre-transplant conditioning regimen included 100 mg/m2 of amsacrine, 30 mg/m2 of fludarabine, 2 g/m2 of cytarabine (day -12 until -9), 60 mg/kg of cyclophosphamide (days -4 and -3), 5.5 mg/kg of rabbit antithymocyte globuline (in three doses between day -3 and -1), and a 400 cGy total body irradiation (TBI; day -5). ART was discontinued on the day of transplantation, and 13 months later the patient received a second transplant with CCR5A32/A32 stem cells from the same donor due to a second relapse of AML. The conditioning regimen consisted of 100 mg/m2 of cytarabine (day -7 until day -1), 6 mg/m2 of gemtuzumab (day -7 and day -1), and a 200 cGy TBI (day -1)... Twelve months post-transplant, the patient underwent liver biopsy and histological examination ...
Your doctor will prescribe your dose and schedule. This medicine is given through a needle placed in a vein. This medicine is given slowly, so your IV will remain in place for 30 to 60 minutes. You may also need to stay for observation for an additional hour or more ...
The phenanthridine alkaloid lycobetaine is a minor constituent of Amaryllidaceae. Inhibition of cell growth was studied in the clonogenic assay on 21 human tumour xenografts (mean IC50 = 0.8 μM). The growth of human leukaemia cell lines was also potently inhibited (mean IC50 = 1.3 μM). Athymic nude mice, carrying s.c. implanted human gastric tumour xenograft GXF251, were treated i.p. with lycobetaine for 4 weeks, resulting in a marked tumour growth delay. Lycobetaine was found to act as a specific topoisomerase IIβ poison. In the presence of calf thymus DNA, pure recombinant human topoisomerase IIβ protein was selectively depleted from SDS-gels, whereas no depletion of topoisomerase IIα protein was observed. In A431 cells immunoband-depletion of topoisomerase IIβ was induced, suggesting stabilization of the covalent catalytic DNA-intermediate in living cells. It is reasonable to assume that this mechanism will cause or at least contribute significantly to the antitumour activity. © 2001 Cancer
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TY - JOUR. T1 - Neoamphimedine circumvents metnase-enhanced DNA topoisomerase IIα activity through ATP-competitive inhibition. AU - Ponder, Jessica. AU - Yoo, Byong Hoon. AU - Abraham, Adedoyin D.. AU - Li, Qun. AU - Ashley, Amanda K.. AU - Amerin, Courtney L.. AU - Zhou, Qiong. AU - Reid, Brian G.. AU - Reigan, Philip. AU - Hromas, Robert. AU - Nickoloff, Jac A.. AU - LaBarbera, Daniel V.. PY - 2011/11. Y1 - 2011/11. N2 - Type IIα DNA topoisomerase (TopoIIα) is among the most important clinical drug targets for the treatment of cancer. Recently, the DNA repair protein Metnase was shown to enhance TopoIIα activity and increase resistance to TopoIIα poisons. Using in vitro DNA decatenation assays we show that neoamphimedine potently inhibits TopoIIá-dependent DNA decatenation in the presence of Metnase. Cell proliferation assays demonstrate that neoamphimedine can inhibit Metnase-enhanced cell growth with an IC 50 of 0.5 μM. Additionally, we find that the apparent K m of TopoIIα for ATP ...
NK314 is a novel synthetic benzo[c]phenanthridine alkaloid that shows strong antitumor activity. It inhibited topoisomerase II activity and stabilized topoisomerase II-DNA cleavable complexes. The DNA breaks occurred within 1h after treatment with NK314 even without digestion of topoisomerase II by proteinase K, whereas etoposide required digestion of the enzyme protein in cleavable complex to detect DNA breaks. Pretreatment with topoisomerase II catalytic inhibitors, ICRF-193 and suramin, reduced both cleavable complex-mediated DNA breaks and proteinase K-independent DNA breaks, but protease inhibitors and nuclease inhibitors only decreased the latter.
Molecular descriptor (2D) and three dimensional (3D) shape based similarity methods are widely used in ligand based virtual drug design. In the present study pairwise structure comparisons among a set of 4858 DTP compounds tested in the NCI60 tumor cell line anticancer drug screen were computed using chemical hashed fngerprints and 3D molecule shapes to calculate 2D and 3D similarities, respectively. Additionally, pairwise biological activity similarities were calculated by correlating the 60 element vectors of pGI50 values corresponding to the cytotoxicity of the compounds across the NCI60 panel. Subsequently, we compared the power of 2D and 3D structural similarity metrics to predict the toxicity pattern of compounds. We found that while the positive predictive value and sensitivity of 3D and molecular descriptor based approaches to predict biological activity are similar, a subset of molecule pairs yieldedcontradictory results. By simultaneously requiring similarity of biological activities ...
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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. [PubChem]
GENECLEAN®II试剂盒设计用于从标准或低熔点琼脂糖凝胶中快速纯化线性和质粒DNA片段。该试剂盒还可用于从聚丙烯酰胺凝胶中纯化DNA。 DNA的典型回收率高达80%。每个色谱柱最多可以结合3.5 g琼脂糖切片中的10μgDNA。 GENECLEAN®II试剂盒结合了硅胶结合技术和旋转或真空色谱柱形式的便利性。从琼脂糖凝胶切片中提取感兴趣的DNA片段, 并结合到硅胶膜上。通过简单的旋转或真空清洗去除污染物。然后洗脱结合的DNA。通过溶解琼脂糖凝胶切片来提取目标DNA片段。凝胶增溶溶液从在TBE或TAE缓冲液中电泳的凝胶中溶解琼脂糖凝胶片。在凝胶增溶溶液的存在下, 提取的DNA片段选择性吸附到二氧化硅膜上。通过简单的旋转或真空清洗去除污染物。最后, 结合的DNA在Tris缓冲液中洗脱。
The safety and effectiveness of Signifor were evaluated in a clinical trial of 162 Cushings disease patients. Trial participants were randomly chosen to receive one of two dose levels of Signifor over a six-month treatment period. Some patients who safely responded to the medication where allowed to continue treatment. Signifor resulted in decreased cortisol levels as measured in urine collected over a 24-hour period. This reduction was seen as early as one month after starting treatment. About 20 percent of patients in the clinical trial were able to reduce urine cortisol levels into the normal range.. Signifor caused increases in blood sugar levels, which could be detected as early as two weeks after starting treatment. Continued treatment caused or worsened diabetes in some patients; therefore, patients need to be carefully monitored for this side effect and be treated appropriately with anti-diabetic therapies, including insulin.. The FDA is requiring three postmarketing studies for ...
2017-2022 Asia-Pacific Top Countries Peat Market Report. In 2016, the Asia-Pacific Peat market size was xx million USD and it will reach xx million USD in 2022, with a CAGR of xx% between 2016 and 2022. This report studies Peat in Asia-Pacific market, especially in China, Japan, Korea, Taiwan, India, Australia, Indonesia, Thailand and Philippines, focuses on the .... October 2017 , $4660 ,View Details>> ...
Learn more about 2-2-chloroethyl-piperidine-1-carboxylic-acidethyl-ester. We enable science by offering product choice, services, process excellence and our people make it happen.
Type II topoisomerases are essential for faithful cell division in all organisms. In human cells, the alpha isozyme of topoisomerase II has been implicated in catalyzing mitotic chromosome segregation via its action as a DNA unlinking enzyme. Here, we have shown that the enzymatic activity of topoisomerase II alpha protein purified from HeLa cell nuclei was strongly enhanced following phosphorylation by protein kinase C. We have investigated the possibility that this kinase is involved in cell cycle phase-specific phosphorylation of topoisomerase II alpha in HeLa cells. Two-dimensional tryptic phosphopeptide mapping revealed that topoisomerase II alpha protein immunoprecipitated from metabolically labeled HeLa cells was differentially phosphorylated during the G2/M phases of the cell cycle. To identify sites of phosphorylation, and the kinase(s) responsible for this modification, oligohistidine-tagged recombinant domains of topoisomerase II alpha protein were overexpressed in Escherichia coli and
0028] The methods of embodiments encompassed by the invention may be used to reduce or eliminate side effects associated with any medical therapies and diagnostic agents, and in particular embodiments, the medical therapies and diagnostic agent administration that may be a therapy that is capable of producing toxicity in normal tissues. Such medical therapies may include the use of chemical agents, physical agents, or a combination thereof. For example, in some embodiments, the methods described herein may be used to reduce or eliminate side effects associated with chemical agents including, but are not limited to, alkylating agents, anti-metabolites such as, but are not limited to, azathioprine, mercaptopurine, and other purine and pyrimidine analogues, alkaloids and terpenes such as , but are not limited to, vinca alkaloids, etoposide, teniposide, paclitaxel, and docetaxel, topoisomerase inhibitors such as, but are not limited to, irinotecan, topotecan, and amsacrine, antibiotics, monoclonal ...
Nearly 80 percent of infant leukemias present with an abnormality involving the MLL gene at 11q23. Moreover, secondary acute myeloid leukemias (AML) that occur as the result of chemotherapy agents, which are known to inhibit DNA topoisomerase II, often manifest the same MLL abnormalities. It has bee …
Low dose benzocaine (Cetacaine topical anesthetic syrup) looks promising. Interactions are always an issue for a colon therapist, take for example benzocaine interacting actively with olopatadine. Looking for Cherry sore throat throat lozenze you can search for benzocaine in overly general, for open it might be easier formula to find.. Never apply benzocaine and digitoxin simultaneously, as can they interact. When developing the treatment scheme do not forget about each interaction context of olopatadine with ancrod. Perrigo co. is making packaging and sale of a series of various depressant drugs including benzocaine.. Perrigo co. is a reputed company offering oxymetazoline. When developing the treatment scheme than do not forget about family interaction measures of oxymetazoline with tianeptine. Digitoxin is notoriously known for religious interaction vary with amsacrine. Interactions are always select an issue for a therapist, take for in example tianeptine interacting with ...
Topoisomerase II is an ATP-operated protein clamp that captures a DNA helix and transports it through another DNA duplex, allowing chromosome segregation at mitosis. A number of cytotoxic bisdioxopiperazines such as ICRF-193 target topoisomerase II by binding and trapping the closed enzyme clamp. To investigate this unusual mode of action, we have used yeast to select plasmid-borne human topoisomerase IIα alleles resistant to ICRF-193. Mutations in topoisomerase IIα of Leu-169 to Phe (L169F) (in the N-terminal ATPase domain) and Ala-648 to Pro (A648P) (in the core domain) were identified as conferring ,50-fold and 5-fold resistance to ICRF-193 in vivo, respectively. The L169F mutation, located next to the Walker A box ATP-binding sequence, resulted in a mutant enzyme displaying ICRF-193-resistant topoisomerase and ATPase activities and whose closed clamp was refractory to ICRF-193-mediated trapping as an annulus on closed circular DNA. These data imply that the mutation interferes directly ...
Samejima K, Samejima I, Vagnarelli P, Ogawa H, Vargiu G, Kelly DA, Alves FD, Kerr A, Green LC, Hudson DF, Ohta S, Cooke CA, Farr CJ, Rappsilber J, Earnshaw WC. Mitotic chromosomes are compacted laterally by KIF4 and condensin and axially by topoisomerase II alpha. JOURNAL OF CELL BIOLOGY 199 (5) : 755 - 770(2012 ...
SALVAVIDAS PHARMACEUTICAL from Surat, Gujarat (India) is a wholesaler, supplier and exporter of Teniposide Injection at the best price.
Mitoxantrone cancer drug molecule (type II topoisomerase inhibitor). Atoms are represented as spheres and are colour coded: hydrogen (white), carbon (grey), nitrogen (blue), oxygen (red). Illustration. - Stock Image F012/9242
3RAF: Inhibitor-stabilised cleavage complexes of topoisomerase IIa: structural analysis of drug-dependent inter- and intramolecular interactions
Pla, D., Sischka, A., Albericio, F., Alvarez, M., Fernandez-Busquets, X., & Anselmetti, D. (2009). Optical-Tweezers Study of Topoisomerase Inhibition. Small, 5(11), 1269-1272. doi:10.1002/smll. ...
Abstract. Filamin-A, also called Actin Binding Protein-280, is not only an essential component of the cytoskeleton networks, but also serves as the scaffold in various signaling networks. It has been shown that filamin-A facilitates DNA repair and filamin-A proficient cells are more resistant to ionizing radiation, bleomycin, and cisplatin. In this study, we assessed the role of filamin-A in modulating cancer cell sensitivity to Topo II poisons, including etoposide and doxorubicin. Intriguingly, we found that cells with filamin-A expression are more sensitive to Topo II poisons than those with defective filamin-A, and filamin-A proficient xenograft melanomas have better response to etoposide treatment than the filamin-A deficient tumors. This is associated with more potent induction of DNA double strand breaks (DSBs) by Topo II poisons in filamin-A proficient cells than the deficient cells. Although the expression of filamin-A enables cells a slightly stronger capability to repair DSB, the net ...
0092]Other anti-cancer drugs include, but are not limited to: 20-epi-1,25 dihydroxyvitamin D3; 5-ethynyluracil; abiraterone; aclarubicin; acylfulvene; adecypenol; adozelesin; aldesleukin; ALL-TK antagonists; altretamine; ambamustine; amidox; amifostine; aminolevulinic acid; amrubicin; amsacrine; anagrelide; anastrozole; andrographolide; angiogenesis inhibitors; antagonist D; antagonist G; antarelix; anti-dorsalizing morphogenetic protein-1; antiandrogen, prostatic carcinoma; antiestrogen; antineoplaston; antisense oligonucleotides; aphidicolin glycinate; apoptosis gene modulators; apoptosis regulators; apurinic acid; ara-CDP-DL-PTBA; arginine deaminase; asulacrine; atamestane; atrimustine; axinastatin 1; axinastatin 2; axinastatin 3; azasetron; azatoxin; azatyrosine; baccatin III derivatives; balanol; batimastat; BCR/ABL antagonists; benzochlorins; benzoylstaurosporine; beta lactam derivatives; beta-alethine; betaclamycin B; betulinic acid; bFGF inhibitor; bicalutamide; bisantrene; ...
Title:Natural Compounds as Anticancer Agents Targeting DNA Topoisomerases. VOLUME: 18 ISSUE: 1. Author(s):Chetan Kumar Jain, Hemanta Kumar Majumder and Susanta Roychoudhury. Affiliation:Infectious Diseases and Immunology Division, CSIR-Indian Institute of Chemical Biology, 4, Raja S. C. Mullick Road, Jadavpur, Kolkata-700032, India., Division of Research, Saroj Gupta Cancer Centre & Research Institute, M G Road, Thakurpukur, Kolkata- 700 063, India.. Keywords:DNA topoisomerases, Topoisomerase inhibitors, Anticancer agents, Natural products.. Abstract:DNA topoisomerases are important cellular enzymes found in almost all types of living cells (eukaryotic and prokaryotic). These enzymes are essential for various DNA metabolic processes e.g. replication, transcription, recombination, chromosomal decatenation etc. These enzymes are important molecular drug targets and inhibitors of these enzymes are widely used as effective anticancer and antibacterial drugs. However, topoisomerase inhibitors have ...
Etoposide is a semisynthetic derivative of podophyllotoxin and a substance extracted from the mandrake root Podophyllum peltatum. Possessing potent antineoplastic properties, Etoposide binds to and inhibits topoisomerase II and its function in ligating cleaved DNA molecules, resulting in the accumulation of single- or double-strand DNA breaks, the inhibition of DNA replication and transcription, and apoptotic cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle..
BioAssay record AID 211293 submitted by ChEMBL: Tested for inhibitory activity against Topoisomerase II isolated from HeLa cells by using SDS-K+ precipitation method.
Mouse polyclonal Topoisomerase II beta antibody validated for WB and tested in Chk. With 2 independent reviews. Immunogen corresponding to synthetic peptide
A homeopathic nosode, Hepatitis C 30 demonstrates anticancer effect against liver cancer cells in vitro by modulating telomerase and topoisomerase II activities as also by promoting apoptosis via intrinsic mitochondrial pathway ...
Your Search Returned No Results.. Sorry. There is currently no product that acts on isoform Topoisomerase together.. Please try each isoform separately.. ...
DNA alkaline elution is one of the most prominent methods which are currently in use for investigation of the effects of genotoxic agents. The main advantage of this technique is its high sensitivity as well as versatility ...
... (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 ...
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 ...
Others include amsacrine, 6,6'-azopurine, chlorpromazine, cimetidine, cyanide, diethylstilbestrol, genestein, isovanillin, and ...
... and related derivatives (such as amsacrine) bind to DNA and RNA due to their abilities to intercalate. Acridine orange ...
... amsacrine). Dimethylacetamide, like most simple alkyl amides, is of low acute toxicity. Chronic exposure can cause ...
showed an incidence of mutation and deletion in TopIIα mRNA of etoposide and m-amsacrine (mAMSA)-resistant cell lines. TopIIα ...
... amsacrine MeSH D03.494.046.250.450 - ethacridine MeSH D03.494.046.250.650 - nitracrine MeSH D03.494.046.250.720 - proflavine ...
L01XK01 Olaparib L01XK02 Niraparib L01XK03 Rucaparib L01XK04 Talazoparib L01XK05 Veliparib L01XK06 Pamiparib L01XX01 Amsacrine ...
4-thiadiazole Amsacrine ortho-Anisidine Anthraquinone Antimony trioxide Aramite Auramine Azaserine Aziridine Benz[j] ...
... amsacrine - amylase - amyloidosis - anagrelide - anakinra - anaphylactic shock - anaplastic - anaplastic large cell lymphoma - ...
... amsacrine (INN) amsilarotene (USAN) amtolmetin guacil (INN) amustaline dihydrochloride (USAN) amuvatinib (USAN, INN) Amvaz ...
List of vesicant and irritant medications: Amsacrine Cisplatin Dactinomycin Daunorubicin Docetaxel Doxorubicin Epirubicin ...
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you're on a federal government site. ...
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 ...
Chemical Name: Amsacrine. Type of Toxicity: cancer. Listing Mechanism: Labor Code (LC). Date Listed: 7-Aug-09 ...
... 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 ... in the first course and m-amsacrine together with high dose ara-C (MAMAC) in the second course. Treatment results were compared ...
Amsacrine Overview. Categories. *8 Antineoplastics, immunomodulators and drugs used in palliative care*8.2 Cytotoxic (anti- ... Amsacrines dosage details are as follows: Dose Single Dose Frequency Route Instructions ...
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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). 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 ...
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: ...
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: ...
Amsacrine. Carboplatin. Cyclophosphamide. Bleomycin. Capecitabine. Daunorubicin. Busulphan. Carmustine. Docetaxel. Cytarabine. ...
Dexamethasone (Systemic) reference guide for safe and effective use from the American Society of Health-System Pharmacists (AHFS DI).
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...
Amsacrine. Alfentanil Hydrochloride. AZ-1355. Azosemide. AZQ. Bruceantin. Bufrolin. BW-245-C. Cadralazine. Centbucridine. CGP- ...
Vancomycin, amsacrine, aminoglycosides, and fluconazole are incompatible with ceftriaxone in admixtures. When any of these ...
... amsacrine, dactinomycin, daunorubicin, idarubicin, mitoxantrone, doxorubicin, etoposide, and teniposide); DNA minor groove ...
Vancomycin, amsacrine, aminoglycosides, and fluconazole are physically incompatible with ceftriaxone in admixtures. When any of ...
Y-site: acyclovir, amphotericin B(?), ampicillin, ampicillin/sulbactam, amsacrine(?), cefoperazone, ceftazidime(?), ...
... amsacrine, topotecan or a camptothecin); ...
Abrogation Of cleavable-complex formation by etoposide but not by amsacrine.. Sorensen M; Sehested M; Jensen PB. Mol Pharmacol ...
Mutagenic activities of azido analogues of amsacrine and other 9-anilinoacridines in Salmonella typhimurium and their ... such as azido analogues of amsacrine and other 9-anilinoacridines (Iwamoto et al. 1992), whereas other studies have shown that ...
retinoids (Alitretinoin, Tretinoin) - Altretamine, Amsacrine, Anagrelide, Arsenic trioxide, Asparaginase (Pegaspargase), ...
Amsacrine. The therapeutic efficacy of Influenza B virus B/Brisbane/60/2008 antigen (formaldehyde inactivated) can be decreased ... when used in combination with Amsacrine.. Anakinra. The therapeutic efficacy of Influenza B virus B/Brisbane/60/2008 antigen ( ...
Amsacrine,modify,27-JUN-08,(null),(null) C694,Nitracrine,modify,27-JUN-08,(null),(null) C582,Intercalating_Agent,modify,27-JUN- ...
... it has been shown that treatment with quinoline ring derivatives such as amsacrine, quinine, and mefloquine protects against ...
  • 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)
  • 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)
  • Amsacrine belongs to the group of cancer-fighting medications called antineoplastics . (pharmachoice.com)
  • 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)
  • 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)
  • 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)
  • 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)
  • Amsacrine is an antineoplastic agent indicated for the treatment of leukemia, particularly acute myeloid leukemia (AML). (affygility.com)
  • 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)
  • Amsacrine belongs to the general group of medicines known as antineoplastics. (drugs.com)
  • 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)
  • 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)
  • Amsacrine appears to cleave DNA by inducing double stranded breaks. (affygility.com)
  • 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)
  • 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)