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.
Acridines are heterocyclic aromatic organic compounds containing two nitrogen atoms at positions 1 and 3 of a planar, unsaturated ring system, which have been widely used in chemotherapy and have also found applications in dye industries and fluorescence microscopy.
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)

Amsacrine is a chemotherapeutic agent, which means it is a medication used to treat cancer. It is classified as an antineoplastic drug, and more specifically, as an intercalating agent and a topoisomerase II inhibitor. Amsacrine works by intercalating, or inserting itself, into the DNA of cancer cells, which prevents the DNA from replicating and ultimately leads to the death of the cancer cell. It is primarily used in the treatment of acute myeloid leukemia (AML) and other hematologic malignancies.

The chemical name for Amsacrine is 5-[3-amino-1-(3-aminopropyl)-2-hydroxybut-1-yloxy]-8-chloro-1,4-naphthoquinone. It has a molecular formula of C16H17ClNO5 and a molecular weight of 359.8 g/mol.

Amsacrine is typically administered intravenously, and its use is usually reserved for patients who have not responded to other forms of chemotherapy. It may be used in combination with other anticancer drugs as part of a treatment regimen. As with any chemotherapeutic agent, Amsacrine can have significant side effects, including nausea, vomiting, and hair loss. It can also cause damage to the heart and other organs, so it is important for patients to be closely monitored during treatment.

It's worth noting that while Amsacrine can be an effective treatment for some types of cancer, it is not a cure-all, and its use must be carefully considered in the context of each individual patient's medical history and current health status.

Aminoacridines are a group of synthetic chemical compounds that contain an acridine nucleus, which is a tricyclic aromatic structure, substituted with one or more amino groups. These compounds have been studied for their potential therapeutic properties, particularly as antiseptics and antibacterial agents. However, their use in medicine has declined due to the development of newer and safer antibiotics. Some aminoacridines also exhibit antimalarial, antifungal, and antiviral activities. They can intercalate into DNA, disrupting its structure and function, which is thought to contribute to their antimicrobial effects. However, this property also makes them potentially mutagenic and carcinogenic, limiting their clinical use.

DNA topoisomerases are enzymes that regulate the topological state of DNA during various cellular processes such as replication, transcription, and repair. They do this by introducing temporary breaks in the DNA strands and allowing the strands to rotate around each other, thereby relieving torsional stress and supercoiling. Topoisomerases are classified into two types: type I and type II.

Type II topoisomerases are further divided into two subtypes: type IIA and type IIB. These enzymes function by forming a covalent bond with the DNA strands, cleaving them, and then passing another segment of DNA through the break before resealing the original strands. This process allows for the removal of both positive and negative supercoils from DNA as well as the separation of interlinked circular DNA molecules (catenanes) or knotted DNA structures.

Type II topoisomerases are essential for cell viability, and their dysfunction has been linked to various human diseases, including cancer and neurodegenerative disorders. They have also emerged as important targets for the development of anticancer drugs that inhibit their activity and induce DNA damage leading to cell death. Examples of type II topoisomerase inhibitors include etoposide, doxorubicin, and mitoxantrone.

Topoisomerase II inhibitors are a class of anticancer drugs that work by interfering with the enzyme topoisomerase II, which is essential for DNA replication and transcription. These inhibitors bind to the enzyme-DNA complex, preventing the relaxation of supercoiled DNA and causing DNA strand breaks. This results in the accumulation of double-stranded DNA breaks, which can lead to apoptosis (programmed cell death) in rapidly dividing cells, such as cancer cells. Examples of topoisomerase II inhibitors include etoposide, doxorubicin, and mitoxantrone.

Teniposide is a synthetic podophyllotoxin derivative, which is an antineoplastic agent. It works by interfering with the DNA synthesis and function of cancer cells, leading to cell cycle arrest and apoptosis (programmed cell death). Teniposide is primarily used in the treatment of acute lymphoblastic leukemia (ALL) and other malignancies in children. It is often administered through intravenous infusion and is typically used in combination with other chemotherapeutic agents.

The medical definition of Teniposide can be stated as:

Teniposide, chemically known as (4'-demethylepipodophyllotoxin 9-[4,6-O-(R)-benzylidene-α-L-glucopyranoside]), is a semi-synthetic podophyllotoxin derivative with antineoplastic activity. It inhibits DNA topoisomerase II, leading to the formation of DNA-topoisomerase II cleavable complexes, G2 arrest, and apoptosis in cancer cells. Teniposide is primarily used in the treatment of acute lymphoblastic leukemia (ALL) and other malignancies in children, often administered through intravenous infusion and typically used in combination with other chemotherapeutic agents.

Intercalating agents are chemical substances that can be inserted between the stacked bases of DNA, creating a separation or "intercalation" of the base pairs. This property is often exploited in cancer chemotherapy, where intercalating agents like doxorubicin and daunorubicin are used to inhibit the replication and transcription of cancer cells by preventing the normal functioning of their DNA. However, these agents can also have toxic effects on normal cells, particularly those that divide rapidly, such as bone marrow and gut epithelial cells. Therefore, their use must be carefully monitored and balanced against their therapeutic benefits.

'Dipodomys' is the genus name for kangaroo rats, which are small rodents native to North America. They are called kangaroo rats due to their powerful hind legs and long tails, which they use to hop around like kangaroos. Kangaroo rats are known for their ability to survive in arid environments, as they are able to obtain moisture from the seeds they eat and can concentrate their urine to conserve water. They are also famous for their highly specialized kidneys, which allow them to produce extremely dry urine.

Aminacrine is a type of medication known as an antineoplastic agent or chemotherapeutic drug. It is primarily used in the treatment of certain types of cancer. Aminacrine works by interfering with the DNA replication process within cancer cells, which helps to inhibit the growth and proliferation of these cells.

The chemical name for aminacrine is 9-aminoacridine hydrochloride monohydrate. It has a yellowish crystalline appearance and is typically administered intravenously in a hospital setting. Common side effects of aminacrine include nausea, vomiting, diarrhea, mouth sores, and hair loss. More serious side effects can include heart rhythm abnormalities, seizures, and lung or kidney damage.

It's important to note that the use of aminacrine is typically reserved for cases where other cancer treatments have not been effective, due to its potential for serious side effects. As with all medications, it should be used under the close supervision of a healthcare professional.

Etoposide is a chemotherapy medication used to treat various types of cancer, including lung cancer, testicular cancer, and certain types of leukemia. It works by inhibiting the activity of an enzyme called topoisomerase II, which is involved in DNA replication and transcription. By doing so, etoposide can interfere with the growth and multiplication of cancer cells.

Etoposide is often administered intravenously in a hospital or clinic setting, although it may also be given orally in some cases. The medication can cause a range of side effects, including nausea, vomiting, hair loss, and an increased risk of infection. It can also have more serious side effects, such as bone marrow suppression, which can lead to anemia, bleeding, and a weakened immune system.

Like all chemotherapy drugs, etoposide is not without risks and should only be used under the close supervision of a qualified healthcare provider. It is important for patients to discuss the potential benefits and risks of this medication with their doctor before starting treatment.

Cytarabine is a chemotherapeutic agent used in the treatment of various types of cancer, including leukemias and lymphomas. Its chemical name is cytosine arabinoside, and it works by interfering with the DNA synthesis of cancer cells, which ultimately leads to their death.

Cytarabine is often used in combination with other chemotherapy drugs and may be administered through various routes, such as intravenous (IV) or subcutaneous injection, or orally. The specific dosage and duration of treatment will depend on the type and stage of cancer being treated, as well as the patient's overall health status.

Like all chemotherapy drugs, cytarabine can cause a range of side effects, including nausea, vomiting, diarrhea, hair loss, and an increased risk of infection. It may also cause more serious side effects, such as damage to the liver, kidneys, or nervous system, and it is important for patients to be closely monitored during treatment to minimize these risks.

It's important to note that medical treatments should only be administered under the supervision of a qualified healthcare professional, and this information should not be used as a substitute for medical advice.

I'm sorry for any confusion, but "Razoxane" is not a medical term that has a widely accepted or specific definition in the field of medicine. It is possible that you may be referring to "razoxane," which is a medication used in the treatment of certain types of cancer. Razoxane is an antineoplastic agent, which means it is a drug that is used to treat cancer. It works by interfering with the formation of blood vessels that supply tumors, which can help to slow or stop the growth of the tumor.

It is important to note that the use of razoxane is not widely accepted and it is not a commonly used cancer treatment. It is typically used only in certain specific circumstances and when other treatments have not been effective. As with any medication, razoxane should be used under the close supervision of a healthcare professional, and it is important to be aware of the potential risks and benefits.

Anticipatory vomiting is a condition characterized by the experience of nausea and vomiting in response to a stimulus that a person has learned to associate with previous episodes of emesis (vomiting). It is often observed in patients who have undergone chemotherapy or radiation therapy for cancer treatment. The sight, smell, taste, or even thought of the treatment setting can trigger the body's vomiting reflex, even before any medication is administered. This condition can be distressing and may negatively impact a patient's quality of life. Various interventions, such as behavioral therapies, relaxation techniques, and medications, can be used to manage anticipatory vomiting.

Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.

Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.

It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.

Mitoxantrone is a synthetic antineoplastic anthracenedione drug, which means it is used to treat cancer. Its medical definition can be found in various authoritative sources such as the Merck Manual or Stedman's Medical Dictionary. Here's a brief version of the definition from MedlinePlus, a service of the US National Library of Medicine:

"Mitoxantrone is used to treat certain types of cancer (e.g., breast cancer, leukemia, non-Hodgkin's lymphoma). It works by slowing or stopping the growth of cancer cells. Mitoxantrone belongs to a class of drugs known as antitumor antibiotics."

Please note that this is a simplified definition meant for general information purposes and does not include all the details that might be present in a comprehensive medical definition. Always consult a healthcare professional or refer to authoritative resources for accurate, detailed, and up-to-date information.

Acridines are a class of heterocyclic aromatic organic compounds that contain a nucleus of three fused benzene rings and a nitrogen atom. They have a wide range of applications, including in the development of chemotherapeutic agents for the treatment of cancer and antibacterial, antifungal, and antiparasitic drugs. Some acridines also exhibit fluorescent properties and are used in research and diagnostic applications.

In medicine, some acridine derivatives have been found to intercalate with DNA, disrupting its structure and function, which can lead to the death of cancer cells. For example, the acridine derivative proflavin has been used as an antiseptic and in the treatment of certain types of cancer. However, many acridines also have toxic side effects, limiting their clinical use.

It is important to note that while acridines have potential therapeutic uses, they should only be used under the supervision of a qualified healthcare professional, as they can cause harm if not used properly.

Topoisomerase I inhibitors are a class of anticancer drugs that work by inhibiting the function of topoisomerase I, an enzyme that plays a crucial role in the relaxation and replication of DNA. By inhibiting this enzyme's activity, these drugs interfere with the normal unwinding and separation of DNA strands, leading to DNA damage and ultimately cell death. Topoisomerase I inhibitors are used in the treatment of various types of cancer, including colon, small cell lung, ovarian, and cervical cancers. Examples of topoisomerase I inhibitors include camptothecin, irinotecan, and topotecan.

Daunorubicin is an anthracycline antibiotic used in the treatment of various types of cancer, including leukemia, Hodgkin's lymphoma, and breast cancer. It works by intercalating with DNA and inhibiting topoisomerase II, which results in DNA damage and ultimately cell death.

The drug is administered intravenously and may cause side effects such as nausea, vomiting, hair loss, mouth sores, and damage to the heart muscle (cardiotoxicity) with long-term use. Regular monitoring of cardiac function is recommended during treatment with daunorubicin.

It's important to note that this medication should only be used under the supervision of a qualified healthcare professional, as it can have serious and potentially life-threatening consequences if not used correctly.

Asparaginase is a medication that is used in the treatment of certain types of cancer, such as acute lymphoblastic leukemia (ALL) and non-Hodgkin lymphoma (NHL). It is an enzyme that breaks down the amino acid asparagine, which is a building block of proteins. Some cancer cells are unable to produce their own asparagine and rely on obtaining it from the bloodstream. By reducing the amount of asparagine in the blood, asparaginase can help to slow or stop the growth of these cancer cells.

Asparaginase is usually given as an injection into a muscle (intramuscularly) or into a vein (intravenously). It may be given alone or in combination with other chemotherapy drugs. The specific dosage and duration of treatment will depend on the individual's medical history, the type and stage of cancer being treated, and how well the person tolerates the medication.

Like all medications, asparaginase can cause side effects. Common side effects include nausea, vomiting, loss of appetite, and changes in liver function tests. Less common but more serious side effects may include allergic reactions, pancreatitis, and blood clotting problems. It is important for patients to discuss the potential risks and benefits of asparaginase with their healthcare provider before starting treatment.

Drug resistance, also known as antimicrobial resistance, is the ability of a microorganism (such as bacteria, viruses, fungi, or parasites) to withstand the effects of a drug that was originally designed to inhibit or kill it. This occurs when the microorganism undergoes genetic changes that allow it to survive in the presence of the drug. As a result, the drug becomes less effective or even completely ineffective at treating infections caused by these resistant organisms.

Drug resistance can develop through various mechanisms, including mutations in the genes responsible for producing the target protein of the drug, alteration of the drug's target site, modification or destruction of the drug by enzymes produced by the microorganism, and active efflux of the drug from the cell.

The emergence and spread of drug-resistant microorganisms pose significant challenges in medical treatment, as they can lead to increased morbidity, mortality, and healthcare costs. The overuse and misuse of antimicrobial agents, as well as poor infection control practices, contribute to the development and dissemination of drug-resistant strains. To address this issue, it is crucial to promote prudent use of antimicrobials, enhance surveillance and monitoring of resistance patterns, invest in research and development of new antimicrobial agents, and strengthen infection prevention and control measures.

... (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 ...
L01XL05 Ciltacabtagene autoleucel L01XL06 Brexucabtagene autoleucel L01XL07 Idecabtagene vicleucel L01XX01 Amsacrine L01XX02 ...
4-thiadiazole Amsacrine Arecoline Aspartame Benz[j]aceanthrylene Benz[a]anthracene Benzo[b]fluoranthene Benzo[j]fluoranthene ...
... 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 ...
Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. It has been used in acute lymphoblastic leukemia ... Ketron AC, Denny WA, Graves DE, Osheroff N (February 2012). "Amsacrine as a Topoisomerase II Poison: Importance of Drug-DNA ... Horstmann MA, Hassenpflug WA, zur Stadt U, Escherich G, Janka G, Kabisch H (December 2005). "Amsacrine combined with etoposide ... Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II. In contrast, the ...
Hazard - P - B - T - Risk Cannot be excluded. Environmental information is missing on fass.se. It is voluntary for manufacturers to provide information about environmental impact on fass.se. ...
Amsacrine (Toxic Effects in Humans- 2) → Amsacrine (Toxic Effects in Humans- 4) ... Amsacrine (Toxic Effects in Humans- 3). In this article we will discuss Amsacrine (Toxic Effects in Humans- 3) ... In this article, we will discuss Amsacrine (Toxic Effects in Humans- 3). So, lets get started. ... Nausea, vomiting and mucositis are common after administration of amsacrine. Diarrhoea occurs in about 10-20% of patients ( ...
Acyclovir reference guide for safe and effective use from the American Society of Health-System Pharmacists (AHFS DI).
Amsacrine / pharmacology * Chromatin / ultrastructure* * Chromosome Mapping / methods* * Chromosomes, Human, Pair 7 * Cosmids ...
Please make sure that HealthWell currently has a fund for your diagnosis/indication and that your medication is covered under that fund by visiting our Disease Funds listing. If we do not have a fund that currently covers your diagnosis, please check back as we frequently open and reopen programs as funding becomes available. The Foundation is able to help patients receiving treatment for indications for which we currently have an open fund. We can only assist with medications that have been prescribed to treat the disease/covered diagnosis. You will be asked to provide the Foundation with the patients diagnosis, which must be verified by a physician, nurse practitioner, or physician assistants signature. The patient must receive treatment in the United States.. ...
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. Date of publication: 30/07/2015. *Anthrax Antigen Filtrate (Biothrax). Date of publication: 31/07/2019 ...
Primary therapy of acute promyelocytic leukemia: results of amsacrine- and daunorubicin-based therapy. Blood 1984; 63: 211-212. ... amsacrine and prednisone. Cunningham et al.15 reported a median survival of 6 weeks following relapse. A variety of reinduction ... Treatment of recurrent promyelocytic leukemia with a combination regimen utilizing amsacrine, cytosine arabinoside and 6- ...
Vancomycin, amsacrine, aminoglycosides, and fluconazole are incompatible with ceftriaxone in admixtures. When any of these ...
Amsacrine. The risk or severity of adverse effects can be increased when Amsacrine is combined with Pegcetacoplan. ...
retinoids (Alitretinoin, Tretinoin) - Altretamine, Amsacrine, Anagrelide, Arsenic trioxide, Asparaginase (Pegaspargase), ...
6. Cytotoxic action and cell cycle effects of ALGA, a peptidic derivative of the antileukemic drug amsacrine. 257-64页 作者:M, ...
Amsacrine 1 mg/ml 253. Lorazepam 0.5 mg/ml Atracurium besylate 0.5 mg/ml 402. ...
Y-site: Amifostine, amsacrine, aztreonam, cefepime, dobutamine, dopamine, fludarabine, foscarnet, gemcitabine, idarubicin, ...
Potential Mechanisms Governing Sensitivity of HL-60 Cells to Amsacrine and Etoposide Dale R. Grabowski, Katherine A. Holmes, ... Potential Mechanisms Governing Sensitivity of HL-60 Cells to Amsacrine and Etoposide Dale R. Grabowski, Katherine A. Holmes, ... Potential Mechanisms Governing Sensitivity of HL-60 Cells to Amsacrine and Etoposide Dale R. Grabowski, Katherine A. Holmes, ... Potential Mechanisms Governing Sensitivity of HL-60 Cells to Amsacrine and Etoposide Dale R. Grabowski, Katherine A. Holmes, ...
... amsacrine; bestrabucil; bisantrene; edatraxate; defofamine; demecolcine; diaziquone; elfornithine; elliptinium acetate; an ...
38] - Amsacrine, bleomycin, busulfan, carboplatin, chlorambucil, cisplatin, cyclophosphamide, cytarabine, daunorubicin, ...
High-Dose Cytarabine Consolidation With or Without Additional Amsacrine and Mitoxantrone in Acute Myeloid Leukemia: Results of ...
Amsacrine (m-AMSA) is an anticancer agent that displays activity against refractory acute leukemias as well as Hodgkins and ...
Amsacrine. ️⏏️ ينتمي Amsacrine إلى مجموعة الأدوية العامة المعروفة باسم مضادات الأورام. يتم استخدامه لعلاج ابيضاض الدم الحاد ...
INSUFFISANCE CARDIAQUE ACLARUBICINE CHLORHYDRATE ALBUMINE HUMAINE PLASMATIQUE ALDESLEUKINE ALPRENOLOL CHLORHYDRATE AMSACRINE ...
Amsacrine Formulary 08.01.05 CDK inhibitors 08.01.05 Arsenic trioxide. Arsenic Trioxide Formulary *NECDAG approved relapsed or ...
Amsa (Amsacrine) should not be used by anyone who:. *is allergic to Amsa (Amsacrine) or to any of the ingredients of the ... These factors may affect how you should use Amsa (Amsacrine).. Blood clotting: Amsa (Amsacrine) can reduce the number of ... Amsa (Amsacrine) belongs to the group of cancer-fighting medications called antineoplastics. Amsa (Amsacrine) is used to treat ... Amsa (Amsacrine) is always given under the supervision of a doctor. Very careful handling of Amsa (Amsacrine) is required. It ...
A knowledge graph of biological entities such as genes, gene functions, diseases, phenotypes and chemicals. Embeddings are generated with Walking RDF and OWL method ...
Looking for Amsacrine found 2 matches. Open monograph to display formulary status. BNF Category. ...
  • High-Dose Cytarabine Consolidation With or Without Additional Amsacrine and Mitoxantrone in Acute Myeloid Leukemia: Results of the Prospective Randomized AML2003 Trial. (stembook.org)
  • Including mitoxantrone and amsacrine. (thehasse.org)
  • Instead of anthracyclins, remission induction programs may incorporate mitoxantrone and amsacrine. (ashpublications.org)
  • When the white blood cell count is under control without medication after treatment with Amsa (Amsacrine), the person is said to be in remission. (pocketpills.com)
  • While in remission, the dose of Amsa (Amsacrine) is usually reduced and given every 4 to 8 weeks, depending on the number of white blood cells in the blood. (pocketpills.com)
  • Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. (wikipedia.org)
  • Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II. (wikipedia.org)
  • Amsa (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. (pocketpills.com)
  • Amsa (Amsacrine) kills cancer cells by interfering with their growth and reproduction. (pocketpills.com)
  • As well as interfering with the growth and reproduction of cancer cells, Amsa (Amsacrine) can interfere with some of your normal cells. (pocketpills.com)
  • Amsa (Amsacrine) belongs to the group of cancer-fighting medications called antineoplastics. (pocketpills.com)
  • Your doctor may have suggested Amsa (Amsacrine) for conditions other than those listed in these drug information articles. (pocketpills.com)
  • Nausea, vomiting and mucositis are common after administration of amsacrine. (ptmasterguide.com)
  • If you miss an appointment to receive Amsa (Amsacrine), contact your doctor as soon as possible to reschedule your appointment. (pocketpills.com)
  • Amsacrine (m-AMSA) is an anticancer agent that displays activity against refractory acute leukemias as well as Hodgkin's and non-Hodgkin's lymphomas. (adooq.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)
  • AT5BIVA cells are sensitive to the topo II inhibitors etoposide (VP16) and amsacrine (m-AMSA), compared to normal human fibroblasts (MRC5-V1 and VA13). (ox.ac.uk)
  • Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. (wikipedia.org)
  • The achieved remission was consolidated using allogeneic bone marrow transplantation after FLAMSA reduced density conditioning without amsacrine. (muni.cz)
  • 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. (mediresource.com)
  • 11. Phase II evaluation of amsacrine (m-AMSA) in solid tumors, myeloma, and lymphoma: a University of Arizona and Southwest Oncology Group Study. (nih.gov)
  • 17. Phase II trial of amsacrine (AMSA) in urinary bladder cancer. (nih.gov)
  • Amsacrine belongs to the group of cancer-fighting medications called antineoplastics . (mediresource.com)
  • Amsacrine kills cancer cells by interfering with their growth and reproduction. (mediresource.com)
  • As well as interfering with the growth and reproduction of cancer cells, amsacrine can interfere with some of your normal cells. (mediresource.com)