AnatomyDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesInformation ScienceHealth Care
EtoposideAntineoplastic Agents, PhytogenicAntineoplastic Combined Chemotherapy ProtocolsTopoisomerase II InhibitorsIfosfamideCisplatinCarcinoma, Small CellDNA Topoisomerases, Type IIPodophyllotoxinVincristineDoxorubicinCyclophosphamideCarboplatinAmsacrineDrug Administration ScheduleBleomycinLung NeoplasmsCombined Modality TherapyCytarabineGerminomaAntineoplastic AgentsTeniposideNucleic Acid Synthesis InhibitorsTopoisomerase InhibitorsLeukopeniaTransplantation, AutologousTesticular NeoplasmsDrug Resistance, NeoplasmMitoxantroneRemission InductionApoptosisNeoplasms, Germ Cell and EmbryonalTreatment OutcomeAdministration, OralDNA DamageHodgkin DiseaseInfusions, IntravenousCamptothecinCarmustineHematologic DiseasesDrug EvaluationSalvage TherapyLymphoma, Non-HodgkinTopotecanTopoisomerase I InhibitorsTumor Cells, CulturedDisease-Free SurvivalSurvival AnalysisRazoxaneNeutropeniaPrednisoneSurvival RateDrug ResistanceThrombocytopeniaDose-Response Relationship, DrugProcarbazineDrug Resistance, MultipleP-GlycoproteinOrganophosphorus CompoundsMelphalanPaclitaxelVinblastineCell SurvivalGranulocyte Colony-Stimulating FactorRetroperitoneal NeoplasmsAlopeciaDaunorubicinBone Marrow DiseasesHematopoietic Stem Cell TransplantationMethotrexateHL-60 CellsLevoleucovorinCell Line, TumorDrug SynergismSmall Cell Lung CarcinomaMesnaCaspasesDrug Screening Assays, AntitumorDNA Topoisomerases, Type I
Etoposide
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
Antineoplastic Agents, Phytogenic
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
Antineoplastic Combined Chemotherapy Protocols
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
Topoisomerase II Inhibitors
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.
Ifosfamide
Positional isomer of CYCLOPHOSPHAMIDE which is active as an alkylating agent and an immunosuppressive agent.
Cisplatin
An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.
Carcinoma, Small Cell
An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)
DNA Topoisomerases, Type II
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.
Podophyllotoxin
A lignan (LIGNANS) found in PODOPHYLLIN resin from the roots of PODOPHYLLUM plants. It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives.
Vincristine
An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.)
Doxorubicin
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
Cyclophosphamide
Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.
Carboplatin
An organoplatinum compound that possesses antineoplastic activity.
Amsacrine
An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.
Drug Administration Schedule
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
Bleomycin
A complex of related glycopeptide antibiotics from Streptomyces verticillus consisting of bleomycin A2 and B2. It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors.
Lung Neoplasms
Tumors or cancer of the LUNG.
Combined Modality Therapy
The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.
Cytarabine
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
Germinoma
A malignant neoplasm of the germinal tissue of the GONADS; MEDIASTINUM; or pineal region. Germinomas are uniform in appearance, consisting of large, round cells with vesicular nuclei and clear or finely granular eosinophilic-staining cytoplasm. (Stedman, 265th ed; from DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, pp1642-3)
Antineoplastic Agents
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Teniposide
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle.
Nucleic Acid Synthesis Inhibitors
Compounds that inhibit cell production of DNA or RNA.
Topoisomerase Inhibitors
Compounds that inhibit the activity of DNA TOPOISOMERASES.
Leukopenia
Transplantation, Autologous
Transplantation of an individual's own tissue from one site to another site.
Testicular Neoplasms
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.
Drug Resistance, Neoplasm
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
Mitoxantrone
An anthracenedione-derived antineoplastic agent.
Remission Induction
Therapeutic act or process that initiates a response to a complete or partial remission level.
Apoptosis
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Neoplasms, Germ Cell and Embryonal
Neoplasms composed of primordial GERM CELLS of embryonic GONADS or of elements of the germ layers of the EMBRYO, MAMMALIAN. The concept does not refer to neoplasms located in the gonads or present in an embryo or FETUS.
Treatment Outcome
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
Administration, Oral
The giving of drugs, chemicals, or other substances by mouth.
DNA Damage
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
Hodgkin Disease
A malignant disease characterized by progressive enlargement of the lymph nodes, spleen, and general lymphoid tissue. In the classical variant, giant usually multinucleate Hodgkin's and REED-STERNBERG CELLS are present; in the nodular lymphocyte predominant variant, lymphocytic and histiocytic cells are seen.
Infusions, Intravenous
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
Camptothecin
An alkaloid isolated from the stem wood of the Chinese tree, Camptotheca acuminata. This compound selectively inhibits the nuclear enzyme DNA TOPOISOMERASES, TYPE I. Several semisynthetic analogs of camptothecin have demonstrated antitumor activity.
Carmustine
A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed)
Hematologic Diseases
Disorders of the blood and blood forming tissues.
Drug Evaluation
Any process by which toxicity, metabolism, absorption, elimination, preferred route of administration, safe dosage range, etc., for a drug or group of drugs is determined through clinical assessment in humans or veterinary animals.
Salvage Therapy
A therapeutic approach, involving chemotherapy, radiation therapy, or surgery, after initial regimens have failed to lead to improvement in a patient's condition. Salvage therapy is most often used for neoplastic diseases.
Lymphoma, Non-Hodgkin
Any of a group of malignant tumors of lymphoid tissue that differ from HODGKIN DISEASE, being more heterogeneous with respect to malignant cell lineage, clinical course, prognosis, and therapy. The only common feature among these tumors is the absence of giant REED-STERNBERG CELLS, a characteristic of Hodgkin's disease.
Topotecan
An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.
Topoisomerase I Inhibitors
Compounds that inhibit the activity of DNA TOPOISOMERASE I.
Tumor Cells, Cultured
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Disease-Free Survival
Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.
Survival Analysis
A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.
Razoxane
An antimitotic agent with immunosuppressive properties.
Neutropenia
A decrease in the number of NEUTROPHILS found in the blood.
Prednisone
A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.
Survival Rate
The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods.
Drug Resistance
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
Thrombocytopenia
A subnormal level of BLOOD PLATELETS.
Dose-Response Relationship, Drug
The relationship between the dose of an administered drug and the response of the organism to the drug.
Procarbazine
An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.
Drug Resistance, Multiple
Simultaneous resistance to several structurally and functionally distinct drugs.
P-Glycoprotein
A 170-kDa transmembrane glycoprotein from the superfamily of ATP-BINDING CASSETTE TRANSPORTERS. It serves as an ATP-dependent efflux pump for a variety of chemicals, including many ANTINEOPLASTIC AGENTS. Overexpression of this glycoprotein is associated with multidrug resistance (see DRUG RESISTANCE, MULTIPLE).
Organophosphorus Compounds
Organic compounds that contain phosphorus as an integral part of the molecule. Included under this heading is broad array of synthetic compounds that are used as PESTICIDES and DRUGS.
Melphalan
An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.
Paclitaxel
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
Vinblastine
Antitumor alkaloid isolated from Vinca rosea. (Merck, 11th ed.)
Cell Survival
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Granulocyte Colony-Stimulating Factor
A glycoprotein of MW 25 kDa containing internal disulfide bonds. It induces the survival, proliferation, and differentiation of neutrophilic granulocyte precursor cells and functionally activates mature blood neutrophils. Among the family of colony-stimulating factors, G-CSF is the most potent inducer of terminal differentiation to granulocytes and macrophages of leukemic myeloid cell lines.
Retroperitoneal Neoplasms
Alopecia
Absence of hair from areas where it is normally present.
Daunorubicin
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
Bone Marrow Diseases
Hematopoietic Stem Cell Transplantation
Transfer of HEMATOPOIETIC STEM CELLS from BONE MARROW or BLOOD between individuals within the same species (TRANSPLANTATION, HOMOLOGOUS) or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). Hematopoietic stem cell transplantation has been used as an alternative to BONE MARROW TRANSPLANTATION in the treatment of a variety of neoplasms.
Methotrexate
An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.
HL-60 Cells
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
Levoleucovorin
A folate analog consisting of the pharmacologically active isomer of LEUCOVORIN.
Cell Line, Tumor
A cell line derived from cultured tumor cells.
Drug Synergism
The action of a drug in promoting or enhancing the effectiveness of another drug.
Small Cell Lung Carcinoma
A form of highly malignant lung cancer that is composed of small ovoid cells (SMALL CELL CARCINOMA).
Mesna
A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.
Caspases
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
Drug Screening Assays, Antitumor
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
DNA Topoisomerases, Type I
DNA TOPOISOMERASES that catalyze ATP-independent breakage of one of the two strands of DNA, passage of the unbroken strand through the break, and rejoining of the broken strand. DNA Topoisomerases, Type I enzymes reduce the topological stress in the DNA structure by relaxing the superhelical turns and knotted rings in the DNA helix.

Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits the p53-Mdm2 autoregulatory feedback loop. (1/3752)

The Mdm2 protein is frequently overexpressed in human non-seminomatous germ cell tumours and transitional carcinoma of the bladder where it may contribute to tolerance of wtp53. Mdm2 forms an autoregulatory feedback loop with p53; the Mdm2 gene is responsive to transactivation by p53 and once synthesized the Mdm2 protein terminates the p53 response. We show here that the topoisomerase poison etoposide, like ultra violet irradiation, inhibits Mdm2 synthesis. Cytotoxic concentrations of etoposide (IC90 for > 3 h) result in inhibition of Mdm2 induction at both the RNA and protein level. Rapid apoptosis ensues. Global transcription is not inhibited: p21waf-1/cip1 and GADD45 expression increase in a dose dependent manner. Inhibition of Mdm2 synthesis depends on the continuous presence of etoposide, suggesting the DNA damage may prevent transcription. Downregulation of Mdm2 transcript occurs in cells expressing HPV16-E6 suggesting that inhibition of Mdm2 transcription is p53-independent. When cells are -treated with a pulse (1 h) of etoposide and reincubated in drug free medium, Mdm2 synthesis commences immediately after damage is repaired (3 h) and the p53 response is attenuated. Induction of apoptosis and loss of clonogenicity are 3-5-fold lower under pulse treatment conditions. This is the first observation of inhibition of Mdm2 transcription following treatment with topoisomerase (topo II) poisons, a feature that may be useful in tumour types where p53 is tolerated by overexpression of Mdm2.  (+info)

1,25-Dihydroxyvitamin D3 enhances the susceptibility of breast cancer cells to doxorubicin-induced oxidative damage. (2/3752)

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3), the hormonal form of vitamin D, has anticancer activity in vivo and in vitro. Doxorubicin exerts its cytotoxic effect on tumor cells mainly by two mechanisms: (a) generation of reactive oxygen species (ROS); and (b) inhibition of topoisomerase II. We studied the combined cytotoxic action of 1,25(OH)2D3 and doxorubicin on MCF-7 breast cancer cells. Pretreatement with 1,25(OH)2D3 resulted in enhanced cytotoxicity of doxorubicin. The average enhancing effect after a 72-h pretreatment with 1,25(OH)2D3 (10 nM) followed by a 24-h treatment with 1 microg/ml doxorubicin was 74+/-9% (mean +/- SE). Under these experimental conditions, 1,25(OH)2D3 on its own did not affect cell number or viability. 1,25(OH)2D3 also enhanced the cytotoxic activity of another ROS generating quinone, menadione, but did not affect cytotoxicity induced by the topoisomerase inhibitor etoposide. The antioxidant N-acetylcysteine slightly reduced the cytotoxic activity of doxorubicin but had a marked protective effect against the combined action of 1,25(OH)2D3 and doxorubicin. These results indicate that ROS are involved in the interaction between 1,25(OH)2D3 and doxorubicin. 1,25(OH)2D3 also increased doxorubicin cytotoxicity in primary cultures of rat cardiomyocytes. Treatment of MCF-7 cells with 1,25(OH)2D3 alone markedly reduced the activity, protein, and mRNA levels of the cytoplasmic antioxidant enzyme Cu/Zn superoxide dismutase, which indicated that the hormone inhibits its biosynthesis. This reduction in the antioxidant capacity of the cells could account for the synergistic interaction between 1,25(OH)2D3 and doxorubicin and may also suggest increased efficacy of 1,25(OH)2D3 or its analogues in combination with other ROS-generating anticancer therapeutic modalities.  (+info)

p27Kip1 induces drug resistance by preventing apoptosis upstream of cytochrome c release and procaspase-3 activation in leukemic cells. (3/3752)

The cyclin-dependent kinase inhibitor p27Kip1 has been implicated as a drug resistance factor in tumor cells grown as spheroids or confluent monolayers. Here, we show that p27Kip1 overexpression also induces resistance to drug-induced apoptosis and cytotoxicity in human leukemic cells growing in suspension. The anti-apoptotic effect of p27Kip1 is not restricted to DNA-damaging agents but extends to the tubulin poison vinblastin, agonistic anti-Fas antibodies and macromolecule synthesis inhibitors. To further identify at which level this protein interferes with the cell death pathway, we investigated its influence on caspase activation and mitochondrial changes. Exposure of mock-transfected U937 cells to 50 microm etoposide activates procaspase-3 and the long isoform of procaspase-2 and induces mitochondrial potential decrease and cytochrome c release from mitochondria to the cytosol. All these events are prevented by p27Kip1 overexpression. p27Kip1 does not modulate Bcl-2, Bcl-X(L), Mcl-1 and Bax protein level in leukemic cells but suppresses Mcl-1 expression decrease observed in mock-transfected U937 cells undergoing etoposide-induced cell death. We conclude that p27Kip1 prevents cell death upstream of the final pathway common to many apoptotic stimuli that involves cytochrome c release from mitochondria and activation of downstream caspases.  (+info)

Bcl-2 overexpression results in reciprocal downregulation of Bcl-X(L) and sensitizes human testicular germ cell tumours to chemotherapy-induced apoptosis. (4/3752)

Testicular germ cell tumours are hypersentive to chemotherapy and cell lines derived from these tumours are chemosensitive in vitro. We have previously shown that these cell lines express undetectable levels of the suppressor of apoptosis Bcl-2 and relatively high levels of the apoptosis inducer Bax (Chresta et al., 1996). To determine whether the absence of Bcl-2 in these cell lines makes them highly susceptible to drug-induced apoptosis, Bcl-2 was expressed ectopically in the 833K testicular germ cell tumour cell line. Stable overexpressing clones were isolated and three clones were studied further. Surprisingly, Bcl-2 overexpressing cells were sensitized to chemotherapy-induced apoptosis compared to the parental and vector control cells. Analysis of potential mechanisms of sensitization revealed there was a reciprocal downregulation of the endogenously expressed Bcl-X(L) in the Bcl-2 overexpressing clones. Downregulation of Bcl-X(L) to the same extent using antisense oligonucleotides enhanced etoposide-induced apoptosis by twofold. Our results indicate that Bcl-2 and Bcl-X(L) have different abilities to protect against chemotherapy-induced apoptosis in testicular germ cell tumours. In contrast to findings in some tumour cell types, Bcl-2 did not act as a gatekeeper to prevent entry of p53 to the nucleus.  (+info)

Effect of cellular ATP depletion on topoisomerase II poisons. Abrogation Of cleavable-complex formation by etoposide but not by amsacrine. (5/3752)

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)

Nuclear foci of mammalian recombination proteins are located at single-stranded DNA regions formed after DNA damage. (6/3752)

A sensitive and rapid in situ method was developed to visualize sites of single-stranded (ss) DNA in cultured cells and in experimental test animals. Anti-bromodeoxyuridine antibody recognizes the halogenated base analog incorporated into chromosomal DNA only when substituted DNA is in the single strand form. After treatment of cells with DNA-damaging agents or gamma irradiation, ssDNA molecules form nuclear foci in a dose-dependent manner within 60 min. The mammalian recombination protein Rad51 and the replication protein A then accumulate at sites of ssDNA and form foci, suggesting that these are sites of recombinational DNA repair.  (+info)

Replication-mediated DNA damage by camptothecin induces phosphorylation of RPA by DNA-dependent protein kinase and dissociates RPA:DNA-PK complexes. (7/3752)

Replication protein A (RPA) is a DNA single-strand binding protein essential for DNA replication, recombination and repair. In human cells treated with the topoisomerase inhibitors camptothecin or etoposide (VP-16), we find that RPA2, the middle-sized subunit of RPA, becomes rapidly phosphorylated. This response appears to be due to DNA-dependent protein kinase (DNA-PK) and to be independent of p53 or the ataxia telangiectasia mutated (ATM) protein. RPA2 phosphorylation in response to camptothecin required ongoing DNA replication. Camptothecin itself partially inhibited DNA synthesis, and this inhibition followed the same kinetics as DNA-PK activation and RPA2 phosphorylation. DNA-PK activation and RPA2 phosphorylation were prevented by the cell-cycle checkpoint abrogator 7-hydroxystaurosporine (UCN-01), which markedly potentiates camptothecin cytotoxicity. The DNA-PK catalytic subunit (DNA-PKcs) was found to bind RPA which was replaced by the Ku autoantigen upon camptothecin treatment. DNA-PKcs interacted directly with RPA1 in vitro. We propose that the encounter of a replication fork with a topoisomerase-DNA cleavage complex could lead to a juxtaposition of replication fork-associated RPA and DNA double-strand end-associated DNA-PK, leading to RPA2 phosphorylation which may signal the presence of DNA damage to an S-phase checkpoint mechanism. KEYWORDS: camptothecin/DNA damage/DNA-dependent protein kinase/RPA2 phosphorylation  (+info)

Mutation of a conserved serine residue in a quinolone-resistant type II topoisomerase alters the enzyme-DNA and drug interactions. (8/3752)

A Ser740 --> Trp mutation in yeast topoisomerase II (top2) and of the equivalent Ser83 in gyrase results in resistance to quinolones and confers hypersensitivity to etoposide (VP-16). We characterized the cleavage complexes induced by the top2(S740W) in the human c-myc gene. In addition to resistance to the fluoroquinolone CP-115,953, top2(S740W) induced novel DNA cleavage sites in the presence of VP-16, azatoxin, amsacrine, and mitoxantrone. Analysis of the VP-16 sites indicated that the changes in the cleavage pattern were reflected by alterations in base preference. C at position -2 and G at position +6 were observed for the top2(S740W) in addition to the previously reported C-1 and G+5 for the wild-type top2. The VP-16-induced top2(S740W) cleavage complexes were also more stable. The most stable sites had strong preference for C-1, whereas the most reversible sites showed no base preference at positions -1 or -2. Different patterns of DNA cleavage were also observed in the absence of drug and in the presence of calcium. These results indicate that the Ser740 --> Trp mutation alters the DNA recognition of top2, enhances its DNA binding, and markedly affects its interactions with inhibitors. Thus, residue 740 of top2 appears critical for both DNA and drug interactions.  (+info)

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Etoposide damages female germ cells in the developing ovary | BMC Cancer | Full TextEtoposide damages female germ cells in the developing ovary | BMC Cancer | Full Text
The Topo II inhibitor etoposide has been administered to women during pregnancy, with healthy babies born, although there are no data on the side-effects of etoposide on the reproductive system of these children, as none have yet reached puberty. Our results, using in vitro systems to assess the effects of etoposide, show that exposure of pre-follicular ovaries to etoposide results in a near-complete elimination of healthy follicles by the end of culture. This observed lack of follicles is a direct result of etoposide-treated pre-follicular germ cells failing to survive, with only a small proportion capable of forming follicles. Etoposide was used in concentrations considerably lower than those measured in the serum of patients, concentrations of 50-150 ng ml−1 being used, compared with 5-60 μg ml−1 in patient serum [38]. In contrast, exposure to oocytes once they were enclosed in follicles had no effect on total follicle numbers or health, the only effect seen on transitional follicles, ...
https://bmccancer.biomedcentral.com/articles/10.1186/s12885-016-2505-9
Carboplatin and Etoposide With or Without Thalidomide in Treating Patients With Limited-Stage or Extensive-Stage Small Cell...Carboplatin and Etoposide With or Without Thalidomide in Treating Patients With Limited-Stage or Extensive-Stage Small Cell...
NOTE: *Patients who are unable to receive etoposide IV on day 2 may receive oral etoposide on days 2 and 3.. In both arms, chemotherapy (carboplatin and etoposide) repeats every 3 weeks for up to 6 courses. Patients receive thalidomide or placebo continuously for up to 2 years. Treatment continues in the absence of disease progression or unacceptable toxicity. Patients who experience disease progression may continue to receive thalidomide or placebo provided the patient is clinically and symptomatically stable.. Quality of life is assessed at baseline, during each course of chemotherapy, at 3-4 weeks after completion of chemotherapy, and at 6, 12, 18, and 24 months.. Patients are followed every 2 months for 2 years after the completion of chemotherapy and then every 3 months thereafter.. Peer Reviewed and Funded or Endorsed by Cancer Research UK. PROJECTED ACCRUAL: A total of 372 patients (186 per treatment arm) will be accrued for this study. ...
https://clinicaltrials.gov/show/NCT00061919
Phase II Evaluation of Low-Dose Oral Etoposide for the Treatment of Relapsed or Progressed AIDS-Related Kaposi's Sarcoma...Phase II Evaluation of Low-Dose Oral Etoposide for the Treatment of Relapsed or Progressed AIDS-Related Kaposi's Sarcoma...
Etoposide may be at least as, or even more, effective and less myelotoxic when given in low doses over prolonged periods of time.. Patients receive low-dose oral etoposide on days 1 through 7 of every 2-week cycle. Patients who achieve a complete or partial response after two cycles and have no toxicity greater than grade 2 may have their dose escalated for subsequent cycles. If there are no responses to therapy among the first 14 evaluable patients, the study will close; if there is at least one objective response to therapy among the first 14 evaluable patients, enrollment will continue until all 41 patients are enrolled. Patients continue therapy until maximal tumor response (either stable disease or complete response) is achieved or disease progression occurs. ...
https://clinicaltrials.gov/show/NCT00000807?order=150
Opioid, ??- | Effect of ATM and HDAC Inhibition on Etoposide-Induced DNA DamageOpioid, ??- | Effect of ATM and HDAC Inhibition on Etoposide-Induced DNA Damage
Supplementary MaterialsSupplementary figure. in medical trials.1 Although several immunotherapeutic and surgical strategies have already been created to boost the prognosis of cutaneous melanoma sufferers, such as for example checkpoint inhibitors, chimeric antigen receptor T-cell (CAR-T) immunotherapy, oncolytic infections and dendritic … Continue reading →. ...
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Etoposide Injection, USP by Hospira: Etoposide belongs to the group of cancer-fighting medications called antineoplastics. Etoposide kills cancer cells by interfering with the genetic material DNA, which is necessary for their growth and reproduction. Etoposide is used alone or in combination with other antineoplastic medications to treat many types of cancer. These include certain types of lung cancer, lymphoma (cancer of the lymph cells), and cancers of the testicles.
http://bodyandhealth.canada.com/drug/getdrug/etoposide-injection-usp-by-hospira
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Etoposide Injection, USP by Mylan: Etoposide belongs to the group of cancer-fighting medications called antineoplastics. Etoposide kills cancer cells by interfering with the genetic material DNA, which is necessary for their growth and reproduction. Etoposide is used alone or in combination with other antineoplastic medications to treat many types of cancer. These include certain types of lung cancer, lymphoma (cancer of the lymph cells), and cancers of the testicles.
http://bodyandhealth.canada.com/drug/getdrug/etoposide-injection-usp-by-mylan
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Etoposide - Side Effects, Uses, Dosage, Overdose, Pregnancy, Alcohol | caas.rxwiki.com
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Etoposide - Side Effects, Uses, Dosage, Overdose, Pregnancy, Alcohol | RxWikiEtoposide - Side Effects, Uses, Dosage, Overdose, Pregnancy, Alcohol | RxWiki
Etoposide - Get up-to-date information on Etoposide side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about Etoposide
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etoposide (oral) | Cignaetoposide (oral) | Cigna
Etoposide is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Etoposide is used to treat small cell lung cancer. It is usually given in combination with other cancer medicines. Etoposide may also be used for purposes not listed in this medication guide.
https://www.cigna.com/individuals-families/health-wellness/hw/medications/etoposide-d00230a1
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Paclitaxel and etoposide are two chemotherapy agents with broad cytotoxic activity and different mechanisms of action and resistance. Preclinical studies of their combined cytotoxicity have yielded conflicting results. We performed two sequential Phase II trials using different sequence schedules of paclitaxel and etoposide as first-line treatment in advanced non-small cell lung cancer (NSCLC). Forty-four patients with stage IIIB or IV NSCLC were included between July 1995 and September 1996. All patients received etoposide at 100 mg/m2, given as an i.v. infusion on days 1, 2, and 3. The first 20 patients (part A) also received paclitaxel at 175 mg/m2 as a 3-h infusion on day 1, immediately prior to etoposide. The subsequent 24 patients (part B) were given the same paclitaxel dose, but on day 4. Grade 3-4 granulocytopenia was seen in 70% of the patients in part A and in 37% of those in part B (P = 0.04). Twenty-five % of the courses in part A and 4% of the courses in part B were associated with ...
http://clincancerres.aacrjournals.org/content/4/11/2723
Reduction of atherosclerotic lesions in rabbits treated with etoposide | IJNReduction of atherosclerotic lesions in rabbits treated with etoposide | IJN
Reduction of atherosclerotic lesions in rabbits treated with etoposide associated with cholesterol-rich nanoemulsions Elaine R Tavares1, Fatima R Freitas1, Jayme Diament1, Raul C Maranhão1,21Heart Institute of the Medical School Hospital (InCor), University of São Paulo, São Paulo, Brazil; 2Faculty of Pharmaceutical Sciences, University of São Paulo, São Paulo, BrazilObjectives: Cholesterol-rich nanoemulsions (LDE) bind to low-density lipoprotein (LDL) receptors and after injection into the bloodstream concentrate in aortas of atherosclerotic rabbits. Association of paclitaxel with LDE markedly reduces the lesions. In previous studies, treatment of refractory cancer patients with etoposide associated with LDE had been shown devoid of toxicity. In this study, the ability of etoposide to reduce lesions and inflammatory factors in atherosclerotic rabbits was investigated.Methods: Eighteen New Zealand rabbits were fed a 1% cholesterol diet for 60 days. Starting from day 30
https://www.dovepress.com/reduction-of-atherosclerotic-lesions-in-rabbits-treated-with-etoposide-peer-reviewed-article-IJN
Cisplatin Plus Etoposide, Irinotecan Possible Treatment Option for Sensitive Relapsed SCLC - Cancer Therapy AdvisorCisplatin Plus Etoposide, Irinotecan Possible Treatment Option for Sensitive Relapsed SCLC - Cancer Therapy Advisor
Cisplatin, etoposide, and irinotecan may be clinically beneficial as a second-line chemotherapy for selected patients with small cell lung cancer (SCLC).
https://www.cancertherapyadvisor.com/lung-cancer/lung-cancer-sclc-cisplatin-etoposide-irinotecan-possible-treatment/article/503708/
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Our results are most consistent with a model for etoposide-induced gene rearrangement shown in Fig. 4C. In this model, etoposide induces DNA damage (Topo II-linked DSBs) somewhere in the chromsomes. Etoposide-induced DNA damage then activates the apoptotic signaling pathway, which leads to activation of caspase-3 followed by ICAD cleavage and activation of CAD. Activated CAD then cleaves DNA within the MLL bcr as well as within MLL partner genes. The repair of the DSB within the MLL bcr through NHEJ results in rearrangement of the MLL gene with one of its ,50 partner genes and hence t-AML.. The role of apoptotic nuclease in genome instability is a surprising finding. It is generally thought that apoptotic nucleases, such as CAD, play a role late in the apoptotic cell death program. Our results suggest that a population of apoptotic cells with activated CAD may escape cell death and survive with a few DSBs ( 15). A possible consequence of this escape is gene rearrangements. It should be pointed ...
http://cancerres.aacrjournals.org/content/66/18/8975
A genome-wide approach to identify genetic variants that contribute to etoposide-induced cytotoxicityA genome-wide approach to identify genetic variants that contribute to etoposide-induced cytotoxicity
Large interindividual variance has been observed in sensitivity to drugs. To comprehensively decipher the genetic contribution to these variations in drug susceptibility, we present a genome-wide model using human lymphoblastoid cell lines from the International HapMap consortium, of which extensive …
https://pubmed.ncbi.nlm.nih.gov/17537913/
Glentham Life Sciences | Product Search: EtoposideGlentham Life Sciences | Product Search: Etoposide
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Etoposide Injection by Fresenius - PharmasaveEtoposide Injection by Fresenius - Pharmasave
Before you begin using a medication, be sure to inform your doctor of any medical conditions or allergies you may have, any medications you are taking, whether you are pregnant or breast-feeding, and any other significant facts about your health. These factors may affect how you should use this medication.. Allergic reactions: Allergic reactions, including difficulty breathing and swelling of the throat and mouth, can occur with the use of this medication. Tell your doctor immediately if you experience any of these symptoms.. Blood clotting: This medication can reduce the number of platelet cells in the blood. Platelets help the blood to clot, and a shortage could make you bleed more easily. Tell your doctor of any signs that your blood is not clotting as quickly as usual. Such symptoms may include black and tarry stools, blood in the urine, easy bruising, or cuts that wont stop bleeding.. Infection: As well as killing cancer cells, etoposide can reduce the number of cells that fight infection ...
http://www.pharmasave.com/medications/etoposide-injection-by-fresenius/
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Both ATM and ATR display a preference for phosphorylating SQ/TQ motifs in their substrates (Kim et al., 1999; Traven and Heierhorst, 2005; Shiloh, 2006). ATR is predominantly activated by UV light and stalled replication forks, whereas ATM is specifically activated by DSBs of DNA, as seen after irradiation, etoposide, or oxidative stress (Abraham, 2001; Shiloh, 2006). In contrast, treatment with the ATP-competitive kinase inhibitor, staurosporine, does not activate ATM or affect the phosphorylation status of ATM-dependent substrates (Kamer et al., 2005). We show here that DNA-damaging agents, such as IR and etoposide, trigger MEF2D phosphorylation. Moreover, MEF2D phosphorylation only increased after etoposide exposure in wt-ATM cells but not in ATM-deficient cells. These results suggest that ATM mediates MEF2D phosphorylation in response to DSBs in DNA.. Furthermore, in the present study, RNA interference-mediated knockdown experiments in cerebellar granule cells indicate that endogenous MEF2D ...
http://www.jneurosci.org/content/34/13/4640
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Introduction: Vorinostat has been shown to potentiate DNA damage induced by topoisomerase II inhibitors in a sequence dependent fashion. A multi-center, open label phase I study with escalating doses of vorinostat in combination with etoposide was conducted to establish the safety of the combination in pediatric patients with refractory solid tumors to determine the maximum tolerated dose (MTD), dose limiting toxicity (DLT) and recommended phase II dose (RP2D) of this regimen.. Methods: Eligible patients were ≤21 years of age with relapsed/refractory solid tumors including central nervous system tumors. Study design consisted of a standard 3+3 dose escalation schema. Vorinostat was administered once daily for days 1-4 of the treatment cycle in escalating doses (125 mg/m2, 160 mg/m2, 210 mg/m2, and 270 mg/m2). Etoposide was administered at a fixed dose of 100 mg/m2/day on days 3-5 of the treatment cycle. Etoposide was administered 4 hours after administration of vorinostat. Each treatment cycle ...
http://mct.aacrjournals.org/content/12/11_Supplement/B81
Etoposide combinations may improve survival and quality of life - CareAcross
Researchers studying etoposide (used in lung & testicular cancer, leukemias and brain tumors) showed that combining it with other compounds can improve outcomes.
https://www.careacross.com/news/etoposide-combinations-may-improve-survival-and-quality-of-life
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Phase 1 Study of Ibrutinib and Immuno-Chemotherapy Using Dose-Adjusted-Temozolomide, Etoposide, Doxil, Dexamethasone, Ibrutinib...Phase 1 Study of Ibrutinib and Immuno-Chemotherapy Using Dose-Adjusted-Temozolomide, Etoposide, Doxil, Dexamethasone, Ibrutinib...
This study is investigating ibrutinib and immuno-chemotherapy using dose-adjusted-temozolomide, etoposide, doxil, dexamethasone, ibrutinib, rituximab
http://adisinsight.springer.com/trials/700248085?error=cookies_not_supported&code=efcc2291-a94c-40a3-a78c-99e711d8a0f8
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The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites ...
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FDA Approves Tecentriq plus Chemotherapy for First-Line Treatment of Extensive-Stage Small-Cell Lung Cancer | Personalized...FDA Approves Tecentriq plus Chemotherapy for First-Line Treatment of Extensive-Stage Small-Cell Lung Cancer | Personalized...
For the second time this month, the FDA has given an approval to Genentechs PD-L1 inhibitor, Tecentriq.. On March 18, 2019, the FDA awarded the immunotherapy agent, Tecentriq (atezolizumab; Genentech), in combination with chemotherapy (carboplatin and etoposide), approval for the first-line treatment of adults with extensive-stage small-cell lung cancer (ES-SCLC).. As evidence of the rapidity with which the immunotherapy field is gaining ground in cancer treatment, this new approval comes only 10 days after the drug received an accelerated approval (in combination with nab-paclitaxel) for the treatment of triple-negative breast cancer. Not only is this the second approval for atezolizumab in close succession to the first, but it is the first novel treatment in 2 decades for ES-SCLC, an aggressive and deadly malignancy.. This latest approval was based on data from the phase 3 IMpower133 trial, which was the first study to show that initial treatment with the immunotherapy-based combination ...
http://www.personalizedmedonc.com/inthenews/fda-approves-tecentriq-plus-chemotherapy-for-first-line-treatment-of-extensive-stage-small-cell-lung-cancer/
Evaluation of the continuous infusion of etoposide plus cisplatin in metastatic breast cancer a collaborative north central...
TY - JOUR. T1 - Evaluation of the continuous infusion of etoposide plus cisplatin in metastatic breast cancer a collaborative north central cancer treatment group/mayo clinic phase ii study. AU - Krook, James E.. AU - Loprinzi, Charles L.. AU - Schaid, Daniel J.. AU - Kardinal, Carl G.. AU - Mailliard, James A.. AU - Pfeifle, Delano M.. AU - Ellison, Neil M.. AU - Reuter, Nicholas F.. AU - Nelimark, Robert A.. N1 - Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1990/2/1. Y1 - 1990/2/1. N2 - A prospective clinical trial was done to evaluate the efficacy and toxicity of cisplatin plus etoposide (VP‐16) in patients with breast cancer who failed one previous chemotherapy regimen for advanced disease or relapsed within 12 months of adjuvant chemotherapy. Partial responses occurred in 11 of 44 evaluable patients (25%; 95% confidence interval (CI), 13% to 40%). The median time to disease progression in responding patients was 4 months (range, 3 to 6+ months), whereas the median ...
https://mayoclinic.pure.elsevier.com/en/publications/evaluation-of-the-continuous-infusion-of-etoposide-plus-cisplatin
Radiotherapy improves the survival of patients with extensive-disease | CMARRadiotherapy improves the survival of patients with extensive-disease | CMAR
Radiotherapy improves the survival of patients with extensive-disease small-cell lung cancer: a propensity score matched analysis of Surveillance, Epidemiology, and End Results database Rui Zhang,* Ping Li,* Qin Li, Yunfeng Qiao, Tangpeng Xu, Peng Ruan, Qibin Song, Zhenming Fu Cancer Center, Renmin Hospital of Wuhan University, Wuhan 430060, China *These authors contributed equally to this work Background: The survival advantage of radiotherapy for patients with extensive-disease small-cell lung cancer (ED-SCLC) has not been adequately evaluated.Methods: We analyzed stage IV SCLC patients enrolled from the Surveillance, Epidemiology, and End Results (SEER) registry through January 2010 and December 2012. Propensity score analysis with 1:1 matching was performed to ensure well-balanced characteristics of all comparison groups. Kaplan–Meier and Cox proportional hazardous model were used to evaluate the overall survival (OS), cancer-specific survival (CSS), and corresponding 95% CI.Results: Overall,
https://www.dovepress.com/radiotherapy-improves-the-survival-of-patients-with-extensive-disease--peer-reviewed-article-CMAR
Salvage therapy in recurrent germ cell cancer: ifosfamide and cisplatin plus either vinblastine or etoposide
To determine the efficacy of the addition of ifosfamide to cisplatin plus etoposide (VIP), or vinblastine (VeIP), in patients with recurrent germ cell tumors. DESIGN: Nonrandomized, prospective phase II trial. SETTING: Tertiary referral university hospital. PATIENTS: Fifty-six of fifty-eight entered patients with measurable and progressive recurrent germ cell tumors of testicular (46 patients), ovarian (1 patient), and extragonadal (9 patients) origin were evaluable for response after not being cured with cisplatin, vinblastine, and etoposide regimens. INTERVENTIONS: Patients were administered cisplatin (20 mg/m2 body surface area daily for 5 days), ifosfamide (1.2 g daily for 5 days), plus either etoposide (75 mg daily for 5 days) or vinblastine (0.11 mg/kg body weight on days 1 and 2). In addition, vigorous intravenous hydration therapy with normal saline (100 to 125 mL/h) was administered during the treatment course. Uroepithelial protective agents, N-acetylcysteine (orally) or mesna ...
https://imsdd.meb.uni-bonn.de/cgi-bin/mycite?ExtRef=MEDL/88339106/PMID/2844110
Etoposide Induces Nuclear Re-Localisation of AIDEtoposide Induces Nuclear Re-Localisation of AID
During B cell activation, the DNA lesions that initiate somatic hypermutation and class switch recombination are introduced by activation-induced cytidine deaminase (AID). AID is a highly mutagenic protein that is maintained in the cytoplasm at steady state, however AID is shuttled across the nuclear membrane and the protein transiently present in the nucleus appears sufficient for targeted alteration of immunoglobulin loci. AID has been implicated in epigenetic reprogramming in primordial germ cells and cell fusions and in induced pluripotent stem cells (iPS cells), however AID expression in non-B cells is very low. We hypothesised that epigenetic reprogramming would require a pathway that instigates prolonged nuclear residence of AID. Here we show that AID is completely re-localised to the nucleus during drug withdrawal following etoposide treatment, in the period in which double strand breaks (DSBs) are repaired. Re-localisation occurs 2-6 hours after etoposide treatment, and AID remains in the
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0082110
Protein Ser/Thr Phosphatases | Effect of ATM and HDAC Inhibition on Etoposide-Induced DNA DamageProtein Ser/Thr Phosphatases | Effect of ATM and HDAC Inhibition on Etoposide-Induced DNA Damage
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http://etoposide.info/category/protein-ser-thr-phosphatases/
Phase II trial of cisplatin/etoposide and concurrent radiotherapy followed by paclitaxel/carboplatin consolidation for limited...
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https://ucdavis.pure.elsevier.com/en/publications/phase-ii-trial-of-cisplatinetoposide-and-concurrent-radiotherapy-/fingerprints/
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Tumors developed in BRCA1 mutation carriers show distinctive cytologic and molecular profiles compared with the sporadic tumor counterparts (1, 24). Nevertheless, at the moment, tailored treatments for this group of patients have only been partially investigated (12, 13). The rarity of human BRCA1-mutated cancer cell lines has further limited the exploitation of such approaches.. In the current study, we used the RNA interference technology to generate several isogenic BRCA1-silenced/nonsilenced breast cancer cell lines to assess whether a biological rational exists to implement therapeutic protocols specific for BRCA1 cancer patients. Our cell models were then challenged with several chemotherapeutics commonly used in breast cancer treatment.. We found no association between BRCA1 down-regulation and sensitivity to the topoisomerase II inhibitors etoposide and doxorubicin. Although differential response was observed in a few clones, this was not correlated to BRCA1 expression levels. ...
http://mct.aacrjournals.org/content/8/4/844
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Although histone deacetylases (HDACs) are involved in the carcinogenesis of solid tumors and HDAC inhibitors (HDACi) have already proved their efficacy in clinical trials, isoenzyme specific functions are still ill defined. In this thesis a high expression of HDAC2 in vivo in human and murine pancreatic ductal adenocarcinomas (PDAC) was demonstrated, suggesting an important role of HDAC2 in the pathogenesis of PDAC. In pancreatic cancer cell lines a HDAC2 dependent signaling pathway was discovered which resulted in resistance towards the topoisomerase II inhibitor etoposide by repression of the BH3-only protein NOXA. Targeting HDAC2 by HDACi will therefore be a promising strategy to overcome therapeutic resistance of PDAC against DNA damage inducing chemotherapeutics. « ...
https://mediatum.ub.tum.de/?id=1081574
Chronic daily administration of oral etoposide - A phase I trial<...
TY - JOUR. T1 - Chronic daily administration of oral etoposide - A phase I trial. AU - Hainsworth, J. D.. AU - Johnson, D. H.. AU - Frazier, S. R.. AU - Greco, F. A.. PY - 1989. Y1 - 1989. N2 - In this phase I study, we administered etoposide (VP-16) orally for 21 consecutive days to patients with advanced refractory cancers. All patients had received previous chemotherapy, and 50% of patients had received more than one combination regimen. When given for 21 consecutive days, the maximum-tolerated dose of oral VP-16 was 50 mg/m2/d. Myelosuppression was the dose-limiting toxicity, and occurred between days 21 and 28. In most patients, blood counts had recovered sufficiently by day 35 to begin another 3-week course. WBC count nadirs of , 1,000/μL occurred in four of 20 courses at this dose, and three patients required hospitalization for treatment of neutropenia and fever. Alopecia occurred in most patients; gastrointestinal (GI) and other toxicities were uncommon. Five of 16 patients with ...
https://utsouthwestern.pure.elsevier.com/en/publications/chronic-daily-administration-of-oral-etoposide-a-phase-i-trial
Chemo drug (etoposide) in pregnancy may cause early menopause in daughters (mice study) Ovarian Cancer and Us ...Chemo drug (etoposide) in pregnancy may cause early menopause in daughters (mice study) Ovarian Cancer and Us ...
Around 1 in 1,000 pregnant women are diagnosed with cancer, requiring consideration for the use of chemotherapy during pregnancy. However, little is known about the possible long-term detrimental effects of etoposide on the reproductive system of the unborn child. ...
https://ovariancancerandus.blogspot.com/2016/08/chemo-drug-etoposide-in-pregnancy-may.html
Paclitaxel and Carboplatin or Bleomycin Sulfate, Etoposide Phosphate, and Cisplatin in Treating Patients With Advanced or...Paclitaxel and Carboplatin or Bleomycin Sulfate, Etoposide Phosphate, and Cisplatin in Treating Patients With Advanced or...
This randomized phase II trial studies paclitaxel and carboplatin to see how well they work compared with bleomycin sulfate, etoposide phosphate, and cisplatin in treating patients with sex cord-ovarian stromal tumors that have spread to other places in the body and usually cannot be cured or controlled with treatment (advanced) or has returned (recurrent). Drugs used in chemotherapy work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Giving more than one drug (combination chemotherapy) may kill more tumor cells. It is not yet known which chemotherapy regimen is more effective in treating sex cord-ovarian stromal tumors. ...
http://www.utswmedicine.org/cancer/clinical-trials/fact-detail.html?primarypurpose=10&studyId=STU%20062010-168
The antitumor drug etoposide (ETO) is widely used in treating several - GLO1 inhibitors for neuropsychiatricThe antitumor drug etoposide (ETO) is widely used in treating several - GLO1 inhibitors for neuropsychiatric
The antitumor drug etoposide (ETO) is widely used in treating several cancers including adrenocortical tumor (ACT). the autophagy inhibitor reduced Take action cell growth and inhibited ETO-induced centrosome amplification. Chloroquine alleviated CDK2 and ERK but not Chk2 activation and thus inhibited centrosome amplification in either ETO- or hydroxyurea-treated ACT cells. In addition chloroquine also inhibited centrosome amplification in osteosarcoma U2OS cell lines when treated with ETO or hydroxyurea. In summary we have exhibited that chloroquine inhibited ACT cell growth and alleviated DNA damage-induced centrosome amplification by inhibiting CDK2 and ERK activity thus preventing genomic instability and recurrence of ACT. Introduction Adrenal gland which is composed of the cortex and medulla is the most important endocrine organ that lies on top of the kidney. Adrenocortex is the major site of steroidogenesis in response to adrenocorticotropic hormone stimulation and its abnormal growth ...
http://bio-zentrum.com/the-antitumor-drug-etoposide-eto-is-widely-used-in-treating-several/
Dose escalation study of high-dose carboplatin and etoposide w...Dose escalation study of high-dose carboplatin and etoposide w...
Dose escalation study of high-dose carboplatin and etoposide with autologous bone marrow support in patients with recurrent and refractory germ cell tumors.: Th
https://www.mysciencework.com/publication/show/dose-escalation-study-high-dose-carboplatin-etoposide-autologous-bone-marrow-support-patients-recurrent-refractory-germ-1773f7a0
FCCC Faculty Publications: show
Background: In an attempt to reduce the toxicity of chemotherapy in good-risk testicular cancer patients the two drug combinations, cisplatin plus etoposide (EP) and carboplatin plus etoposide (EC), have been compared. Methods: Good risk was defined according to the MSKCC and IU criteria. 39 Patients have been treated with EP (cisplatin 20 mg/m2 i.v. and etoposide 100 mg/m2 i.v. on days 1 to 5), and 23 patients received EC (carboplatin 350 mg/m2 on day 1 and etoposide 100 mg/m2 on days 1 to 5). Four cycles of chemotherapy were given at 21- and 28-day intervals, respectively, with delays of up to 7 days in istances of leukocyte counts less than 3.0 x 10(9)/l or platelet counts less than 100 x 10(9)/l. Results: In the EP group 34 (87%) of 39 patients achieved CR (26 with chemotherapy alone, 8 with additional surgery). After a median follow-up of 26 (12-58) months 3 (9%) patients relapsed from CR. Currently 38 patients are alive, and 37 (94%) are NED. In the EC group 20 (87%) of 23 patients ...
http://staffpubs.fccc.edu/abstracts/11403
HIC1 (hypermethylated in cancer 1) SUMOylation is dispensable for DNA by Sonia Paget, Marion Dubuissez et al.HIC1 (hypermethylated in cancer 1) SUMOylation is dispensable for DNA by Sonia Paget, Marion Dubuissez et al.
The tumor suppressor gene HIC1 (Hypermethylated In Cancer 1) encodes a transcriptional repressor mediating the p53-dependent apoptotic response to irreparable DNA double-strand breaks (DSBs) through direct transcriptional repression of SIRT1. HIC1 is also essential for DSB repair as silencing of endogenous HIC1 in BJ-hTERT fibroblasts significantly delays DNA repair in functional Comet assays. HIC1 SUMOylation favours its interaction with MTA1, a component of NuRD complexes. In contrast with irreparable DSBs induced by 16-hours of etoposide treatment, we show that repairable DSBs induced by 1 h etoposide treatment do not increase HIC1 SUMOylation or its interaction with MTA1. Furthermore, HIC1 SUMOylation is dispensable for DNA repair since the non-SUMOylatable E316A mutant is as efficient as wt HIC1 in Comet assays. Upon induction of irreparable DSBs, the ATM-mediated increase of HIC1 SUMOylation is independent of its effector kinase Chk2. Moreover, irreparable DSBs strongly increase both the
https://hsrc.himmelfarb.gwu.edu/smhs_surgery_facpubs/493/
Phase II study of rapid-scheduled etoposide in paediatric soft tissue sarcomas - UQ eSpace
Twenty three patients with paediatric soft tissue sarcomas who had relapsed or refractory disease were treated with a rapid schedule of intravenous etoposide (100 mg/m2 daily on three consecutive days, weekly over 3 weeks). The regimen was well tolerated with predictable myelotoxicity. In 19 patients with rhabdomyosarcoma, there was a response rate of 42%. This appears to be better than previously reported with conventional three weekly schedules. These data indicate that for rhabdomyosarcoma, as for some other tumours, a divided dose regimen may be the optimal schedule and is worthy of further evaluation ...
https://espace.library.uq.edu.au/view/UQ:394480
MedlinePlus - Search Results for: Etoposide
Etoposide injection is used in combination with other medications to treat cancer of the testicles that has ... after treatment with other medications or radiation therapy. Etoposide injection is also used in combination with other ...
https://vsearch.nlm.nih.gov/vivisimo/cgi-bin/query-meta?v%3Aproject=medlineplus&v%3Asources=medlineplus-bundle&query=Etoposide
Non-canonical Activation of the DNA Sensing Adaptor STING by ATM and IFI16 Mediates NF-κB Signaling after Nuclear DNA DamageNon-canonical Activation of the DNA Sensing Adaptor STING by ATM and IFI16 Mediates NF-κB Signaling after Nuclear DNA Damage
DNA damage can be sensed as a danger-associated molecular pattern by the innate immune system. Here we find that keratinocytes and other human cells mount an innate immune response within hours of etoposide-induced DNA damage, which involves the DNA sensing adaptor STING but is independent of the cy …
https://pubmed.ncbi.nlm.nih.gov/30193098/?dopt=Abstract
Transposases in Etoposide Resistance - Robert HromasTransposases in Etoposide Resistance - Robert Hromas
Transposase activity was thought to be extinct in humans because DNA movement can be deleterious in higher organisms, resulting in genomic instability and perha...
http://grantome.com/grant/NIH/R01-CA140422-04
Plus itPlus it
Etoposide is a widely used anticancer drug successfully used for the treatment of many types of cancer in children and adults. Its use, however, is associated with an increased risk of development of secondary acute myelogenous leukemia involving the mixed-lineage leukemia (MLL) gene (11q23) translocations. Previous studies demonstrated that the phenoxyl radical of etoposide can be produced by action of myeloperoxidase (MPO), an enzyme found in developing myeloid progenitor cells, the likely origin for myeloid leukemias. We hypothesized, therefore, that one-electron oxidation of etoposide by MPO to its phenoxyl radical is important for converting this anticancer drug to genotoxic and carcinogenic species in human CD34+ myeloid progenitor cells. In the present study, using electron paramagnetic resonance spectroscopy, we provide conclusive evidence for MPO-dependent formation of etoposide phenoxyl radicals in growth factor-mobilized CD34+ cells isolated from human umbilical cord blood and ...
https://molpharm.aspetjournals.org/content/79/3/479
Objectives To compare the efficacy of rituximab, dose-adjusted etoposide, prednisone, vincristine,
Objectives To compare the efficacy of rituximab, dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide and doxorubicin (DA-EPOCH-R) with traditional rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) regimens in CD5+ double-hit lymphoma (DHL) and to evaluate prognostic factors. PFS (85.7% vs 23.0%, em P /em =0.029), but there was no statistical difference in OS (87.7% vs 34.4.0%, em P /em =0.064). However, in DA-EPOCH-R protocol, there was no significant difference between CD5+ DHL (MYC/BCl2 and MYC/BCL6) and triple-hit lymphoma ( em buy IWP-2 P /em =0.776 for PFS; em P /em =0.728 for OS). Multivariate analysis showed that CD5+ treatment regimen and disease stage were independent prognostic factors. Conclusion Our retrospective study shows that CD5+ has a poorer prognosis than CD5? patients. Based on its improved lifetime and good tolerance on CD5+ patients, which is expected to become the first-line treatment for high-risk DLBCL types based on more ...
http://www.techbizstrategy.com/2019/12/24/objectives-to-compare-the-efficacy-of-rituximab-dose-adjusted-etoposide-prednisone-vincristine/
KEYNOTE-604: Phase 3 trial of pembrolizumab plus etoposide/platinum (EP) for first-line treatment of extensive stage small-cell...KEYNOTE-604: Phase 3 trial of pembrolizumab plus etoposide/platinum (EP) for first-line treatment of extensive stage small-cell...
In this international, double-blind, phase 3 trial, adults with newly diagnosed ES-SCLC, ECOG PS ≤ 1, and no previous systemic therapy for SCLC are randomized 1:1 to receive either EP plus a 200-mg fixed dose of pembrolizumab intravenously (IV) once every 3 weeks (Q3W) or EP plus pbo IV Q3W. Randomization is stratified by the chosen platinum therapy (carboplatin vs cisplatin), ECOG PS (0 vs 1), and baseline lactate dehydrogenase concentration (≤ upper limit of normal [ULN] vs > ULN). Study treatment includes a total of 4 cycles of EP and 2 y of pembrolizumab/pbo and continues until documented PD, intolerable toxicity, or withdrawal of consent. Pts with a response after 4 cycles of EP plus pbo or pembrolizumab may receive prophylactic cranial irradiation. Pts who complete 2 y of pembrolizumab treatment or stop pembrolizumab for reasons other than PD/intolerability, but subsequently have documented PD, may receive an additional 1 y of pembrolizumab. Tumor response is assessed every 6 wk for 48 ...
http://oncologypro.esmo.org/Meeting-Resources/ESMO-2017-Congress/KEYNOTE-604-Phase-3-trial-of-pembrolizumab-plus-etoposide-platinum-EP-for-first-line-treatment-of-extensive-stage-small-cell-lung-cancer-ES-SCLC
Etoposide | トポイソメラーゼ 阻害剤Etoposide | トポイソメラーゼ 阻害剤
Etoposide is a semisynthetic derivative of podophyllotoxin, which inhibits DNA synthesis via topoisomerase II inhibition activity.
http://www.selleck.co.jp/products/Etopophos.html
Brevet US6713454 - Prodrugs of etoposide and etoposide analogs - Google BrevetsBrevet US6713454 - Prodrugs of etoposide and etoposide analogs - Google Brevets
The present invention provides amphiphilic prodrugs comprising a therapeutic compound conjugated to an PEG-oligomer/polymer and methods for using said prodrugs to enable oral drug delivery and/or delivery of drugs across the blood brain barrier into the central nervous system.
http://www.google.fr/patents/US6713454
एपोप्टोसिस - विकिपीडियाएपोप्टोसिस - विकिपीडिया
An etoposide-treated DU145 prostate cancer cell exploding into a cascade of apoptotic bodies. The sub images were extracted from a 61-hour time-lapse microscopy video, created using quantitative phase-contrast microscopy. The optical thickness is color-coded. With increasing thickness, color changes from gray to yellow, red, purple and finally black.[1] ...
https://hi.wikipedia.org/wiki/%E0%A4%8F%E0%A4%AA%E0%A5%8B%E0%A4%AA%E0%A5%8D%E0%A4%9F%E0%A5%8B%E0%A4%B8%E0%A4%BF%E0%A4%B8
FORUM WSB SZCZECIN zarządzanie - Migraine headachetherapy treatment etoposide cisplatin gimme, avamigran price in eng
Golf great Phil Mickelson has been finding it a struggle on the course in recent weeks so could have done without a freak occurrence which left his participation in the final round of the BMW Championship at Medinah in some doubt. Teenage girls have designed Africas first private satellite due to launch into space in 2017. Its hoped it can monitor and find answers to South Africas drought crisis. There are currently1277 DSP recipients who list their only medical condition asdrug or alcohol dependence, official figures have revealed. 1000 mg generic avamigran ...
http://forumwsb.website.pl/archive/index.php/thread-74852.html
Study of Palifosfamide-tris in Combination With Carboplatin and Etoposide in Chemotherapy Naïve Patients With Extensive-Stage...Study of Palifosfamide-tris in Combination With Carboplatin and Etoposide in Chemotherapy Naïve Patients With Extensive-Stage...
This is a multinational, multicenter, randomized controlled, open-label, adaptive study to evaluate the efficacy of PaCE chemotherapy in chemotherapy na
http://www.knowcancer.com/cancer-trials/NCT01555710/
Dr. Jack C Yalowich - Cancer Researcher at OSUCCC - JamesDr. Jack C Yalowich - Cancer Researcher at OSUCCC - James
Jack Yalowich, PhD, is a member of the Translational Therapeutics Program at OSUCCC - James, where his research focuses on therapeutic treatment and prevention of cancers. In particular, he is exploring how to improve ability of the clinically effective anticancer agent etoposide (VP-16) in
https://cancer.osu.edu/research-and-education/find-a-researcher/search-researcher-directory/jack-c-yalowich
Lets Do It!: January 2006Lets Do It!: January 2006
Just a quickie today. Erin had blood counts done yesterday. It was Day 11 of 21 days (hump day for this cycle). With all the chemos Erin has done in the past Day 11 was usually a pretty important day. It was the day Erin was most likely to have the lowest white blood counts and be the most susceptible to germs or infections. We tended to keep a low profile on Days 10 to Day 13 or so, just to be on the safe side. I knew that oral etoposide was supposed to be easy on the counts, but so was topo/cyclo. Even with neulasta support (the injection to build her white counts), with topo/cyclo her ANC would drop down under 1000 every time. [To refresh your memory, normal ANC is over 2000. Under 500 is considered neutropenic and requires her to stay home from school, etc. ] With the etoposide, she didnt have the benefit of neulasta (thats akin to saying she doesnt have the benefit of being beaten with a stick), and she has bone marrow that has faced down almost a year of toxic chemo. ...
http://erinbuenger.blogspot.com/2006_01_01_archive.html
Terminal<...Terminal<...
Despite the premature end of her first chemotherapy cycle, Sadie remained remarkably stable. Between no etoposide and lots of dexamethasone, she was feeling great. We wondered if wed heard the doctors correctly on August 27th. Sadie didnt look like someone with only weeks to live.. Sadies second chemotherapy cycle should have started on September 18, but her bloodwork wasnt good enough. She did have an MRI that day, a month ahead of schedule. The MRI confirmed her prognosis: the tumor had grown dramatically since Sadies last MRI. What cisplatinum and etoposide shed gotten were having no effect. On September 22, the doctors recommended we stop treatment and enjoy the time Sadie had left. Sadie and we concurred.. We went home. Wed cried on August 27th, but today we were just numb. Her prognosis wasnt new, and despite the hard evidence in black-and-white MRI images, it still seemed unreal. I remember feeling mostly relieved that Sadie wouldnt be so miserably sick now that chemotherapy was ...
http://www.sadies-brain-tumor.org/sadies-story/terminal/
Etoposide - wikidocEtoposide - wikidoc
Content is available under Creative Commons Attribution/Share-Alike License unless otherwise noted; All rights reserved on Board Review content ...
http://wikidoc.org/index.php/Etoposide
ZFIN Chebi: etoposideZFIN Chebi: etoposide
5S,5aR,8aR,9R)-9-(4-hydroxy-3,5-dimethoxyphenyl)-8-oxo-5,5a,6,8,8a,9-hexahydrofuro[3,4:6,7]naphtho[2,3-d][1,3]dioxol-5-yl 4,6-O-[(1R)-ethylidene]-beta-D- ...
http://zfin.org/action/ontology/term-detail/CHEBI:4911
Radiation Pneumonitis - 1263781 | CancerGRACERadiation Pneumonitis - 1263781 | CancerGRACE
Background: IIIA T1N2M0 NSCL Lung Cancer. 10/2013 URL Removal followed up with chemoradiation; Radiation to Mediastinum and area of lobectomy. Carbo/Taxol concurrent with 35 radiation treatments; Chemo only 3 treatments - allergic reaction to Taxol replaced with 3 treatments of Cisplatin/Etoposide. 4 months post treatment, ER visit and Pulmonary DR visit follow-up for extreme
https://cancergrace.org/comment/18596
NU7441 | KU-57788 | CAS#503468-95-9 | PI3K inhibitor | MedKoo BiosciencesNU7441 | KU-57788 | CAS#503468-95-9 | PI3K inhibitor | MedKoo Biosciences
NU7441, also known as KU-57788, is a highly potent and selective DNA-PK inhibitor (IC50=14 nM), exhibiting ATP-competitive inhibition kinetics. NU7441 increased the cytotoxicity of ionizing radiation and etoposide in SW620, LoVo, and V3-YAC cells but not in V3 cells, confirming that potentiation was due to DNA-PK inhibition. NU7441 substantially retarded the repair of ionizing radiation-induced and etoposide-induced DSB.
http://www.medkoo.com/products/6239
IV filters with Chemo??? - pg.2 | allnursesIV filters with Chemo??? - pg.2 | allnurses
Page 2 - Okay, this is really bugging me. My friend (and coworker) had to give Etoposide the other night. And like a good little doo-bee, she looked up the med on the hospitals computerized drug reference
http://allnurses.com/oncology-nursing/iv-filters-with-101243-page2.html
EtoposideEtoposide
... is in the topoisomerase inhibitor family of medication. It is believed to work by damaging DNA. Etoposide was ... "Etoposide". Drug Information Portal. U.S. National Library of Medicine. "Etoposide phosphate". Drug Information Portal. U.S. ... It is used in form of its salt etoposide phosphate. Etoposide was first synthesized in 1966 and U.S. Food and Drug ... "Etoposide". National Cancer Institute. 12 August 2008. "Etoposide". NCI Drug Dictionary. National Cancer Institute. Portal: ...
https://en.wikipedia.org/wiki/Etoposide
Plasmablastic lymphomaPlasmablastic lymphoma
... etoposide, and high-dose cytarabine); COMB (i.e. cyclophosphamide, oncovin, methyl-CCNU, and bleomycin); and infusional EPOCH ( ... CHOP plus etoposide); hyper-CVAD-MA (i.e. cyclophosphamide, vincristine, doxorubicin, dexamethasone and high dose methotrexate ... i.e. etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin). While the experience treating PBL with radiation ...
https://en.wikipedia.org/wiki/Plasmablastic_lymphoma
GenisteinGenistein
etoposide and doxorubicin. In high doses it was found to be strongly toxic to normal cells. This effect may be responsible for ...
https://en.wikipedia.org/wiki/Genistein
ADE (chemotherapy)ADE (chemotherapy)
Etoposide - a topoisomerase inhibitor. Fludarabine and cytosine are less effective than standard ADE chemotherapy in high-risk ...
https://en.wikipedia.org/wiki/ADE_(chemotherapy)
MINE (chemotherapy)MINE (chemotherapy)
Etoposide - a topoisomerase inhibitor. A phase II trial of mesna / ifosfamide, mitoxantrone and etoposide for refractory ...
https://en.wikipedia.org/wiki/MINE_(chemotherapy)
Drug discoveryDrug discovery
Etoposide · Teniposide); 3a. Anthracyclines (Aclarubicin · Daunorubicin · Doxorubicin · Epirubicin · Idarubicin · Amrubicin · ...
https://en.wikipedia.org/wiki/Drug_discovery
ICE (chemotherapy)ICE (chemotherapy)
Etoposide - a topoisomerase inhibitor. Cycles are repeated every 14 days for 3 cycles, then high-dose chemotherapy with ... and Etoposide: A Highly Effective Cytoreduction and Peripheral-Blood Progenitor-Cell Mobilization Regimen for Transplant- ...
https://en.wikipedia.org/wiki/ICE_(chemotherapy)
EpipodophyllotoxinEpipodophyllotoxin
These include etoposide and teniposide. They act as anti-cancer drugs by inhibiting topoisomerase II. Podophyllotoxin Takimoto ...
https://en.wikipedia.org/wiki/Epipodophyllotoxin
Undifferentiated pleomorphic sarcomaUndifferentiated pleomorphic sarcoma
... or etoposide, ifosfamide, and cisplatin. These treatment regimens have been reported to lower local recurrence rates, prolong ...
https://en.wikipedia.org/wiki/Undifferentiated_pleomorphic_sarcoma
Small-cell carcinomaSmall-cell carcinoma
Cisplatin and etoposide, Carboplatin and etoposide. The drug paclitaxel may be useful in the treatment of cisplatin-resistant ... In this study, patients with ES-SCLC were treated with standard carboplatin plus etoposide and were randomized to receive ... First-line treatment is usually with cisplatin and etoposide. In Japan, first-line treatment is shifting to irinotecan and ... In cases of LS-SCLC, combination chemotherapy (usually cisplatin or carboplatin plus etoposide) is administered together with ...
https://en.wikipedia.org/wiki/Small-cell_carcinoma
EI24EI24
Etoposide-induced protein 2.4 homolog is a protein that in humans is encoded by the EI24 gene. This gene has higher expression ... "Entrez Gene: EI24 etoposide induced 2.4 mRNA". Maruyama K, Sugano S (1994). "Oligo-capping: a simple method to replace the cap ...
https://en.wikipedia.org/wiki/EI24
Hartmann F. StähelinHartmann F. Stähelin
A few years later, in November 1983, etoposide was approved by the U.S. Food and Drug Administration. Etoposide is still ... etoposide, Vepesid, discovered on 21 October 1966), which remains very clinically successful. Teniposide and etoposide were ... there are an astonishing number of coincidences between etoposide and cyclosporine. The first coincidence was that etoposide ... After a landmark clinical comparative analysis by F. Muggia and M. Rozencweig, etoposide and teniposide were licensed to ...
https://en.wikipedia.org/wiki/Hartmann_F._Stähelin
ChemotherapyChemotherapy
Podophyllotoxin is used to produce two other drugs with different mechanisms of action: etoposide and teniposide. Topoisomerase ... ifosfamide and etoposide. Permanent thinning or hair loss can result from some standard chemotherapy regimens. Chemotherapy ... These agents include etoposide, doxorubicin, mitoxantrone and teniposide. The second group, catalytic inhibitors, are drugs ...
https://en.wikipedia.org/wiki/Chemotherapy
Quinine 3-monooxygenaseQuinine 3-monooxygenase
Relling MV, Evans R, Dass C, Desiderio DM, Nemec J (1992). "Human cytochrome P450 metabolism of teniposide and etoposide". J. ... Zhao XJ, Kawashiro T, Ishizaki T (1998). "Mutual inhibition between quinine and etoposide by human liver microsomes. Evidence ...
https://en.wikipedia.org/wiki/Quinine_3-monooxygenase
Grapefruit-drug interactionsGrapefruit-drug interactions
Etoposide interferes with grapefruit, orange, and apple juices. Fexofenadine (Allegra) concentrations are decreased rather than ... Bitter oranges (such as the Seville oranges often used in marmalade) can interfere with drugs including etoposide, a ... Apple juice has been implicated in interfering with etoposide, a chemotherapy drug, and cyclosporine, taken by transplant ...
https://en.wikipedia.org/wiki/Grapefruit–drug_interactions
PodophyllotoxinPodophyllotoxin
For instance, etoposide binds and stabilizes the temporary DNA break caused by the enzyme, disrupts the reparation of the break ... Lau W, Sattely ES (September 2015). "Six enzymes from mayapple that complete the biosynthetic pathway to the etoposide aglycone ... Mutants resistant to either podophyllotoxin, or to its topoisomerase II inhibitory derivatives such as etoposide (VP-16), have ... Podophyllotoxin derived antitumor agents include etoposide and teniposide. These drugs have been successfully used in therapy ...
https://en.wikipedia.org/wiki/Podophyllotoxin
Endodermal sinus tumorEndodermal sinus tumor
Treatment with cisplatin, etoposide, and bleomycin has been described. Before modern chemotherapy, this type of neoplasm was ...
https://en.wikipedia.org/wiki/Endodermal_sinus_tumor
EPOCH (chemotherapy)EPOCH (chemotherapy)
If the nadir ANC > 500/μL, then the doses of etoposide, doxorubicin, and cyclophosphamide for the next cycle are all increased ... but doxorubicin and etoposide should not be reduced below the initial dose (dose in first course). W H Wilson, G Bryant, S ... Etoposide: a topoisomerase inhibitor from the group of epipodophyllotoxins; Prednisolone: a glucocorticoid hormone that can ... then the doses of etoposide, doxorubicin and cyclophosphamide are reduced by 20% below the doses used in the previous cycle, ...
https://en.wikipedia.org/wiki/EPOCH_(chemotherapy)
Metronomic therapyMetronomic therapy
Etoposide may also be effective in these frail patients. Although metastatic or recurrent lung cancer is difficult to be ... In addition, some chemotherapeutic agents including cyclophosphamide, methotrexate, vinblastine, paclitaxel and etoposide can ...
https://en.wikipedia.org/wiki/Metronomic_therapy
Epithelioid sarcomaEpithelioid sarcoma
Etoposide, vincristine, dactinomycin, and cyclophosphamide have also traditionally been given. Newer chemotherapies, such as ...
https://en.wikipedia.org/wiki/Epithelioid_sarcoma
DiazirineDiazirine
Examples include: The synthesis of a diazirine containing analog of etoposide, a widely used cancer drug targeting ... "A diazirine-based photoaffinity etoposide probe for labeling topoisomerase II". Bioorganic & Medicinal Chemistry. 18 (2): 830- ... topoisomerase II, which holds promise for the identification of the etoposide binding site. The discovery that caprolactam-type ...
https://en.wikipedia.org/wiki/Diazirine
EsthesioneuroblastomaEsthesioneuroblastoma
Cisplatin and etoposide are often used to treat esthesioneuroblastoma as neoadjuvants or adjuvants with radiotherapy or surgery ... November 2004). "Neoadjuvant etoposide, ifosfamide, and cisplatin for the treatment of olfactory neuroblastoma". Cancer. 101 ( ...
https://en.wikipedia.org/wiki/Esthesioneuroblastoma
SPTLC1SPTLC1
"Serine palmitoyltransferase regulates de novo ceramide generation during etoposide-induced apoptosis". The Journal of ...
https://en.wikipedia.org/wiki/SPTLC1
Lipid signalingLipid signaling
Chemotherapeutic agents such as daunorubicin and etoposide enhance the de novo synthesis of ceramide in studies done on ... 2000). "Serine palmitoyltransferase regulates de novo ceramide generation during etoposide-induced apoptosis". J. Biol. Chem. ...
https://en.wikipedia.org/wiki/Lipid_signaling
PAFAH1B2PAFAH1B2
"Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis". Proteomics. 5 (15): 3876-84. doi: ...
https://en.wikipedia.org/wiki/PAFAH1B2
TXNDC5TXNDC5
"Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis". Proteomics. 5 (15): 3876-84. doi: ...
https://en.wikipedia.org/wiki/TXNDC5
SARNPSARNP
"Identification of apoptotic tyrosine-phosphorylated proteins after etoposide or retinoic acid treatment". Proteomics. 4 (4): ...
https://en.wikipedia.org/wiki/SARNP
CAPZBCAPZB
"Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis". Proteomics. 5 (15): 3876-84. doi: ...
https://en.wikipedia.org/wiki/CAPZB
PFDN5PFDN5
"Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis". Proteomics. 5 (15): 3876-84. doi: ...
https://en.wikipedia.org/wiki/PFDN5
CLIC2CLIC2
2006). "Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis". Proteomics. 5 (15): 3876- ...
https://en.wikipedia.org/wiki/CLIC2
Etoposide: MedlinePlus Drug InformationEtoposide: MedlinePlus Drug Information
Etoposide: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Before taking etoposide,. *tell your doctor and pharmacist if you are allergic to etoposide, any other medications, or any of ... You should not become pregnant or breast-feed while you are taking etoposide. If you become pregnant while taking etoposide, ... Etoposide comes as a capsule to take by mouth. It is usually taken once a day for 4 or 5 days in a row. This cycle may be ...
https://medlineplus.gov/druginfo/meds/a684055.html
DailyMed - ETOPOSIDE injectionDailyMed - ETOPOSIDE injection
ETOPOSIDE (UNII: 6PLQ3CP4P3) (ETOPOSIDE - UNII:6PLQ3CP4P3) ETOPOSIDE. 20 mg in 1 mL. ... Etoposide has been shown to be teratogenic in mice and rats. In rats, an intravenous etoposide dose of 0.4 mg/kg/day (about 1/ ... Etoposide has been shown to be mutagenic in Ames assay.. Treatment of Swiss-Albino mice with 1.5 mg/kg IP of etoposide ... Etoposide Injection USP is contraindicated in patients who have demonstrated a previous hypersensitivity to etoposide or any ...
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4f850eb2-3542-43a0-90e8-bb37fa05cf15&audience=consumer
Jurkat Apoptosis Cell Extracts (etoposide) | Cell Signaling TechnologyJurkat Apoptosis Cell Extracts (etoposide) | Cell Signaling Technology
Apoptosis Cell Extracts (Jurkat + Etoposide): Total cell extracts from Jurkat cells treated with 25 μM etoposide for 5 hours ... Load 10 µl of untreated and etoposide treated Jurkat Apoptosis Control Cell Extracts (etoposide) per lane. ... Jurkat Apoptosis Cell Extracts (etoposide) 2043. Toggle Between Dark and Light Modes Filter: *WB ... Etoposide treatment induces proteolytic cleavage of various apoptosis-related proteins including caspases, IAP, and PARP. ...
https://www.cellsignal.com/products/experimental-controls/jurkat-apoptosis-cell-extracts-etoposide/2043
Etoposide InjectionEtoposide Injection
... can be used by cancer patients. Learn more about this medicine, the early and delayed side effects of using ... Etoposide Injection - Handling. How should I handle Etoposide Injection safely?. Etoposide Injection - Storage. How should I ... Before taking Etoposide Injection , what precautions must I follow?. What food or medicine must I avoid when I take Etoposide ... Etoposide Injection - What is it for. ​Etoposide Injection is an intravenous chemotherapy used alone or in combination with ...
https://www.singhealth.com.sg/patient-care/medicine/etoposide-injection
Etoposide Phosphate - Health Information Library | PeaceHealthEtoposide Phosphate - Health Information Library | PeaceHealth
... has decreased toxicity and improved effectiveness of chemotherapy with cisplatin plus etoposide and cisplatin plus 5-FU. ... has decreased toxicity and improved effectiveness of chemotherapy with cisplatin plus etoposide and cisplatin plus 5-FU. ...
https://www.peacehealth.org/medical-topics/id/hn-10001035
Etoposide (VP-16) | ≥99%(HPLC) | Topoisomerase II inhibitor | AdooQ®Etoposide (VP-16) | ≥99%(HPLC) | Topoisomerase II inhibitor | AdooQ®
Etoposide forms a ternary complex with DNA and the topoisomerase II enzyme (which aids in DNA unwinding), prevents re-ligation ... Keywords:buy Etoposide (VP-16) , Etoposide (VP-16) Supplier , purchase , cost , manufacturer , order , distributor , buy 33419- ... VP16, Vepesid, etoposide phosphate. SMILES. C[[email protected]@H]1OC[[email protected]@H]2[[email protected]@H](O1)[[email ... Publications Citing Use of Adooq Etoposide (VP-16) *Reiko Watanabe, .et al. Development of an In Silico Prediction Model for P- ...
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Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide. | Molecular...Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide. | Molecular...
Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide.. K Mizumoto, R J ... Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide.. K Mizumoto, R J ... Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide.. K Mizumoto, R J ... Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide. ...
https://molpharm.aspetjournals.org/content/46/5/890/tab-e-letters
Impact of cyclophosphamide and etoposide on outcome of clear cell sarcoma of the kidney treated on the National Wilms Tumor...Impact of cyclophosphamide and etoposide on outcome of clear cell sarcoma of the kidney treated on the National Wilms Tumor...
Impact of cyclophosphamide and etoposide on outcome of clear cell sarcoma of the kidney treated on the National Wilms Tumor ... Research InnovationPublications Impact of cyclophosphamide and etoposide on outcome of clear cell sarcoma of the kidney treated ... Treatment consisted of vincristine/doxorubicin/cyclophosphamide alternating with cyclophosphamide/etoposide for 24 weeks and ... by incorporating cyclophosphamide and etoposide into treatment on National Wilms Tumor Study (NWTS)-5. PATIENTS AND METHODS: ...
https://www.luriechildrens.org/en/research/publications/impact-of-cyclophosphamide-and-etoposide-on-outcome-of-clear-cell-sarcoma-of-the-kidney-treated-on-the-national-wilms-tumor-study-5-nwts-5/
Treatment of high-risk gestational trophoblastic neoplasia with etoposide, methotrexate, actinomycin D, cyclophosphamide, and...
N2 - Objective The objective of the study was to evaluate the efficacy and toxicity of etoposide, methotrexate, actinomycin D, ... AB - Objective The objective of the study was to evaluate the efficacy and toxicity of etoposide, methotrexate, actinomycin D, ... Objective The objective of the study was to evaluate the efficacy and toxicity of etoposide, methotrexate, actinomycin D, ... abstract = "Objective The objective of the study was to evaluate the efficacy and toxicity of etoposide, methotrexate, ...
https://www.scholars.northwestern.edu/en/publications/treatment-of-high-risk-gestational-trophoblastic-neoplasia-with-e
Evaluation of clinical process in osteosarcoma patients treated with chemotherapy including cisplatin, adriamycin, ifosfamide,...Evaluation of clinical process in osteosarcoma patients treated with chemotherapy including cisplatin, adriamycin, ifosfamide,...
Goorin AM, Harris MB, Bernstein M, Ferguson W, Devidas M, Siegal GP, et al. Phase II/III trial of etoposide and high-dose ... Each 21-day alternative with etoposide 100 mg/m 2 for 3 days and ifosfamide 2 g/m 2 in an infusion of 6 h simultaneous with ... Miser JS, Kinsella TJ, Triche TJ, Tsokos M, Jarosinski P, Forquer R, et al. Ifosfamide with mesna uroprotection and etoposide: ... Aim: The aim of this study was to evaluate the effect of adding etoposide and ifosfamide chemotherapy drugs to treatment ...
https://cancerjournal.net/article.asp?issn=0973-1482
Efficacy and Safety of Apatinib Combined with Etoposide in Patients with Recurrent Platinum-resistant Epithelial Ovarian Cancer...Efficacy and Safety of Apatinib Combined with Etoposide in Patients with Recurrent Platinum-resistant Epithelial Ovarian Cancer...
Keywords: Apatinib, Etoposide, Epithelial ovarian cancer, Efficacy, Safety Citation styles. APA Copy. Huang, Q., Chu, C., Tang ... Huang Q, Chu C, Tang J, Dai Z. Efficacy and Safety of Apatinib Combined with Etoposide in Patients with Recurrent Platinum- ... Huang Q, Chu C, Tang J, Dai Z. Efficacy and Safety of Apatinib Combined with Etoposide in Patients with Recurrent Platinum- ... Huang, Q.; Chu, C.; Tang, J.; Dai, Z. Efficacy and Safety of Apatinib Combined with Etoposide in Patients with Recurrent ...
https://jcancer.org/v11p5353
Pediatric Acute Myelocytic Leukemia Medication: Chemotherapeutic agents, Antiemetic agents, Antimicrobials, prophylactic,...Pediatric Acute Myelocytic Leukemia Medication: Chemotherapeutic agents, Antiemetic agents, Antimicrobials, prophylactic,...
Etoposide is a podophyllotoxin derivative. It is used in the induction and consolidation phases of treatment. ...
https://www.medscape.com/answers/987228-175617/what-medications-are-used-in-pediatric-acute-myelocytic-leukemia-aml-treatment
Arctigenin Inhibits Etoposide Resistance in HT-29 Colon Cancer CellsArctigenin Inhibits Etoposide Resistance in HT-29 Colon Cancer Cells
Arctigenin is a novel therapeutic agent that inhibits resistance to etoposide associated with microenvironmental stress ... Arctigenin was also highly toxic to etoposide-resistant HT-29 cells, with an ICvalue of 10μM for colony formation. We further ... Thus, these results suggest that arctigenin is a novel therapeutic agent that inhibits resistance to etoposide associated with ... Arctigenin Inhibits Etoposide Resistance in HT-29 Colon Cancer Cells during Microenvironmental Stress. ...
http://cdn.greenmedinfo.com/article/arctigenin-novel-therapeutic-agent-inhibits-resistance-etoposide-associated-mi
Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide<...
Etoposide at 10 μM killed 70% of the cells within 4 days, a result that was accompanied by DNA fragmentation. A characteristic ... Etoposide at 10 μM killed 70% of the cells within 4 days, a result that was accompanied by DNA fragmentation. A characteristic ... Etoposide at 10 μM killed 70% of the cells within 4 days, a result that was accompanied by DNA fragmentation. A characteristic ... Etoposide at 10 μM killed 70% of the cells within 4 days, a result that was accompanied by DNA fragmentation. A characteristic ...
https://kyushu-u.pure.elsevier.com/en/publications/programmed-cell-death-apoptosis-of-mouse-fibroblasts-is-induced-b
ETOPOSIDE - TopMedsETOPOSIDE - TopMeds
Etoposide is used in combination with other medications to treat a certain type of lung cancer (small cell lung cancer; SCLC). ... Etoposide is used in combination with other medications to treat a certain type of lung cancer (small cell lung cancer; SCLC). ... Etoposide is in a class of medications known as podophyllotoxin derivatives. It works by slowing or stopping the growth of ... Etoposide is in a class of medications known as podophyllotoxin derivatives. It works by slowing or stopping the growth of ...
https://topmeds.net/product-category/cancer-medicines/etoposide/
PQR | EtoposidePQR | Etoposide
You are viewing an interactive 3D depiction of the molecule etoposide (C29H32O13) from the PQR. ...
http://pqr.pitt.edu/mol/VJJPUSNTGOMMGY-ATGQWNQNSA-N
EFFETTI SUL CAMPO VISIVO DELLA TERAPIA CON CARBOPLATINO-ETOPOSIDE<...
keywords = "carboplatin, chemotherapy, etoposide, visual field",. author = "C. Gelmi and A. Bruno and R. Ceccuzzi and Castagni ... EFFETTI SUL CAMPO VISIVO DELLA TERAPIA CON CARBOPLATINO-ETOPOSIDE. / Gelmi, C.; Bruno, A.; Ceccuzzi, R. et al. ... EFFETTI SUL CAMPO VISIVO DELLA TERAPIA CON CARBOPLATINO-ETOPOSIDE. In: Annali di Ottalmologia e Clinica Oculistica. 1995 ; Vol ... EFFETTI SUL CAMPO VISIVO DELLA TERAPIA CON CARBOPLATINO-ETOPOSIDE. Translated title of the contribution. : Visual field after ...
https://moh-it.pure.elsevier.com/en/publications/visual-field-after-carboplatin-and-etoposide-therapy
Etoposide - Dr. AdemEtoposide - Dr. Adem
Etoposide is a chemotherapy drug and in medical use since 1983. It is classified as a "plant alkaloid". Etoposide blocks an ... Fact Sheet - Everything You Should Know In this Etoposide fact sheet, youll get to know about the precautions, usage, possible ...
https://dr-adem.com/tag/etoposide/
Physicians Poster Sessions | Bone Marrow TransplantationPhysicians Poster Sessions | Bone Marrow Transplantation
Cytarabine/etoposide/lomustine/melphalan Reactions Weekly (2016). * Antineoplastics Reactions Weekly (2016). * Ciclosporin/ ...
https://www.nature.com/articles/bmt201648?error=cookies_not_supported&code=787a5d71-e23d-4006-9e4f-f79e19de096c
Superiority of sequential versus concurrent administration of paclitaxel with etoposide in advanced non-small cell lung cancer:...
All patients received etoposide at 100 mg/m2, given as an i.v. infusion on days 1, 2, and 3. The first 20 patients (part A) ... Our findings suggest that etoposide followed by paclitaxel is well tolerated and has greater activity in NSCLC than concurrent ... We performed two sequential Phase II trials using different sequence schedules of paclitaxel and etoposide as first-line ... also received paclitaxel at 175 mg/m2 as a 3-h infusion on day 1, immediately prior to etoposide. The subsequent 24 patients ( ...
https://www.well.ox.ac.uk/publications/1212590
etoposide - New Developments in Lymphomaetoposide - New Developments in Lymphoma
Tag: etoposide. Oral Chemotherapy Bill Signed into Law in New York State. On September 23 New York Governor Andrew Cuomo signed ... Categories Lymphoma News, Patient EducationTags cancer treatment, cyclophosphamide, etoposide, health insurance, New York State ... For lymphoma patients, oral chemotherapy agents that are sometimes used include cyclophosphamide (cytoxan), etoposide (VP-16), ...
https://cornell-lymphoma.com/tag/etoposide/
Perbandingan Rejimen Kemoterapi Cisplatin Etoposide dengan Cisplatin-Docetaxel dalam Hal Kesintasan 2 Tahun dan Progression...
Harahap, S. P., Sutandyo, N., R., C. M., & Shatri, H. (2016). Perbandingan Rejimen Kemoterapi Cisplatin Etoposide dengan ... Harahap, SP, Sutandyo, N, R., CM & Shatri, H 2016, Perbandingan Rejimen Kemoterapi Cisplatin Etoposide dengan Cisplatin- ... The survival with cisplatin-docexatel is better compared to cisplatin-etoposide, this applies to PFS as well. ... The survival with cisplatin-docexatel is better compared to cisplatin-etoposide, this applies to PFS as well.", ...
https://scholar.ui.ac.id/en/publications/perbandingan-rejimen-kemoterapi-cisplatin-etoposide-dengan-cispla
Retinoblastoma Medication: Anticancer drugs, ImmunosuppressantsRetinoblastoma Medication: Anticancer drugs, Immunosuppressants
The addition of cyclosporine in combination with chemotherapy regimen of carboplatin, etoposide, and vincristine reportedly ...
https://emedicine.medscape.com/article/1222849-medication
Cisplatin, Etoposide and Radiotherapy - SWAG Cancer AllianceCisplatin, Etoposide and Radiotherapy - SWAG Cancer Alliance
SWAG Cancer Alliance is not responsible for the content or reliability of the websites we link to and do not necessarily endorse the views expressed within them. We aim to replace broken links to other sites but cannot guarantee that these links will always work as we have no control over the availability of other sites. Due to the very nature of the internet we cannot guarantee our site or other sites we link to will always be available to you.. ...
https://www.swagcanceralliance.nhs.uk/protocols/cisplatin-etoposide-and-radiotherapy/
Paraplatin + etoposide Chemotherapy, Side Effects - Navigating CareParaplatin + etoposide Chemotherapy, Side Effects - Navigating Care
... etoposide treatment for Small Cell Lung Cancer, how its given and possible side effects. Get free tools to track your health. ... Paraplatin + etoposide for the treatment of Small Cell Lung Cancer Paraplatin + etoposide is a chemotherapy regimen used in the ... This treatment involves two chemotherapy drugs: Paraplatin (carboplatin) and etoposide. Chemotherapy is often given as a ... How Paraplatin + etoposide chemotherapy is given and possible side effects.. ...
https://rhopa.navigatingcare.com/chemotherapy_treatments/carboplatin-etoposide-sclc
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In vitro comparison of podophyllotoxin analogues; etoposide, teniposide and NK 611 using human lung cancer cell lines<...
In vitro comparison of podophyllotoxin analogues; etoposide, teniposide and NK 611 using human lung cancer cell lines. In: ... In vitro comparison of podophyllotoxin analogues; etoposide, teniposide and NK 611 using human lung cancer cell lines. Japanese ... In vitro comparison of podophyllotoxin analogues; etoposide, teniposide and NK 611 using human lung cancer cell lines. / ... In vitro comparison of podophyllotoxin analogues; etoposide, teniposide and NK 611 using human lung cancer cell lines. ...
https://okayama.pure.elsevier.com/en/publications/in-vitro-comparison-of-podophyllotoxin-analogues-etoposide-tenipo
IfosfamideCarboplatin and EtoposideDoxorubicinMethotrexateVincristinePodophyllotoxinPrecautionsEffect of etoposideCisplatin or CarboplatinCyclophosphamide and etoposideTopoisomeraseOral etoposidePaclitaxelDoseCapsuleCombination chemotherapyIntravenousPatientsTreatmentMouse fibroblastsInjectionMetastaticRenalInhibitsCancerTumorsDosageVitroCellsSynthesis
Ifosfamide9
  • Patients who had incomplete responses or developed resistance to EMA-CO were treated with drug combinations employing cisplatin and etoposide with or without bleomycin or ifosfamide. (northwestern.edu)
  • The aim of this study was to evaluate the effect of adding etoposide and ifosfamide chemotherapy drugs to treatment regimen of patients affected with osteosarcoma and to determine the clinical process and response to treatment during a follow-up period of 11 years. (cancerjournal.net)
  • The initial chemotherapy which consisted of four cycles of cisplatin and adriamycin alternative with ifosfamide and etoposide was provided. (cancerjournal.net)
  • This phase II trial studies the effect of polatuzumab vedotin, rituximab, ifosfamide, carboplatin, and etoposide as initial salvage therapy in treating patients with diffuse large B-cell lymphoma that has come back (relapsed) or does not respond to treatment (refractory). (survivornet.com)
  • Chemotherapy drugs, such as ifosfamide, carboplatin, and etoposide, work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. (survivornet.com)
  • I. Evaluate the safety and tolerability of polatuzumab vedotin (Pola) added to rituximab, ifosfamide, carboplatin, and etoposide (PolaR-ICE) as first salvage therapy for relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL). (survivornet.com)
  • SALVAGE THERAPY: Patients receive polatuzumab vedotin intravenously (IV) on day 1, rituximab IV on day 1, etoposide IV on days 1-3, carboplatin IV on day 2, and ifosfamide IV on day 2 or days 1-3. (survivornet.com)
  • To improve the results of salvage therapy we studied the efficacy and toxicity of a combination of etoposide (100 mg/m 2 IV qd × 5), ifosfamide (1.5 g/m 2 /d × 5), and mitoxantrone (8 mg/m 2 /d IV × 3) in 11 adult patients with relapsed or refractory ALL. (elsevier.com)
  • These results demonstrate that the combination of etoposide, ifosfamide, and mitoxantrone can be used as an effective salvage therapy for patients with resistant ALL. (elsevier.com)
Carboplatin and Etoposide6
  • Visual field was performed in thirteen patients affected by cerebral neoplasms after treatment with intra-arterial Carboplatin and Etoposide therapy, in order to evaluate a possible toxic effect. (elsevier.com)
  • This trial is looking at a new drug called LY2940680 with carboplatin and etoposide chemotherapy for small cell lung cancer that has spread beyond the lungs. (cancerresearchuk.org)
  • One combination of drugs they use is carboplatin and etoposide . (cancerresearchuk.org)
  • In this trial some people will have LY2940680 with carboplatin and etoposide. (cancerresearchuk.org)
  • with carboplatin and etoposide. (cancerresearchuk.org)
  • In part 1, the first few people will have a low dose of LY2940680 with carboplatin and etoposide. (cancerresearchuk.org)
Doxorubicin2
  • Treatment consisted of vincristine/doxorubicin/cyclophosphamide alternating with cyclophosphamide/etoposide for 24 weeks and radiation to sites of disease. (luriechildrens.org)
  • In these patients, we recommend either mitotane monotherapy or mitotane, etoposide, doxorubicin and cisplatin depending on prognostic parameters. (bvsalud.org)
Methotrexate3
  • Objective The objective of the study was to evaluate the efficacy and toxicity of etoposide, methotrexate, actinomycin D, cyclophosphamide, and vincristine (EMA-CO) chemotherapy for the treatment of high-risk gestational trophoblastic neoplasia. (northwestern.edu)
  • High-dose methotrexate, etoposide, dexamethasone and pegaspargase (MEDA) combination chemotherapy is effective for advanced and relapsed/refractory extranodal natural killer/T cell lymphoma: a retrospective study. (bvsalud.org)
  • In this study, we retrospectively assessed the efficacy and safety of MEDA regimen ( methotrexate , etoposide , dexamethasone and pegaspargase) in the treatment of advanced and relapsed/refractory ENK/TCL patients . (bvsalud.org)
Vincristine1
  • The addition of cyclosporine in combination with chemotherapy regimen of carboplatin, etoposide, and vincristine reportedly have showed enhanced efficacy of chemotherapy. (medscape.com)
Podophyllotoxin4
  • Etoposide is in a class of medications known as podophyllotoxin derivatives. (medlineplus.gov)
  • Etoposide (also commonly known as VP-16) is a semisynthetic derivative of podophyllotoxin used in the treatment of certain neoplastic diseases. (nih.gov)
  • Etoposide is a podophyllotoxin derivative. (medscape.com)
  • Etoposide (VP-16), a semisynthetic plant derivative of podophyllotoxin. (medscape.com)
Precautions2
  • Before taking Etoposide Injection , what precautions must I follow? (singhealth.com.sg)
  • Fact Sheet - Everything You Should Know In this Etoposide fact sheet, you'll get to know about the precautions, usage, possible side effects, and the. (dr-adem.com)
Effect of etoposide1
  • The predominant macromolecular effect of etoposide appears to be the induction of DNA strand breaks by an interaction with DNA topoisomerase II or the formation of free radicals. (nih.gov)
Cisplatin or Carboplatin1
  • Patients were treated on sequential dose escalation cohorts of tarextumab (5-15mg/kg) administered every three weeks with etoposide and either cisplatin or carboplatin (platinum-based therapy). (globenewswire.com)
Cyclophosphamide and etoposide2
  • PURPOSE: To improve the event-free survival (EFS) and overall survival (OS) for patients with clear cell sarcoma of the kidney (CCSK) by incorporating cyclophosphamide and etoposide into treatment on National Wilms Tumor Study (NWTS)-5. (luriechildrens.org)
  • Dose-intense cyclophosphamide and etoposide for patients with refractory or high-risk non-Hodgkin's lymphoma. (duke.edu)
Topoisomerase5
  • Etoposide forms a ternary complex with DNA and the topoisomerase II enzyme (which aids in DNA unwinding), prevents re-ligation of the DNA strands, and by doing so causes DNA strands to break. (adooq.com)
  • Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide. (aspetjournals.org)
  • The mechanism by which etoposide, a topoisomerase II inhibitor, killed replicating mouse L929 fibroblasts was investigated. (elsevier.com)
  • Farber, John L. / Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide . (elsevier.com)
  • Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA . (bvsalud.org)
Oral etoposide1
  • Chemotherapy comprises oral estramustine 3 times daily and oral etoposide twice daily on days 1-14 and paclitaxel IV over 1 hour on day 2. (clinicaltrials.gov)
Paclitaxel10
  • Superiority of sequential versus concurrent administration of paclitaxel with etoposide in advanced non-small cell lung cancer: comparison of two Phase II trials. (ox.ac.uk)
  • Paclitaxel and etoposide are two chemotherapy agents with broad cytotoxic activity and different mechanisms of action and resistance. (ox.ac.uk)
  • We performed two sequential Phase II trials using different sequence schedules of paclitaxel and etoposide as first-line treatment in advanced non-small cell lung cancer (NSCLC). (ox.ac.uk)
  • The first 20 patients (part A) also received paclitaxel at 175 mg/m2 as a 3-h infusion on day 1, immediately prior to etoposide. (ox.ac.uk)
  • In conclusion, toxicity and antitumor activity of the paclitaxel/etoposide combination may be sequence dependent. (ox.ac.uk)
  • Our findings suggest that etoposide followed by paclitaxel is well tolerated and has greater activity in NSCLC than concurrent administration. (ox.ac.uk)
  • IMSEAR at SEARO: Phase II study of cisplatin, etoposide and paclitaxel in locally advanced or metastatic adenocarcinoma of gastric/gastroesophageal junction. (who.int)
  • AIMS: To evaluate safety and efficacy of low-dose cisplatin, etoposide and paclitaxel (CEP) based combination chemotherapy in locally advanced or metastatic adenocarcinoma of gastric/gastroesophageal junction. (who.int)
  • MATERIALS AND METHODS: Thirty-three patients were enrolled onto this study, out of which, all but one received cisplatin 15 mg/m 2, etoposide 40 mg/m 2 and paclitaxel 50 mg/m 2, given on day 1 and 4 every week for three weeks in a 28-day cycle. (who.int)
  • Compare the efficacy of androgen suppression and radiotherapy with or without subsequent paclitaxel, estramustine, and etoposide, in terms of overall and disease-free survival, biochemical and local control, and freedom from distant metastasis, in patients with localized high-risk prostate cancer. (clinicaltrials.gov)
Dose6
  • Etoposide Injection USP is available for intravenous use as 20 mg/mL solution in 100 mg (5 mL), 250 mg (12.5 mL), 500 mg (25 mL), and 1 g (50 mL) sterile, multiple-dose vials. (nih.gov)
  • After intravenous administration of 14 C-etoposide (100 to 124 mg/m 2 ), mean recovery of radioactivity in the urine was 56% of the dose at 120 hours, 45% of which was excreted as etoposide: fecal recovery of radioactivity was 44% of the dose at 120 hours. (nih.gov)
  • A retrospective review was performed on the toxicity and response to one cycle of dose-intense cyclophosphamide/etoposide, followed by consolidation in patients with refractory or previously untreated, high-risk non-Hodgkin's lymphoma (NHL). (duke.edu)
  • However, the metabolites did exhibit dose-dependent depletion of glutathione, resembling the behavior of etoposide, a hindered phenol with antioxidant properties against lipid peroxidation. (cdc.gov)
  • In this study we evaluated the results of low dose, continuous infusion etoposide over 21 days added to a conventional high-dose regimen of carboplatin and thiotepa in eight patients with relapsed pediatric CNS tumors. (mssm.edu)
  • A Phase 2 dose of tarextumab 15mg/kg every three weeks with etoposide and platinum-based therapy was selected with consideration to safety, pharmacodynamics, radiographic tumor reduction and potentially longer survival in biomarker positive patients. (globenewswire.com)
Capsule2
Combination chemotherapy2
  • Ninety-two patients with advanced non-small cell lung cancer were treated with a combination chemotherapy regimen containing cisplatin, vindesine, and etoposide. (elsevier.com)
  • Combination chemotherapy consisting of irinotecan, etoposide, and carboplatin for refractory or relapsed neuroblastoma. (cdc.gov)
Intravenous2
  • On intravenous administration, the disposition of etoposide is best described as a biphasic process with a distribution half-life of about 1.5 hours and terminal elimination half-life ranging from 4 to 11 hours. (nih.gov)
  • Etoposide Injection is an intravenous chemotherapy used alone or in combination with other agents for the treatment of certain types of cancer. (singhealth.com.sg)
Patients9
  • Etoposide binding ratio correlates directly with serum albumin in patients with cancer and in normal volunteers. (nih.gov)
  • The unbound fraction of etoposide significantly correlated with bilirubin in a population of cancer patients. (nih.gov)
  • This study aimed to assess the efficacy and safety of apatinib combined with etoposide in patients with recurrent platinum-resistant EOC. (jcancer.org)
  • We have reviewed a total of 33 patients with recurrent platinum-resistant EOC from July 2017 to July 2018, who were regularly treated with apatinib and etoposide until disease progression or unacceptable toxic effects occurred. (jcancer.org)
  • At the date of the review finished, 15 of 33 (45.5%) patients remained on the combined treatment of apatinib and etoposide, while the other 18 (54.5%) had discontinued. (jcancer.org)
  • The efficacy of apatinib combined with etoposide is encouraging in patients with platinum-resistant EOC. (jcancer.org)
  • All patients received etoposide at 100 mg/m2, given as an i.v. infusion on days 1, 2, and 3. (ox.ac.uk)
  • For lymphoma patients, oral chemotherapy agents that are sometimes used include cyclophosphamide (cytoxan), etoposide (VP-16), and procarbazine (matulane). (cornell-lymphoma.com)
  • Fifty-five patients with refractory NHL and 13 with untreated, high-risk NHL were administered one cycle of daily cyclophosphamide 1.5 g/m2 intravenously on days 1-4 and etoposide 300 mg/m2 intravenously every 12 hours on days 1-3. (duke.edu)
Treatment4
  • Etoposide treatment induces proteolytic cleavage of various apoptosis-related proteins including caspases, IAP, and PARP. (cellsignal.com)
  • When added 6-24 hr after treatment with etoposide, cycloheximide lost the ability to protect cells. (elsevier.com)
  • Paraplatin + etoposide is a chemotherapy regimen used in the treatment of small cell lung cancer. (navigatingcare.com)
  • You have etoposide on the first 3 days of each 4 week cycle of treatment. (cancerresearchuk.org)
Mouse fibroblasts1
  • The data document that the killing of replicating mouse fibroblasts by etoposide represents an example of programmed cell death (apoptosis) that depends on protein synthesis. (elsevier.com)
Injection6
Metastatic1
  • iii) We recommend that adrenal surgery for (suspected) ACC should be performed only by surgeons experienced in adrenal and oncological surgery aiming at a complete en bloc resection (including resection of oligo-metastatic disease). (bvsalud.org)
Renal2
  • An inverse relationship between plasma albumin levels and etoposide renal clearance is found in children. (nih.gov)
  • In people with renal illness, Etoposide should be taken with care. (fedeltyhealthcare.com)
Inhibits2
  • Arctigenin is a novel therapeutic agent that inhibits resistance to etoposide associated with microenvironmental stress conditions. (greenmedinfo.com)
  • Arctigenin Inhibits Etoposide Resistance in HT-29 Colon Cancer Cells during Microenvironmental Stress. (greenmedinfo.com)
Cancer4
  • Etoposide is also sometimes used to treat certain types of ovarian cancer (cancer that begins in the female reproductive organs where eggs are formed). (medlineplus.gov)
  • Etoposide should be administered under the supervision of a qualified physician experienced in the use of cancer chemotherapeutic agents. (nih.gov)
  • Attention California Residents: This product can expose you to chemicals including Etoposide (VP-16) , which is known to the State of California to cause cancer and birth defects or other reproductive harm. (adooq.com)
  • Etoposide is a cancer-fighting drug. (fedeltyhealthcare.com)
Tumors1
  • Etoposide concentrations are higher in normal lung than in lung metastases and are similar in primary tumors and normal tissues of the myometrium. (nih.gov)
Dosage1
Vitro1
  • In vitro , etoposide is highly protein bound (97%) to human plasma proteins. (nih.gov)
Cells9
  • Etoposide can cause a severe decrease in the number of blood cells in your bone marrow. (medlineplus.gov)
  • Apoptosis Cell Extracts (Jurkat + Etoposide): Total cell extracts from Jurkat cells treated with 25 μM etoposide for 5 hours serve as a positive control for activated apoptotic cascades. (cellsignal.com)
  • In this study, we investigated the active compound arctigenin, which inhibited microenvironmental stress-induced etoposide resistance in HT-29 cells. (greenmedinfo.com)
  • Arctigenin was also highly toxic to etoposide-resistant HT-29 cells, with an ICvalue of 10μM for colony formation. (greenmedinfo.com)
  • Etoposide at 10 μM killed 70% of the cells within 4 days, a result that was accompanied by DNA fragmentation. (elsevier.com)
  • Simultaneous exposure of the cells to 10 μM etoposide plus 1 μM cycloheximide reduced both the extent of cell killing and the fragmentation of DNA. (elsevier.com)
  • Delayed addition of cycloheximide protected cells only if cycloheximide was added 1-6 hr after exposure to etoposide. (elsevier.com)
  • Etoposide blocks an enzyme in cells called. (dr-adem.com)
  • Prostate epithelial cells exposed to NO for prolonged periods displayed increased resistance to apoptosis, coupled with a dampened p53/p21 response to the DNA damaging agent etoposide. (nuigalway.ie)
Synthesis4
  • Furthermore, DNA synthesis was inhibited by either etoposide or cycloheximide within 6 hr. (elsevier.com)
  • Protein synthesis, however, was not inhibited by etoposide. (elsevier.com)
  • Thus, an imbalance between protein synthesis and DNA synthesis cannot explain the cell killing by etoposide. (elsevier.com)
  • Although protein synthesis is required during the first 24 hr of exposure to etoposide, cell death is delayed until several days later. (elsevier.com)
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