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.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
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.
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.
Positional isomer of CYCLOPHOSPHAMIDE which is active as an alkylating agent and an immunosuppressive agent.
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.
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 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.
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.
An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.)
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
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.
An organoplatinum compound that possesses antineoplastic activity.
An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
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.
Tumors or cancer of the LUNG.
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.
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)
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)
Substances that inhibit or prevent the proliferation of NEOPLASMS.
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.
Compounds that inhibit cell production of DNA or RNA.
Compounds that inhibit the activity of DNA TOPOISOMERASES.
Leukopenia is a condition characterized by an abnormally low white blood cell count (less than 4,000 cells per microliter of blood) in peripheral blood, increasing the risk of infection due to decreased immune defense.
Transplantation of an individual's own tissue from one site to another site.
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
An anthracenedione-derived antineoplastic agent.
Therapeutic act or process that initiates a response to a complete or partial remission level.
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 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.
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.
The giving of drugs, chemicals, or other substances by mouth.
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.
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.
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.
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.
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)
Disorders of the blood and blood forming tissues.
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.
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.
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.
An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.
Compounds that inhibit the activity of DNA TOPOISOMERASE I.
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.
Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.
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.
An antimitotic agent with immunosuppressive properties.
A decrease in the number of NEUTROPHILS found in the blood.
A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.
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.
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.
A subnormal level of BLOOD PLATELETS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.
Simultaneous resistance to several structurally and functionally distinct drugs.
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).
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.
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.
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
Antitumor alkaloid isolated from Vinca rosea. (Merck, 11th ed.)
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.
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 are a diverse group of tumors that originate in the retroperitoneal space, which is the area behind the peritoneum and includes the kidneys, adrenal glands, pancreas, and major blood vessels.
Absence of hair from areas where it is normally present.
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
Bone marrow diseases, also known as hematologic or blood disorders, refer to conditions that affect the production and function of blood cells within the bone marrow, such as leukemia, lymphoma, myeloma, and aplastic anemia, potentially leading to complications like anemia, neutropenia, thrombocytopenia, and increased susceptibility to infections or bleeding.
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.
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.
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)
A folate analog consisting of the pharmacologically active isomer of LEUCOVORIN.
A cell line derived from cultured tumor cells.
The action of a drug in promoting or enhancing the effectiveness of another drug.
A form of highly malignant lung cancer that is composed of small ovoid cells (SMALL CELL CARCINOMA).
A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.
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.
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 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)

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

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

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

Antineoplastic agents, phytogenic, also known as plant-derived anticancer drugs, are medications that are derived from plants and used to treat cancer. These agents have natural origins and work by interfering with the growth and multiplication of cancer cells, helping to slow or stop the spread of the disease. Some examples of antineoplastic agents, phytogenic include paclitaxel (Taxol), vincristine, vinblastine, and etoposide. These drugs are often used in combination with other treatments such as surgery, radiation therapy, and other medications to provide a comprehensive approach to cancer care.

Antineoplastic combined chemotherapy protocols refer to a treatment plan for cancer that involves the use of more than one antineoplastic (chemotherapy) drug given in a specific sequence and schedule. The combination of drugs is used because they may work better together to destroy cancer cells compared to using a single agent alone. This approach can also help to reduce the likelihood of cancer cells becoming resistant to the treatment.

The choice of drugs, dose, duration, and frequency are determined by various factors such as the type and stage of cancer, patient's overall health, and potential side effects. Combination chemotherapy protocols can be used in various settings, including as a primary treatment, adjuvant therapy (given after surgery or radiation to kill any remaining cancer cells), neoadjuvant therapy (given before surgery or radiation to shrink the tumor), or palliative care (to alleviate symptoms and prolong survival).

It is important to note that while combined chemotherapy protocols can be effective in treating certain types of cancer, they can also cause significant side effects, including nausea, vomiting, hair loss, fatigue, and an increased risk of infection. Therefore, patients undergoing such treatment should be closely monitored and managed by a healthcare team experienced in administering chemotherapy.

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

Ifosfamide is an alkylating agent, which is a type of chemotherapy medication. It works by interfering with the DNA of cancer cells, preventing them from dividing and growing. Ifosfamide is used to treat various types of cancers, such as testicular cancer, small cell lung cancer, ovarian cancer, cervical cancer, and certain types of sarcomas.

The medical definition of Ifosfamide is:

Ifosfamide is a synthetic antineoplastic agent, an oxazaphosphorine derivative, with the chemical formula C6H15Cl2N2O2P. It is used in the treatment of various malignancies, including germ cell tumors, sarcomas, lymphomas, and testicular cancer. The drug is administered intravenously and exerts its cytotoxic effects through the alkylation and cross-linking of DNA, leading to the inhibition of DNA replication and transcription. Ifosfamide can cause significant myelosuppression and has been associated with urotoxicity, neurotoxicity, and secondary malignancies. Therefore, it is essential to monitor patients closely during treatment and manage any adverse effects promptly.

Cisplatin is a chemotherapeutic agent used to treat various types of cancers, including testicular, ovarian, bladder, head and neck, lung, and cervical cancers. It is an inorganic platinum compound that contains a central platinum atom surrounded by two chloride atoms and two ammonia molecules in a cis configuration.

Cisplatin works by forming crosslinks between DNA strands, which disrupts the structure of DNA and prevents cancer cells from replicating. This ultimately leads to cell death and slows down or stops the growth of tumors. However, cisplatin can also cause damage to normal cells, leading to side effects such as nausea, vomiting, hearing loss, and kidney damage. Therefore, it is essential to monitor patients closely during treatment and manage any adverse effects promptly.

Carcinoma, small cell is a type of lung cancer that typically starts in the bronchi (the airways that lead to the lungs). It is called "small cell" because the cancer cells are small and appear round or oval in shape. This type of lung cancer is also sometimes referred to as "oat cell carcinoma" due to the distinctive appearance of the cells, which can resemble oats when viewed under a microscope.

Small cell carcinoma is a particularly aggressive form of lung cancer that tends to spread quickly to other parts of the body. It is strongly associated with smoking and is less common than non-small cell lung cancer (NSCLC), which accounts for about 85% of all lung cancers.

Like other types of lung cancer, small cell carcinoma may not cause any symptoms in its early stages. However, as the tumor grows and spreads, it can cause a variety of symptoms, including coughing, chest pain, shortness of breath, hoarseness, and weight loss. Treatment for small cell carcinoma typically involves a combination of chemotherapy, radiation therapy, and sometimes surgery.

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

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

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

Podophyllotoxin is a pharmaceutical agent derived from the podophyllum plant. It is an antimitotic compound that inhibits microtubule assembly, leading to cell cycle arrest and apoptosis. It is primarily used in topical form as a treatment for genital warts, caused by certain types of human papillomavirus (HPV). Podophyllotoxin works by interfering with the growth of the wart cells, eventually causing them to die off.

It's important to note that podophyllotoxin is a potent cytotoxic agent and should only be used under the supervision of a healthcare professional. It should not be taken orally or applied to open wounds, and it should be kept out of reach of children.

Vincristine is an antineoplastic agent, specifically a vinca alkaloid. It is derived from the Madagascar periwinkle plant (Catharanthus roseus). Vincristine binds to tubulin, a protein found in microtubules, and inhibits their polymerization, which results in disruption of mitotic spindles leading to cell cycle arrest and apoptosis (programmed cell death). It is used in the treatment of various types of cancer including leukemias, lymphomas, and solid tumors. Common side effects include peripheral neuropathy, constipation, and alopecia.

Doxorubicin is a type of chemotherapy medication known as an anthracycline. It works by interfering with the DNA in cancer cells, which prevents them from growing and multiplying. Doxorubicin is used to treat a wide variety of cancers, including leukemia, lymphoma, breast cancer, lung cancer, ovarian cancer, and many others. It may be given alone or in combination with other chemotherapy drugs.

Doxorubicin is usually administered through a vein (intravenously) and can cause side effects such as nausea, vomiting, hair loss, mouth sores, and increased risk of infection. It can also cause damage to the heart muscle, which can lead to heart failure in some cases. For this reason, doctors may monitor patients' heart function closely while they are receiving doxorubicin treatment.

It is important for patients to discuss the potential risks and benefits of doxorubicin therapy with their healthcare provider before starting treatment.

Cyclophosphamide is an alkylating agent, which is a type of chemotherapy medication. It works by interfering with the DNA of cancer cells, preventing them from dividing and growing. This helps to stop the spread of cancer in the body. Cyclophosphamide is used to treat various types of cancer, including lymphoma, leukemia, multiple myeloma, and breast cancer. It can be given orally as a tablet or intravenously as an injection.

Cyclophosphamide can also have immunosuppressive effects, which means it can suppress the activity of the immune system. This makes it useful in treating certain autoimmune diseases, such as rheumatoid arthritis and lupus. However, this immunosuppression can also increase the risk of infections and other side effects.

Like all chemotherapy medications, cyclophosphamide can cause a range of side effects, including nausea, vomiting, hair loss, fatigue, and increased susceptibility to infections. It is important for patients receiving cyclophosphamide to be closely monitored by their healthcare team to manage these side effects and ensure the medication is working effectively.

Carboplatin is a chemotherapeutic agent used to treat various types of cancers, including ovarian, lung, and head and neck cancer. It is a platinum-containing compound that works by forming crosslinks in DNA, which leads to the death of rapidly dividing cells, such as cancer cells. Carboplatin is often used in combination with other chemotherapy drugs and is administered intravenously.

The medical definition of Carboplatin is:

"A platinum-containing antineoplastic agent that forms crosslinks with DNA, inducing cell cycle arrest and apoptosis. It is used to treat a variety of cancers, including ovarian, lung, and head and neck cancer."

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

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

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

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

A "Drug Administration Schedule" refers to the plan for when and how a medication should be given to a patient. It includes details such as the dose, frequency (how often it should be taken), route (how it should be administered, such as orally, intravenously, etc.), and duration (how long it should be taken) of the medication. This schedule is often created and prescribed by healthcare professionals, such as doctors or pharmacists, to ensure that the medication is taken safely and effectively. It may also include instructions for missed doses or changes in the dosage.

Bleomycin is a type of chemotherapeutic agent used to treat various types of cancer, including squamous cell carcinoma, testicular cancer, and lymphomas. It works by causing DNA damage in rapidly dividing cells, which can inhibit the growth and proliferation of cancer cells.

Bleomycin is an antibiotic derived from Streptomyces verticillus and is often administered intravenously or intramuscularly. While it can be effective in treating certain types of cancer, it can also have serious side effects, including lung toxicity, which can lead to pulmonary fibrosis and respiratory failure. Therefore, bleomycin should only be used under the close supervision of a healthcare professional who is experienced in administering chemotherapy drugs.

Lung neoplasms refer to abnormal growths or tumors in the lung tissue. These tumors can be benign (non-cancerous) or malignant (cancerous). Malignant lung neoplasms are further classified into two main types: small cell lung carcinoma and non-small cell lung carcinoma. Lung neoplasms can cause symptoms such as cough, chest pain, shortness of breath, and weight loss. They are often caused by smoking or exposure to secondhand smoke, but can also occur due to genetic factors, radiation exposure, and other environmental carcinogens. Early detection and treatment of lung neoplasms is crucial for improving outcomes and survival rates.

Combined modality therapy (CMT) is a medical treatment approach that utilizes more than one method or type of therapy simultaneously or in close succession, with the goal of enhancing the overall effectiveness of the treatment. In the context of cancer care, CMT often refers to the combination of two or more primary treatment modalities, such as surgery, radiation therapy, and systemic therapies (chemotherapy, immunotherapy, targeted therapy, etc.).

The rationale behind using combined modality therapy is that each treatment method can target cancer cells in different ways, potentially increasing the likelihood of eliminating all cancer cells and reducing the risk of recurrence. The specific combination and sequence of treatments will depend on various factors, including the type and stage of cancer, patient's overall health, and individual preferences.

For example, a common CMT approach for locally advanced rectal cancer may involve preoperative (neoadjuvant) chemoradiation therapy, followed by surgery to remove the tumor, and then postoperative (adjuvant) chemotherapy. This combined approach allows for the reduction of the tumor size before surgery, increases the likelihood of complete tumor removal, and targets any remaining microscopic cancer cells with systemic chemotherapy.

It is essential to consult with a multidisciplinary team of healthcare professionals to determine the most appropriate CMT plan for each individual patient, considering both the potential benefits and risks associated with each treatment method.

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

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

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

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

A germinoma is a type of tumor that develops in the brain or the spine, primarily in the pituitary gland or pineal gland. It is a rare form of primary central nervous system (CNS) cancer and is classified as a type of germ cell tumor. These tumors arise from cells that normally develop into sperm or eggs, which can migrate to unusual locations during embryonic development.

Germinomas are highly sensitive to radiation therapy and chemotherapy, making them generally treatable and curable with appropriate medical intervention. Symptoms of a germinoma may include headaches, nausea, vomiting, visual disturbances, hormonal imbalances, and neurological deficits, depending on the location and size of the tumor. Diagnosis typically involves imaging studies like MRI or CT scans, followed by a biopsy to confirm the presence of malignant cells.

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

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

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

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

The medical definition of Teniposide can be stated as:

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

Nucleic acid synthesis inhibitors are a class of antimicrobial, antiviral, or antitumor agents that block the synthesis of nucleic acids (DNA or RNA) by interfering with enzymes involved in their replication. These drugs can target various stages of nucleic acid synthesis, including DNA transcription, replication, and repair, as well as RNA transcription and processing.

Examples of nucleic acid synthesis inhibitors include:

1. Antibiotics like quinolones (e.g., ciprofloxacin), rifamycins (e.g., rifampin), and trimethoprim, which target bacterial DNA gyrase, RNA polymerase, or dihydrofolate reductase, respectively.
2. Antiviral drugs like reverse transcriptase inhibitors (e.g., zidovudine, lamivudine) and integrase strand transfer inhibitors (e.g., raltegravir), which target HIV replication by interfering with viral enzymes required for DNA synthesis.
3. Antitumor drugs like antimetabolites (e.g., methotrexate, 5-fluorouracil) and topoisomerase inhibitors (e.g., etoposide, doxorubicin), which interfere with DNA replication and repair in cancer cells.

These drugs have been widely used for treating various bacterial and viral infections, as well as cancers, due to their ability to selectively inhibit the growth of target cells without affecting normal cellular functions significantly. However, they may also cause side effects related to their mechanism of action or off-target effects on non-target cells.

Topoisomerase inhibitors are a class of anticancer drugs that work by interfering with the function of topoisomerases, which are enzymes responsible for relaxing supercoiled DNA during processes such as replication and transcription. Topoisomerase I inhibitors selectively bind to and stabilize the cleavage complex formed between topoisomerase I and DNA, preventing the relegation of the broken DNA strand and resulting in DNA damage and cell death. Examples include irinotecan and topotecan. Topoisomerase II inhibitors, on the other hand, bind to and stabilize the cleavage complex formed between topoisomerase II and DNA, leading to double-stranded DNA breaks and cell death. Examples include doxorubicin, etoposide, and mitoxantrone. These drugs are used in the treatment of various types of cancer.

Leukopenia is a medical term used to describe an abnormally low white blood cell (WBC) count in the blood. White blood cells are crucial components of the body's immune system, helping to fight infections and diseases. A normal WBC count ranges from 4,500 to 11,000 cells per microliter (μL) of blood in most laboratories. Leukopenia is typically diagnosed when the WBC count falls below 4,500 cells/μL.

There are several types of white blood cells, including neutrophils, lymphocytes, monocytes, eosinophils, and basophils. Neutropenia, a specific type of leukopenia, refers to an abnormally low neutrophil count (less than 1,500 cells/μL). Neutropenia increases the risk of bacterial and fungal infections since neutrophils play a significant role in combating these types of pathogens.

Leukopenia can result from various factors, such as viral infections, certain medications (like chemotherapy or radiation therapy), bone marrow disorders, autoimmune diseases, or congenital conditions affecting white blood cell production. It is essential to identify the underlying cause of leukopenia to provide appropriate treatment and prevent complications.

Autologous transplantation is a medical procedure where cells, tissues, or organs are removed from a person, stored and then returned back to the same individual at a later time. This is different from allogeneic transplantation where the tissue or organ is obtained from another donor. The term "autologous" is derived from the Greek words "auto" meaning self and "logos" meaning study.

In autologous transplantation, the patient's own cells or tissues are used to replace or repair damaged or diseased ones. This reduces the risk of rejection and eliminates the need for immunosuppressive drugs, which are required in allogeneic transplants to prevent the body from attacking the foreign tissue.

Examples of autologous transplantation include:

* Autologous bone marrow or stem cell transplantation, where stem cells are removed from the patient's blood or bone marrow, stored and then reinfused back into the same individual after high-dose chemotherapy or radiation therapy to treat cancer.
* Autologous skin grafting, where a piece of skin is taken from one part of the body and transplanted to another area on the same person.
* Autologous chondrocyte implantation, where cartilage cells are harvested from the patient's own knee, cultured in a laboratory and then implanted back into the knee to repair damaged cartilage.

Testicular neoplasms are abnormal growths or tumors in the testicle that can be benign (non-cancerous) or malignant (cancerous). They are a type of genitourinary cancer, which affects the reproductive and urinary systems. Testicular neoplasms can occur in men of any age but are most commonly found in young adults between the ages of 15 and 40.

Testicular neoplasms can be classified into two main categories: germ cell tumors and non-germ cell tumors. Germ cell tumors, which arise from the cells that give rise to sperm, are further divided into seminomas and non-seminomas. Seminomas are typically slow-growing and have a good prognosis, while non-seminomas tend to grow more quickly and can spread to other parts of the body.

Non-germ cell tumors are less common than germ cell tumors and include Leydig cell tumors, Sertoli cell tumors, and lymphomas. These tumors can have a variety of clinical behaviors, ranging from benign to malignant.

Testicular neoplasms often present as a painless mass or swelling in the testicle. Other symptoms may include a feeling of heaviness or discomfort in the scrotum, a dull ache in the lower abdomen or groin, and breast enlargement (gynecomastia).

Diagnosis typically involves a physical examination, imaging studies such as ultrasound or CT scan, and blood tests to detect tumor markers. Treatment options depend on the type and stage of the neoplasm but may include surgery, radiation therapy, chemotherapy, or a combination of these modalities. Regular self-examinations of the testicles are recommended for early detection and improved outcomes.

Drug resistance in neoplasms (also known as cancer drug resistance) refers to the ability of cancer cells to withstand the effects of chemotherapeutic agents or medications designed to kill or inhibit the growth of cancer cells. This can occur due to various mechanisms, including changes in the cancer cell's genetic makeup, alterations in drug targets, increased activity of drug efflux pumps, and activation of survival pathways.

Drug resistance can be intrinsic (present at the beginning of treatment) or acquired (developed during the course of treatment). It is a significant challenge in cancer therapy as it often leads to reduced treatment effectiveness, disease progression, and poor patient outcomes. Strategies to overcome drug resistance include the use of combination therapies, development of new drugs that target different mechanisms, and personalized medicine approaches that consider individual patient and tumor characteristics.

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

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

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

Remission induction is a treatment approach in medicine, particularly in the field of oncology and hematology. It refers to the initial phase of therapy aimed at reducing or eliminating the signs and symptoms of active disease, such as cancer or autoimmune disorders. The primary goal of remission induction is to achieve a complete response (disappearance of all detectable signs of the disease) or a partial response (a decrease in the measurable extent of the disease). This phase of treatment is often intensive and may involve the use of multiple drugs or therapies, including chemotherapy, immunotherapy, or targeted therapy. After remission induction, patients may receive additional treatments to maintain the remission and prevent relapse, known as consolidation or maintenance therapy.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

Neoplasms, germ cell and embryonal are types of tumors that originate from the abnormal growth of cells. Here's a brief medical definition for each:

1. Neoplasms: Neoplasms refer to abnormal tissue growths or masses, which can be benign (non-cancerous) or malignant (cancerous). They result from uncontrolled cell division and may invade surrounding tissues or spread to other parts of the body through a process called metastasis.
2. Germ Cell Tumors: These are rare tumors that develop from the germ cells, which give rise to sperm and eggs in the reproductive organs (ovaries and testes). They can be benign or malignant and may occur in both children and adults. Germ cell tumors can also arise outside of the reproductive organs, a condition known as extragonadal germ cell tumors.
3. Embryonal Tumors: These are a type of malignant neoplasm that primarily affects infants and young children. They develop from embryonic cells, which are immature cells present during fetal development. Embryonal tumors can occur in various organs, including the brain (medulloblastomas), nervous system (primitive neuroectodermal tumors or PNETs), and other areas like the kidneys and liver.

It is essential to note that these conditions require professional medical evaluation and treatment by healthcare professionals with expertise in oncology and related fields.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

Oral administration is a route of giving medications or other substances by mouth. This can be in the form of tablets, capsules, liquids, pastes, or other forms that can be swallowed. Once ingested, the substance is absorbed through the gastrointestinal tract and enters the bloodstream to reach its intended target site in the body. Oral administration is a common and convenient route of medication delivery, but it may not be appropriate for all substances or in certain situations, such as when rapid onset of action is required or when the patient has difficulty swallowing.

DNA damage refers to any alteration in the structure or composition of deoxyribonucleic acid (DNA), which is the genetic material present in cells. DNA damage can result from various internal and external factors, including environmental exposures such as ultraviolet radiation, tobacco smoke, and certain chemicals, as well as normal cellular processes such as replication and oxidative metabolism.

Examples of DNA damage include base modifications, base deletions or insertions, single-strand breaks, double-strand breaks, and crosslinks between the two strands of the DNA helix. These types of damage can lead to mutations, genomic instability, and chromosomal aberrations, which can contribute to the development of diseases such as cancer, neurodegenerative disorders, and aging-related conditions.

The body has several mechanisms for repairing DNA damage, including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. However, if the damage is too extensive or the repair mechanisms are impaired, the cell may undergo apoptosis (programmed cell death) to prevent the propagation of potentially harmful mutations.

Hodgkin disease, also known as Hodgkin lymphoma, is a type of cancer that originates in the white blood cells called lymphocytes. It typically affects the lymphatic system, which is a network of vessels and glands spread throughout the body. The disease is characterized by the presence of a specific type of abnormal cell, known as a Reed-Sternberg cell, within the affected lymph nodes.

The symptoms of Hodgkin disease may include painless swelling of the lymph nodes in the neck, armpits, or groin; fever; night sweats; weight loss; and fatigue. The exact cause of Hodgkin disease is unknown, but it is thought to involve a combination of genetic, environmental, and infectious factors.

Hodgkin disease is typically treated with a combination of chemotherapy, radiation therapy, and/or immunotherapy, depending on the stage and extent of the disease. With appropriate treatment, the prognosis for Hodgkin disease is generally very good, with a high cure rate. However, long-term side effects of treatment may include an increased risk of secondary cancers and other health problems.

Intravenous (IV) infusion is a medical procedure in which liquids, such as medications, nutrients, or fluids, are delivered directly into a patient's vein through a needle or a catheter. This route of administration allows for rapid absorption and distribution of the infused substance throughout the body. IV infusions can be used for various purposes, including resuscitation, hydration, nutrition support, medication delivery, and blood product transfusion. The rate and volume of the infusion are carefully controlled to ensure patient safety and efficacy of treatment.

Camptothecin is a topoisomerase I inhibitor, which is a type of chemotherapeutic agent used in cancer treatment. It works by interfering with the function of an enzyme called topoisomerase I, which helps to uncoil DNA during cell division. By inhibiting this enzyme, camptothecin prevents the cancer cells from dividing and growing, ultimately leading to their death.

Camptothecin is found naturally in the bark and stem of the Camptotheca acuminata tree, also known as the "happy tree," which is native to China. It was first isolated in 1966 and has since been developed into several synthetic derivatives, including irinotecan and topotecan, which are used clinically to treat various types of cancer, such as colon, lung, and ovarian cancers.

Like other chemotherapeutic agents, camptothecin can have significant side effects, including nausea, vomiting, diarrhea, and myelosuppression (suppression of bone marrow function). It is important for patients receiving camptothecin-based therapies to be closely monitored by their healthcare team to manage these side effects effectively.

Carmustine is a chemotherapy drug used to treat various types of cancer, including brain tumors, multiple myeloma, and Hodgkin's lymphoma. It belongs to a class of drugs called alkylating agents, which work by damaging the DNA in cancer cells, preventing them from dividing and growing.

Carmustine is available as an injectable solution that is administered intravenously (into a vein) or as implantable wafers that are placed directly into the brain during surgery. The drug can cause side effects such as nausea, vomiting, hair loss, and low blood cell counts, among others. It may also increase the risk of certain infections and bleeding complications.

As with all chemotherapy drugs, carmustine can have serious and potentially life-threatening side effects, and it should only be administered under the close supervision of a qualified healthcare professional. Patients receiving carmustine treatment should be closely monitored for signs of toxicity and other adverse reactions.

Hematologic diseases, also known as hematological disorders, refer to a group of conditions that affect the production, function, or destruction of blood cells or blood-related components, such as plasma. These diseases can affect erythrocytes (red blood cells), leukocytes (white blood cells), and platelets (thrombocytes), as well as clotting factors and hemoglobin.

Hematologic diseases can be broadly categorized into three main types:

1. Anemia: A condition characterized by a decrease in the total red blood cell count, hemoglobin, or hematocrit, leading to insufficient oxygen transport to tissues and organs. Examples include iron deficiency anemia, sickle cell anemia, and aplastic anemia.
2. Leukemia and other disorders of white blood cells: These conditions involve the abnormal production or function of leukocytes, which can lead to impaired immunity and increased susceptibility to infections. Examples include leukemias (acute lymphoblastic leukemia, chronic myeloid leukemia), lymphomas, and myelodysplastic syndromes.
3. Platelet and clotting disorders: These diseases affect the production or function of platelets and clotting factors, leading to abnormal bleeding or clotting tendencies. Examples include hemophilia, von Willebrand disease, thrombocytopenia, and disseminated intravascular coagulation (DIC).

Hematologic diseases can have various causes, including genetic defects, infections, autoimmune processes, environmental factors, or malignancies. Proper diagnosis and management of these conditions often require the expertise of hematologists, who specialize in diagnosing and treating disorders related to blood and its components.

"Drug evaluation" is a medical term that refers to the systematic process of assessing the pharmacological, therapeutic, and safety profile of a drug or medication. This process typically involves several stages, including preclinical testing in the laboratory, clinical trials in human subjects, and post-marketing surveillance.

The goal of drug evaluation is to determine the efficacy, safety, and optimal dosage range of a drug, as well as any potential interactions with other medications or medical conditions. The evaluation process also includes an assessment of the drug's pharmacokinetics, or how it is absorbed, distributed, metabolized, and eliminated by the body.

The findings from drug evaluations are used to inform regulatory decisions about whether a drug should be approved for use in clinical practice, as well as to provide guidance to healthcare providers about how to use the drug safely and effectively.

Salvage therapy, in the context of medical oncology, refers to the use of treatments that are typically considered less desirable or more aggressive, often due to greater side effects or lower efficacy, when standard treatment options have failed. These therapies are used to attempt to salvage a response or delay disease progression in patients with refractory or relapsed cancers.

In other words, salvage therapy is a last-resort treatment approach for patients who have not responded to first-line or subsequent lines of therapy. It may involve the use of different drug combinations, higher doses of chemotherapy, immunotherapy, targeted therapy, or radiation therapy. The goal of salvage therapy is to extend survival, improve quality of life, or achieve disease stabilization in patients with limited treatment options.

Non-Hodgkin lymphoma (NHL) is a type of cancer that originates in the lymphatic system, which is part of the immune system. It involves the abnormal growth and proliferation of malignant lymphocytes (a type of white blood cell), leading to the formation of tumors in lymph nodes, spleen, bone marrow, or other organs. NHL can be further classified into various subtypes based on the specific type of lymphocyte involved and its characteristics.

The symptoms of Non-Hodgkin lymphoma may include:

* Painless swelling of lymph nodes in the neck, armpits, or groin
* Persistent fatigue
* Unexplained weight loss
* Fever
* Night sweats
* Itchy skin

The exact cause of Non-Hodgkin lymphoma is not well understood, but it has been associated with certain risk factors such as age (most common in people over 60), exposure to certain chemicals, immune system deficiencies, and infection with viruses like Epstein-Barr virus or HIV.

Treatment for Non-Hodgkin lymphoma depends on the stage and subtype of the disease, as well as the patient's overall health. Treatment options may include chemotherapy, radiation therapy, immunotherapy, targeted therapy, stem cell transplantation, or a combination of these approaches. Regular follow-up care is essential to monitor the progression of the disease and manage any potential long-term side effects of treatment.

Topotecan is a chemotherapeutic agent, specifically a topoisomerase I inhibitor. It is a semi-synthetic derivative of camptothecin and works by interfering with the function of topoisomerase I, an enzyme that helps to relax supercoiled DNA during transcription and replication. By inhibiting this enzyme, topotecan causes DNA damage and apoptosis (programmed cell death) in rapidly dividing cells, such as cancer cells. It is used in the treatment of various types of cancer, including small cell lung cancer and ovarian cancer.

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

'Tumor cells, cultured' refers to the process of removing cancerous cells from a tumor and growing them in controlled laboratory conditions. This is typically done by isolating the tumor cells from a patient's tissue sample, then placing them in a nutrient-rich environment that promotes their growth and multiplication.

The resulting cultured tumor cells can be used for various research purposes, including the study of cancer biology, drug development, and toxicity testing. They provide a valuable tool for researchers to better understand the behavior and characteristics of cancer cells outside of the human body, which can lead to the development of more effective cancer treatments.

It is important to note that cultured tumor cells may not always behave exactly the same way as they do in the human body, so findings from cell culture studies must be validated through further research, such as animal models or clinical trials.

Disease-free survival (DFS) is a term used in medical research and clinical practice, particularly in the field of oncology. It refers to the length of time after primary treatment for a cancer during which no evidence of the disease can be found. This means that the patient shows no signs or symptoms of the cancer, and any imaging studies or other tests do not reveal any tumors or other indications of the disease.

DFS is often used as an important endpoint in clinical trials to evaluate the effectiveness of different treatments for cancer. By measuring the length of time until the cancer recurs or a new cancer develops, researchers can get a better sense of how well a particular treatment is working and whether it is improving patient outcomes.

It's important to note that DFS is not the same as overall survival (OS), which refers to the length of time from primary treatment until death from any cause. While DFS can provide valuable information about the effectiveness of cancer treatments, it does not necessarily reflect the impact of those treatments on patients' overall survival.

Survival analysis is a branch of statistics that deals with the analysis of time to event data. It is used to estimate the time it takes for a certain event of interest to occur, such as death, disease recurrence, or treatment failure. The event of interest is called the "failure" event, and survival analysis estimates the probability of not experiencing the failure event until a certain point in time, also known as the "survival" probability.

Survival analysis can provide important information about the effectiveness of treatments, the prognosis of patients, and the identification of risk factors associated with the event of interest. It can handle censored data, which is common in medical research where some participants may drop out or be lost to follow-up before the event of interest occurs.

Survival analysis typically involves estimating the survival function, which describes the probability of surviving beyond a certain time point, as well as hazard functions, which describe the instantaneous rate of failure at a given time point. Other important concepts in survival analysis include median survival times, restricted mean survival times, and various statistical tests to compare survival curves between groups.

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

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

Neutropenia is a condition characterized by an abnormally low concentration (less than 1500 cells/mm3) of neutrophils, a type of white blood cell that plays a crucial role in fighting off bacterial and fungal infections. Neutrophils are essential components of the innate immune system, and their main function is to engulf and destroy microorganisms that can cause harm to the body.

Neutropenia can be classified as mild, moderate, or severe based on the severity of the neutrophil count reduction:

* Mild neutropenia: Neutrophil count between 1000-1500 cells/mm3
* Moderate neutropenia: Neutrophil count between 500-1000 cells/mm3
* Severe neutropenia: Neutrophil count below 500 cells/mm3

Severe neutropenia significantly increases the risk of developing infections, as the body's ability to fight off microorganisms is severely compromised. Common causes of neutropenia include viral infections, certain medications (such as chemotherapy or antibiotics), autoimmune disorders, and congenital conditions affecting bone marrow function. Treatment for neutropenia typically involves addressing the underlying cause, administering granulocyte-colony stimulating factors to boost neutrophil production, and providing appropriate antimicrobial therapy to prevent or treat infections.

Prednisone is a synthetic glucocorticoid, which is a type of corticosteroid hormone. It is primarily used to reduce inflammation in various conditions such as asthma, allergies, arthritis, and autoimmune disorders. Prednisone works by mimicking the effects of natural hormones produced by the adrenal glands, suppressing the immune system's response and reducing the release of substances that cause inflammation.

It is available in oral tablet form and is typically prescribed to be taken at specific times during the day, depending on the condition being treated. Common side effects of prednisone include increased appetite, weight gain, mood changes, insomnia, and easy bruising. Long-term use or high doses can lead to more serious side effects such as osteoporosis, diabetes, cataracts, and increased susceptibility to infections.

Healthcare providers closely monitor patients taking prednisone for extended periods to minimize the risk of adverse effects. It is essential to follow the prescribed dosage regimen and not discontinue the medication abruptly without medical supervision, as this can lead to withdrawal symptoms or a rebound of the underlying condition.

Medical survival rate is a statistical measure used to determine the percentage of patients who are still alive for a specific period of time after their diagnosis or treatment for a certain condition or disease. It is often expressed as a five-year survival rate, which refers to the proportion of people who are alive five years after their diagnosis. Survival rates can be affected by many factors, including the stage of the disease at diagnosis, the patient's age and overall health, the effectiveness of treatment, and other health conditions that the patient may have. It is important to note that survival rates are statistical estimates and do not necessarily predict an individual patient's prognosis.

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

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

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

Thrombocytopenia is a medical condition characterized by an abnormally low platelet count (thrombocytes) in the blood. Platelets are small cell fragments that play a crucial role in blood clotting, helping to stop bleeding when a blood vessel is damaged. A healthy adult typically has a platelet count between 150,000 and 450,000 platelets per microliter of blood. Thrombocytopenia is usually diagnosed when the platelet count falls below 150,000 platelets/µL.

Thrombocytopenia can be classified into three main categories based on its underlying cause:

1. Immune thrombocytopenia (ITP): An autoimmune disorder where the immune system mistakenly attacks and destroys its own platelets, leading to a decreased platelet count. ITP can be further divided into primary or secondary forms, depending on whether it occurs alone or as a result of another medical condition or medication.
2. Decreased production: Thrombocytopenia can occur when there is insufficient production of platelets in the bone marrow due to various causes, such as viral infections, chemotherapy, radiation therapy, leukemia, aplastic anemia, or vitamin B12 or folate deficiency.
3. Increased destruction or consumption: Thrombocytopenia can also result from increased platelet destruction or consumption due to conditions like disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or severe bacterial infections.

Symptoms of thrombocytopenia may include easy bruising, prolonged bleeding from cuts, spontaneous nosebleeds, bleeding gums, blood in urine or stools, and skin rashes like petechiae (small red or purple spots) or purpura (larger patches). The severity of symptoms can vary depending on the degree of thrombocytopenia and the presence of any underlying conditions. Treatment for thrombocytopenia depends on the cause and may include medications, transfusions, or addressing the underlying condition.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Procarbazine is an antineoplastic agent, specifically an alkylating agent, used in the treatment of certain types of cancer such as Hodgkin's lymphoma and brain tumors. It works by interfering with the DNA of cancer cells, preventing them from dividing and growing. Procarbazine is often used in combination with other chemotherapy drugs to increase its effectiveness.

It is important to note that procarbazine can have significant side effects, including nausea, vomiting, loss of appetite, and weakness. It can also suppress the immune system, increasing the risk of infection. Additionally, it can cause damage to cells outside of the cancerous tissue, which can result in side effects such as hair loss and mouth sores.

Procarbazine is a prescription medication that should only be used under the supervision of a healthcare professional. It is important for patients to follow their doctor's instructions carefully when taking this medication and to report any side effects or concerns promptly.

"Multiple drug resistance" (MDR) is a term used in medicine to describe the condition where a patient's infection becomes resistant to multiple antimicrobial drugs. This means that the bacteria, virus, fungus or parasite that is causing the infection has developed the ability to survive and multiply despite being exposed to medications that were originally designed to kill or inhibit its growth.

In particular, MDR occurs when an organism becomes resistant to at least one drug in three or more antimicrobial categories. This can happen due to genetic changes in the microorganism that allow it to survive in the presence of these drugs. The development of MDR is a significant concern for public health because it limits treatment options and can make infections harder, if not impossible, to treat.

MDR can develop through several mechanisms, including mutations in the genes that encode drug targets or enzymes involved in drug metabolism, as well as the acquisition of genetic elements such as plasmids and transposons that carry resistance genes. The overuse and misuse of antimicrobial drugs are major drivers of MDR, as they create selective pressure for the emergence and spread of resistant strains.

MDR infections can occur in various settings, including hospitals, long-term care facilities, and communities. They can affect people of all ages and backgrounds, although certain populations may be at higher risk, such as those with weakened immune systems or chronic medical conditions. Preventing the spread of MDR requires a multifaceted approach that includes surveillance, infection control, antimicrobial stewardship, and research into new therapies and diagnostics.

P-glycoprotein (P-gp) is a type of membrane transport protein that plays a crucial role in the efflux (extrusion) of various substrates, including drugs and toxins, out of cells. It is also known as multidrug resistance protein 1 (MDR1).

P-gp is encoded by the ABCB1 gene and is primarily located on the apical membrane of epithelial cells in several tissues, such as the intestine, liver, kidney, and blood-brain barrier. Its main function is to protect these organs from harmful substances by actively pumping them out of the cells and back into the lumen or bloodstream.

In the context of pharmacology, P-gp can contribute to multidrug resistance (MDR) in cancer cells. When overexpressed, P-gp can reduce the intracellular concentration of various anticancer drugs, making them less effective. This has led to extensive research on inhibitors of P-gp as potential adjuvants for cancer therapy.

In summary, P-glycoprotein is a vital efflux transporter that helps maintain homeostasis by removing potentially harmful substances from cells and can impact drug disposition and response in various tissues, including the intestine, liver, kidney, and blood-brain barrier.

Organophosphorus compounds are a class of chemical substances that contain phosphorus bonded to organic compounds. They are used in various applications, including as plasticizers, flame retardants, pesticides (insecticides, herbicides, and nerve gases), and solvents. In medicine, they are also used in the treatment of certain conditions such as glaucoma. However, organophosphorus compounds can be toxic to humans and animals, particularly those that affect the nervous system by inhibiting acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine. Exposure to these compounds can cause symptoms such as nausea, vomiting, muscle weakness, and in severe cases, respiratory failure and death.

Melphalan is an antineoplastic agent, specifically an alkylating agent. It is used in the treatment of multiple myeloma and other types of cancer. The medical definition of Melphalan is:

A nitrogen mustard derivative that is used as an alkylating agent in the treatment of cancer, particularly multiple myeloma and ovarian cancer. Melphalan works by forming covalent bonds with DNA, resulting in cross-linking of the double helix and inhibition of DNA replication and transcription. This ultimately leads to cell cycle arrest and apoptosis (programmed cell death) in rapidly dividing cells, such as cancer cells.

Melphalan is administered orally or intravenously, and its use is often accompanied by other anticancer therapies, such as radiation therapy or chemotherapy. Common side effects of Melphalan include nausea, vomiting, diarrhea, and bone marrow suppression, which can lead to anemia, neutropenia, and thrombocytopenia. Other potential side effects include hair loss, mucositis, and secondary malignancies.

It is important to note that Melphalan should be used under the close supervision of a healthcare professional, as it can cause serious adverse reactions if not administered correctly.

Paclitaxel is a chemotherapeutic agent derived from the bark of the Pacific yew tree (Taxus brevifolia). It is an antimicrotubule agent that promotes the assembly and stabilization of microtubules, thereby interfering with the normal dynamic reorganization of the microtubule network that is essential for cell division.

Paclitaxel is used in the treatment of various types of cancer including ovarian, breast, lung, and pancreatic cancers. It works by inhibiting the disassembly of microtubules, which prevents the separation of chromosomes during mitosis, leading to cell cycle arrest and apoptosis (programmed cell death).

Common side effects of paclitaxel include neutropenia (low white blood cell count), anemia (low red blood cell count), alopecia (hair loss), peripheral neuropathy (nerve damage causing numbness or tingling in the hands and feet), myalgias (muscle pain), arthralgias (joint pain), and hypersensitivity reactions.

Vinblastine is an alkaloid derived from the Madagascar periwinkle plant (Catharanthus roseus) and is primarily used in cancer chemotherapy. It is classified as a vinca alkaloid, along with vincristine, vinorelbine, and others.

Medically, vinblastine is an antimicrotubule agent that binds to tubulin, a protein involved in the formation of microtubules during cell division. By binding to tubulin, vinblastine prevents the assembly of microtubules, which are essential for mitosis (cell division). This leads to the inhibition of cell division and ultimately results in the death of rapidly dividing cells, such as cancer cells.

Vinblastine is used to treat various types of cancers, including Hodgkin's lymphoma, non-Hodgkin's lymphoma, testicular cancer, breast cancer, and others. It is often administered intravenously in a healthcare setting and may be given as part of a combination chemotherapy regimen with other anticancer drugs.

As with any medication, vinblastine can have side effects, including bone marrow suppression (leading to an increased risk of infection, anemia, and bleeding), neurotoxicity (resulting in peripheral neuropathy, constipation, and jaw pain), nausea, vomiting, hair loss, and mouth sores. Regular monitoring by a healthcare professional is necessary during vinblastine treatment to manage side effects and ensure the safe and effective use of this medication.

Cell survival refers to the ability of a cell to continue living and functioning normally, despite being exposed to potentially harmful conditions or treatments. This can include exposure to toxins, radiation, chemotherapeutic drugs, or other stressors that can damage cells or interfere with their normal processes.

In scientific research, measures of cell survival are often used to evaluate the effectiveness of various therapies or treatments. For example, researchers may expose cells to a particular drug or treatment and then measure the percentage of cells that survive to assess its potential therapeutic value. Similarly, in toxicology studies, measures of cell survival can help to determine the safety of various chemicals or substances.

It's important to note that cell survival is not the same as cell proliferation, which refers to the ability of cells to divide and multiply. While some treatments may promote cell survival, they may also inhibit cell proliferation, making them useful for treating diseases such as cancer. Conversely, other treatments may be designed to specifically target and kill cancer cells, even if it means sacrificing some healthy cells in the process.

Granulocyte Colony-Stimulating Factor (G-CSF) is a type of growth factor that specifically stimulates the production and survival of granulocytes, a type of white blood cell crucial for fighting off infections. G-CSF works by promoting the proliferation and differentiation of hematopoietic stem cells into mature granulocytes, primarily neutrophils, in the bone marrow.

Recombinant forms of G-CSF are used clinically as a medication to boost white blood cell production in patients undergoing chemotherapy or radiation therapy for cancer, those with congenital neutropenia, and those who have had a bone marrow transplant. By increasing the number of circulating neutrophils, G-CSF helps reduce the risk of severe infections during periods of intense immune suppression.

Examples of recombinant G-CSF medications include filgrastim (Neupogen), pegfilgrastim (Neulasta), and lipegfilgrastim (Lonquex).

Retroperitoneal neoplasms refer to abnormal growths or tumors that develop in the retroperitoneal space. This is the area located behind the peritoneum, which is the membrane that lines the abdominal cavity and covers the abdominal organs. The retroperitoneal space contains several vital structures such as the kidneys, adrenal glands, pancreas, aorta, and lymphatic vessels.

Retroperitoneal neoplasms can be benign or malignant (cancerous). Malignant retroperitoneal neoplasms are often aggressive and can invade surrounding tissues and organs, leading to various complications. Common types of retroperitoneal neoplasms include lymphomas, sarcomas, and metastatic tumors from other primary sites. Symptoms may vary depending on the size and location of the tumor but can include abdominal or back pain, weight loss, and swelling in the legs. Diagnosis typically involves imaging studies such as CT scans or MRI, followed by a biopsy to determine the type and grade of the tumor. Treatment options may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

Alopecia is a medical term that refers to the loss of hair or baldness. It can occur in various parts of the body, but it's most commonly used to describe hair loss from the scalp. Alopecia can have several causes, including genetics, hormonal changes, medical conditions, and aging.

There are different types of alopecia, such as:

* Alopecia Areata: It is a condition that causes round patches of hair loss on the scalp or other parts of the body. The immune system attacks the hair follicles, causing the hair to fall out.
* Androgenetic Alopecia: Also known as male pattern baldness or female pattern baldness, it's a genetic condition that causes gradual hair thinning and eventual hair loss, typically following a specific pattern.
* Telogen Effluvium: It is a temporary hair loss condition caused by stress, medication, pregnancy, or other factors that can cause the hair follicles to enter a resting phase, leading to shedding and thinning of the hair.

The treatment for alopecia depends on the underlying cause. In some cases, such as with telogen effluvium, hair growth may resume without any treatment. However, other forms of alopecia may require medical intervention, including topical treatments, oral medications, or even hair transplant surgery in severe cases.

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

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

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

Bone marrow diseases, also known as hematologic disorders, are conditions that affect the production and function of blood cells in the bone marrow. The bone marrow is the spongy tissue inside bones where all blood cells are produced. There are various types of bone marrow diseases, including:

1. Leukemia: A cancer of the blood-forming tissues, including the bone marrow. Leukemia causes the body to produce large numbers of abnormal white blood cells, which can crowd out healthy blood cells and impair their function.
2. Lymphoma: A cancer that starts in the lymphatic system, which is part of the immune system. Lymphoma can affect the bone marrow and cause an overproduction of abnormal white blood cells.
3. Multiple myeloma: A cancer of the plasma cells, a type of white blood cell found in the bone marrow. Multiple myeloma causes an overproduction of abnormal plasma cells, which can lead to bone pain, fractures, and other complications.
4. Aplastic anemia: A condition in which the bone marrow does not produce enough new blood cells. This can lead to symptoms such as fatigue, weakness, and an increased risk of infection.
5. Myelodysplastic syndromes (MDS): A group of disorders in which the bone marrow does not produce enough healthy blood cells. MDS can lead to anemia, infections, and bleeding.
6. Myeloproliferative neoplasms (MPNs): A group of disorders in which the bone marrow produces too many abnormal white or red blood cells, or platelets. MPNs can lead to symptoms such as fatigue, itching, and an increased risk of blood clots.

Treatment for bone marrow diseases depends on the specific condition and its severity. Treatment options may include chemotherapy, radiation therapy, stem cell transplantation, or targeted therapies that target specific genetic mutations.

Hematopoietic Stem Cell Transplantation (HSCT) is a medical procedure where hematopoietic stem cells (immature cells that give rise to all blood cell types) are transplanted into a patient. This procedure is often used to treat various malignant and non-malignant disorders affecting the hematopoietic system, such as leukemias, lymphomas, multiple myeloma, aplastic anemia, inherited immune deficiency diseases, and certain genetic metabolic disorders.

The transplantation can be autologous (using the patient's own stem cells), allogeneic (using stem cells from a genetically matched donor, usually a sibling or unrelated volunteer), or syngeneic (using stem cells from an identical twin).

The process involves collecting hematopoietic stem cells, most commonly from the peripheral blood or bone marrow. The collected cells are then infused into the patient after the recipient's own hematopoietic system has been ablated (or destroyed) using high-dose chemotherapy and/or radiation therapy. This allows the donor's stem cells to engraft, reconstitute, and restore the patient's hematopoietic system.

HSCT is a complex and potentially risky procedure with various complications, including graft-versus-host disease, infections, and organ damage. However, it offers the potential for cure or long-term remission in many patients with otherwise fatal diseases.

Methotrexate is a medication used in the treatment of certain types of cancer and autoimmune diseases. It is an antimetabolite that inhibits the enzyme dihydrofolate reductase, which is necessary for the synthesis of purines and pyrimidines, essential components of DNA and RNA. By blocking this enzyme, methotrexate interferes with cell division and growth, making it effective in treating rapidly dividing cells such as cancer cells.

In addition to its use in cancer treatment, methotrexate is also used to manage autoimmune diseases such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease. In these conditions, methotrexate modulates the immune system and reduces inflammation.

It's important to note that methotrexate can have significant side effects and should be used under the close supervision of a healthcare provider. Regular monitoring of blood counts, liver function, and kidney function is necessary during treatment with methotrexate.

HL-60 cells are a type of human promyelocytic leukemia cell line that is commonly used in scientific research. They are named after the hospital where they were first isolated, the Hospital of the University of Pennsylvania (HUP) and the 60th culture attempt to grow these cells.

HL-60 cells have the ability to differentiate into various types of blood cells, such as granulocytes, monocytes, and macrophages, when exposed to certain chemical compounds or under specific culturing conditions. This makes them a valuable tool for studying the mechanisms of cell differentiation, proliferation, and apoptosis (programmed cell death).

HL-60 cells are also often used in toxicity studies, drug discovery and development, and research on cancer, inflammation, and infectious diseases. They can be easily grown in the lab and have a stable genotype, making them ideal for use in standardized experiments and comparisons between different studies.

Levoleucovorin is the pharmaceutical form of the active isomer of folinic acid, which is a reduced and readily usable form of folate. It is used in medicine as a medication to reduce the toxic effects of methotrexate, an antifolate chemotherapeutic agent, when high-dose methotrexate therapy is used.

Methotrexate works by blocking the action of an enzyme called dihydrofolate reductase, which is necessary for the production of thymidine, one of the four nucleosides in DNA. By inhibiting this enzyme, methotrexate prevents the synthesis of DNA and RNA, thereby interfering with cell division and growth. However, methotrexate can also block the action of other enzymes that require reduced folates as cofactors, leading to toxicity in normal cells.

Levoleucovorin is a form of folate that can bypass the blocked enzyme and provide the necessary cofactor for these other enzymes, thereby reducing the toxic effects of methotrexate on normal cells. It is usually given 24 hours after the start of high-dose methotrexate therapy, and its administration is continued until the serum concentration of methotrexate falls below a certain level.

It's important to note that levoleucovorin should not be given at the same time as methotrexate, as it can reduce the efficacy of methotrexate in killing cancer cells.

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

Drug synergism is a pharmacological concept that refers to the interaction between two or more drugs, where the combined effect of the drugs is greater than the sum of their individual effects. This means that when these drugs are administered together, they produce an enhanced therapeutic response compared to when they are given separately.

Drug synergism can occur through various mechanisms, such as:

1. Pharmacodynamic synergism - When two or more drugs interact with the same target site in the body and enhance each other's effects.
2. Pharmacokinetic synergism - When one drug affects the metabolism, absorption, distribution, or excretion of another drug, leading to an increased concentration of the second drug in the body and enhanced therapeutic effect.
3. Physiochemical synergism - When two drugs interact physically, such as when one drug enhances the solubility or permeability of another drug, leading to improved absorption and bioavailability.

It is important to note that while drug synergism can result in enhanced therapeutic effects, it can also increase the risk of adverse reactions and toxicity. Therefore, healthcare providers must carefully consider the potential benefits and risks when prescribing combinations of drugs with known or potential synergistic effects.

Small Cell Lung Carcinoma (SCLC) is a type of lung cancer that typically originates in the central part of the lungs. It is called "small cell" because the tumor cells appear small and round under a microscope. SCLC is an aggressive form of lung cancer that tends to spread rapidly to other parts of the body, such as the lymph nodes, liver, bones, and brain.

SCLC is strongly associated with smoking and is relatively uncommon in people who have never smoked. It accounts for about 10-15% of all lung cancer cases. SCLC is often diagnosed at a later stage because it can grow quickly and cause symptoms such as coughing, chest pain, shortness of breath, and weight loss.

Treatment for SCLC typically involves a combination of chemotherapy and radiation therapy. Surgery is not usually an option due to the advanced stage of the disease at diagnosis. The prognosis for SCLC is generally poor, with a five-year survival rate of less than 7%. However, early detection and treatment can improve outcomes in some cases.

Mesna is a medication used in the prevention and treatment of hemorrhagic cystitis (inflammation and bleeding of the bladder) caused by certain chemotherapy drugs, specifically ifosfamide and cyclophosphamide. Mesna works by neutralizing the toxic metabolites of these chemotherapy agents, which can cause bladder irritation and damage.

Mesna is administered intravenously (into a vein) along with ifosfamide or cyclophosphamide, and it may also be given as a separate infusion after the chemotherapy treatment. The dosage and timing of Mesna administration are determined by the healthcare provider based on the patient's weight, kidney function, and the dose of chemotherapy received.

It is important to note that Mesna does not have any direct anticancer effects and is used solely to manage the side effects of chemotherapy.

Caspases are a family of protease enzymes that play essential roles in programmed cell death, also known as apoptosis. These enzymes are produced as inactive precursors and are activated when cells receive signals to undergo apoptosis. Once activated, caspases cleave specific protein substrates, leading to the characteristic morphological changes and DNA fragmentation associated with apoptotic cell death. Caspases also play roles in other cellular processes, including inflammation and differentiation. There are two types of caspases: initiator caspases (caspase-2, -8, -9, and -10) and effector caspases (caspase-3, -6, and -7). Initiator caspases are activated in response to various apoptotic signals and then activate the effector caspases, which carry out the proteolytic cleavage of cellular proteins. Dysregulation of caspase activity has been implicated in a variety of diseases, including neurodegenerative disorders, ischemic injury, and cancer.

Drug screening assays for antitumor agents are laboratory tests used to identify and evaluate the effectiveness of potential drugs or compounds that can inhibit the growth of tumor cells or induce their death. These assays are typically performed in vitro (in a test tube or petri dish) using cell cultures of various types of cancer cells.

The assays measure different parameters such as cell viability, proliferation, apoptosis (programmed cell death), and cytotoxicity to determine the ability of the drug to kill or inhibit the growth of tumor cells. The results of these assays can help researchers identify promising antitumor agents that can be further developed for clinical use in cancer treatment.

There are different types of drug screening assays for antitumor agents, including high-throughput screening (HTS) assays, which allow for the rapid and automated testing of a large number of compounds against various cancer cell lines. Other types of assays include phenotypic screening assays, target-based screening assays, and functional screening assays, each with its own advantages and limitations.

Overall, drug screening assays for antitumor agents play a critical role in the development of new cancer therapies by providing valuable information on the activity and safety of potential drugs, helping to identify effective treatments and reduce the time and cost associated with bringing new drugs to market.

DNA topoisomerases are enzymes that modify the topological structure of DNA by regulating the number of twists or supercoils in the double helix. There are two main types of DNA topoisomerases: type I and type II.

Type I DNA topoisomerases function by cutting one strand of the DNA duplex, allowing the uncut strand to rotate around the break, and then resealing the break. This process can relieve both positive and negative supercoiling in DNA, as well as introduce single-stranded breaks into the DNA molecule.

Type I topoisomerases are further divided into three subtypes: type IA, type IB, and type IC. These subtypes differ in their mechanism of action and the structure of the active site tyrosine residue that makes the transient break in the DNA strand.

Overall, DNA topoisomerases play a crucial role in many cellular processes involving DNA, including replication, transcription, recombination, and chromosome segregation. Dysregulation of these enzymes has been implicated in various human diseases, including cancer and genetic disorders.

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An alternative, equally effective treatment involves the use of four cycles of Etoposide-Cisplatin (EP). Lymph node surgery may ... Reyhanoglu, Gizem; Tadi, Prasanna (11 July 2022). Etoposide. StatPearls Publishing. PMID 32491787. "MRC trial shows single dose ... rounds of Bleomycin-Etoposide-Cisplatin (BEP). BEP as a first-line treatment was first reported by Professor Michael Peckham in ... etoposide and cisplatin (BEP)". British Journal of Cancer. 47 (5): 613-619. doi:10.1038/bjc.1983.99. PMC 2011384. PMID 6189504 ...
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Etoposide · Teniposide); 3a. Anthracyclines (Aclarubicin · Daunorubicin · Doxorubicin · Epirubicin · Idarubicin · Amrubicin · ...
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These include etoposide and teniposide. They act as anti-cancer drugs by inhibiting topoisomerase II. Podophyllotoxin Takimoto ...
... or etoposide, ifosfamide, and cisplatin. These treatment regimens have been reported to lower local recurrence rates, prolong ...
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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 ...
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 ...
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 ...
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 ...
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 ...
It consists of cyclophosphamide, etoposide, procarbazine, and prednisone. Unlike CHOP, this chemotherapy regimen does not ... etoposide, procarbazine and prednisone) as initial treatment for Hodgkin lymphoma patients presenting with severe abnormal ... an alkylating antineoplastic agent Etoposide- a topoisomerase inhibitor from the epipodophyllotoxin group Procarbazine - an ...
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 ...
Treatment with cisplatin, etoposide, and bleomycin has been described. Before modern chemotherapy, this type of neoplasm was ...
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, ...
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 ...
Etoposide, vincristine, dactinomycin, and cyclophosphamide have also traditionally been given. Newer chemotherapies, such as ...
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 ...
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 ( ...
"Serine palmitoyltransferase regulates de novo ceramide generation during etoposide-induced apoptosis". The Journal of ...
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. ...
"Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis". Proteomics. 5 (15): 3876-84. doi: ...
"Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis". Proteomics. 5 (15): 3876-84. doi: ...
"Identification of apoptotic tyrosine-phosphorylated proteins after etoposide or retinoic acid treatment". Proteomics. 4 (4): ...
"Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis". Proteomics. 5 (15): 3876-84. doi: ...
Etoposide 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: ...
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 ...
Ei24 etoposide induced 2.4 mRNA [Mus musculus] Ei24 etoposide induced 2.4 mRNA [Mus musculus]. Gene ID:13663 ... etoposide induced 2.4 mRNAprovided by MGI. Primary source. MGI:MGI:108090 See related. Ensembl:ENSMUSG00000062762 ... Etoposide-induced protein 2.4 functions as a regulator of the calcium ATPase and protects pancreatic beta-cell survival Title: ... Ei24 etoposide induced 2.4 mRNA [ Mus musculus (house mouse) ] Gene ID: 13663, updated on 23-Nov-2023 ...
CanMED: NDC. The Cancer Medications Enquiry Database (CanMED) is a two-part resource for cancer drug treatment related studies.
Etoposide) drug information. Find its price or cost, dose, when to use, how to use, side effects, adverse effects, substitutes ... Etoposide (Lastet (50 mg)) is an anti-cancer agent, prescribed for lung cancer and testicular cancer. It slows or stops the ...
All patients received high-dose etoposide (60 mg/kg) and allogeneic stem cell transplantation following the TBI. All patients ... that TBI dose escalation above the previously used 13.5 Gy dose is feasible using a high-energy source and high-dose etoposide ... High-dose etoposide, cyclophosphamide, and total body irradiation with allogeneic bone marrow transplantation for patients with ... Etoposide in combination with cyclophosphamide and total body irradiation or busulfan as conditioning for marrow ...
The justification for the substitution of epirubicin for etoposide reflects the fact that etoposide is not very effective as a ... etoposide/cisplatin (EP)[4] or etoposide/doxorubicin (Adriamycin)/cisplatin (EAP).[5] With this background, FLEP appeared to be ... The UFT/Leucovorin/Etoposide Regimen for the Treatment of Advanced Gastric Cancer. Sep 2, 1997. Manuel González Barón, MD. ... The FLEP regimen we used consisted of leucovorin 300 mg/m2/day, followed by etoposide 100 mg/m2/day, 5-FU 500 mg/m2/day, and ...
OUTLINE: Patients receive etoposide by mouth once daily on days 1-21 every 4 weeks. Patients. with responding disease continue ... Chemotherapy: No more than 1 prior chemotherapy trial No prior etoposide At least 3 weeks. since chemotherapy and recovered ... OBJECTIVES: I. Determine the efficacy of prolonged oral etoposide (VP-16) in patients with. advanced ovarian epithelial or ...
inquireetoposide CAS NO : 33419-42-0; MF : C29H32O13 ;4-demethylepipodophyllotoxin-(4,6-o-(r)-ethylidene-beta-d- ...
Check out this study to learn about the clinical efficacy of the first-line anti-PD-L1 blockades with etoposide & platinum for ... According to IMpower133 and CASPIAN, anti-PD-L1 blockades combined with etoposide and platinum (EP) were the conventional first ... ES-SCLC: Anti-PD-L1 Blockades With Etoposide & Platinum. May 31, 2022 ...
Kagan investigated the interaction between dietary antioxidants, vitamins C and E, BHT and BHA, and etoposide VP-16, a widely ... Role of Dietary Antioxidants in Free Radical Enhancement of Etoposide (VP-16) Antitumor Activity. ...
... presented a pathological complete response in the surgical specimen after neoadjuvant chemotherapy with cisplatin and etoposide ... Once localized colon primary SCC was confirmed, it was decided to start treatment with platinum and Etoposide scheme with ... Localized Colonic Small-Cell Carcinoma with Pathological Complete Response after Neoadjuvant Cisplatin and Etoposide: A Case ... "Localized Colonic Small-Cell Carcinoma with Pathological Complete Response after Neoadjuvant Cisplatin and Etoposide: A Case ...
... etoposide), frequency-based adverse effects, comprehensive interactions, contraindications, pregnancy & lactation schedules, ... etoposide intravenous ETOPOSIDE - INJECTION (e-TOE-poe-side) COMMON BRAND NAME(S): Toposar WARNING: This medication may cause ... USES: Etoposide is used to treat testicular cancer and certain forms of lung cancer (such as small cell lung cancer). Etoposide ... Etoposide. *Y-site: cefepime, filgrastim, idarubicin. Etoposide PO4. *Y-site: amphotericin B, cefepime, chlorpromazine, ...
Intervention: One cycle comprising bleomycin 30000 IU on days 1, 8, and 15, etoposide 165 mg/m2 on days 1-3, and cisplatin 50 ... The 111 Study: A Single-arm, Phase 3 Trial Evaluating One Cycle of Bleomycin, Etoposide, and Cisplatin as Adjuvant Chemotherapy ... etoposide (360 mg/m2), and cisplatin (BE360P) chemotherapy, or surveillance. ...
Pembrolizumab Plus Ifosfamide, Carboplatin, and Etoposide in Relapsed or Refractory Classical Hodgkin Lymphoma. By Matthew ... and etoposide) produced a high rate of complete response in patients with relapsed or refractory classical Hodgkin lymphoma who ...
Etoposide/carboplatin chemotherapy for the treatment of metastatic myxomatous cerebral aneurysms. Journal of Neurology, 261(4): ...
Arriola E. L., Lopez A. R., Chresta C. M. Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits ... The Role of the DNA Mismatch Repair System in the Cytotoxicity of the Topoisomerase Inhibitors Camptothecin and Etoposide to ... The abbreviations used are: ETP, etoposide; CPT,camptothecin; topoII, topoisomerase II; topoI, topoisomerase I; DSB,double- ... and etoposide, a topoisomerase II inhibitor. Sensitivity to these drugs cannot be predicted by measuring endogenous levels of ...
The Foundation for Thymic Cancer Research is a tax-exempt, non-profit 501(c)(3) organization registered in the State of New York and donations are tax exempt as allowed by the Internal Revenue Code.. Contact Term of Service. ...
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 ...
Rapid emergence of acquired resistance to standard platinum-etoposide chem... ... Soluble guanylate cyclase signalling mediates etoposide resistance inprogressing small cell lung cancer. Schenk MW et al. ... Rapid emergence of acquired resistance to standard platinum-etoposide chemotherapy is common and improved therapies are ...
Liposomal Doxorubicin and Etoposide in Treating Patients With Recurrent or Persistent Ovarian, Fallopian Tube, or Peritoneal ... Topotecan Plus Etoposide in Treating Patients With Recurrent Ovarian, Peritoneal, or Fallopian Tube Cancer TLK286 in Treating ... Liposomal Doxorubicin and Etoposide in Treating Patients With Recurrent or Persistent Ovarian, Fallopian Tube, or Peritoneal ... First-line Intraperitoneal Cisplatin and Etoposide Chemotherapy for Ovarian Cancer A Study LY2228820 for Recurrent Ovarian ...
Etoposide does not influence phenotype of this sub-population of melanoma cells, while a combined treatment with Etoposide and ... 2 × 106 Hs294T melanoma cells either treated with Etoposide or Etoposide plus Bevacizumab and suspended in 0.2 ml of PBS were ... D) Hs294T cells were treated in hypoxic condition with Etoposide (50 μM) alone or with Etoposide (50 μM) plus Bevacizumab (250 ... On the other hand, Etoposide results ineffective on this subpopulation of cells (Figure 4C). Data revealed that Etoposide but ...
The etoposide concentrations in the CSF were much lower than those in plasma, and bevacizumab did not increase etoposide ... The impact of VEGF inhibition on etoposide penetration into the CSF was analyzed. Eight patients were enrolled. The CNS- ... Eligible patients were scheduled to receive bevacizumab combined with etoposide and cisplatin (BEEP) every 3 weeks for a ... From: A pilot study of bevacizumab combined with etoposide and cisplatin in breast cancer patients with leptomeningeal ...
Dose-intense cyclophosphamide and etoposide for patients with refractory or high-risk non-Hodgkins lymphoma.. Publication , ... "Dose-intense cyclophosphamide and etoposide for patients with refractory or high-risk non-Hodgkins lymphoma." Clin Lymphoma 5 ... "Dose-intense cyclophosphamide and etoposide for patients with refractory or high-risk non-Hodgkins lymphoma." Clin Lymphoma, ... Dose-intense cyclophosphamide/etoposide has promising efficacy; however, nonhematologic toxicity can be considerable. The ...
Etoposide / Etoposide is used for Small Cell Lung Cancer, Acute Leukemia, Bladder Cancer, Spread Of Cancer Cells, Cancer Of ... Etoposide / Etoposide is used for the treatment, control, prevention, & improvement of the following diseases, conditions and ... Etoposide / Etoposide improves the patients condition by performing the following functions like Inhibiting the tumor cells ... Etoposide. This is not a comprehensive list. These side-effects are possible, but do not always occur. Some of the side-effects ...
Tag: etoposide. Day 748/120. Laura Gilkey on January 18, 2017. May 11, 2017. ... Categories: Uncategorized Tags: acute lymphoblastic leukemia, CAR-T, cyclophosphamide, etoposide, family, fever, platelets, ... Categories: Uncategorized Tags: acute lymphoblastic leukemia, blood transfusion, cyclophosphamide, etoposide, kytril, lumbar ... etoposide, hemoglobin, Neupogen, platelets, relapse6 Comments. Day 685/57. Laura Gilkey on November 16, 2016. November 16, 2016 ...
Find information on Etoposide in Daviss Drug Guide including dosage, side effects, interactions, nursing implications, ... "Etoposide." Daviss Drug Guide, 18th ed., F.A. Davis Company, 2023. Emergency Central, emergency.unboundmedicine.com/emergency/ ... view/Davis-Drug-Guide/109244/11.0/etoposide. Vallerand AHA, Sanoski CAC, Quiring CC. Etoposide. Daviss Drug Guide. F.A. Davis ... Vallerand, A. H., Sanoski, C. A., & Quiring, C. (2023). Etoposide. In Daviss Drug Guide (18th ed.). F.A. Davis Company. https ...
K DIAM EXIM is leading Exporter,Manufacturer and Supplier company of Etoposide Injection from Surat, Gujarat, India at best ... Due to its excellent quality and long shelf life, the offered Etoposide Injection is extremely valued by the clients. This ... We are offering optimum quality Etoposide Injection, which is used in combination with other medications to treat cancer of the ...
... studies have focused on the regimen etoposide and cisplatin and on etoposide, doxorubicin, and cisplatin. ... Etoposide is a glycosidic derivative of podophyllotoxin that exerts a cytotoxic effect by stabilizing the normally transient ... Adjuvant or palliative treatment for adrenocortical carcinoma (AC) has been studied by using mitotane, cisplatin, etoposide, ... Chemotherapy has focused on 3 antineoplastics-cisplatin, etoposide, and doxorubicin-given alone or in combination; ...
Etoposide (Toposar). *View full drug information. A glycosidic derivative of podophyllotoxin that exerts a cytotoxic effect by ...
  • Etoposide, sold under the brand name Vepesid among others, is a chemotherapy medication used for the treatments of a number of types of cancer including testicular cancer, lung cancer, lymphoma, leukemia, neuroblastoma, and ovarian cancer. (wikipedia.org)
  • Etoposide is used as a form of chemotherapy for cancers such as Kaposi's sarcoma, Ewing's sarcoma, lung cancer, testicular cancer, lymphoma, nonlymphocytic leukemia, and glioblastoma multiforme. (wikipedia.org)
  • This is a case report of a 77-year-old Spanish male patient with localized SCC of the colon, who presented a pathological complete response in the surgical specimen after neoadjuvant chemotherapy with cisplatin and etoposide. (mdpi.com)
  • Standard management in the UK for high-risk stage 1 nonseminoma germ cell tumours of the testis (NSGCTT) is two cycles of adjuvant bleomycin, etoposide (360 mg/m 2 ), and cisplatin (BE 360 P) chemotherapy, or surveillance. (nih.gov)
  • In a phase II trial reported in JAMA Oncology , Locke J. Bryan, MD , and colleagues found that the combination of pembrolizumab with ICE chemotherapy (a regimen including ifosfamide, carboplatin, and etoposide) produced a high rate of complete response in patients with relapsed or refractory classical Hodgkin lymphoma who were candidates for autologous stem cell transplantation (SCT). (ascopost.com)
  • Rapid emergence of acquired resistance to standard platinum-etoposide chemotherapy is common and improved therapies are required for this recalcitrant tumour. (diagenode.com)
  • Chang, AY 1995, ' Introduction to ifosfamide/carboplatin/etoposide chemotherapy ', Seminars in oncology , vol. 22, no. 3 SUPPL. (johnshopkins.edu)
  • Chemotherapy doses were cisplatin 20 mg/m 2 and ifosfamide 1,200 mg/m 2 on days 1 to 3 and etoposide 40 mg/m 2 administered orally days 1 through 14. (psu.edu)
  • First-line therapy in ES-SCLC currently consists of chemotherapy, combining a platinum drug with either etoposide or irinotecan as a possible alternative. (ersjournals.com)
  • The first-line treatment of ES-SCLC currently consists of chemotherapy with a platinum derivative and etoposide, a combination that was first reported to be effective in the treatment of SCLC in 1985 8 , 9 . (ersjournals.com)
  • For example, a study using human Burkitt lymphoma cells found that oxidative stress actually interferes with the ability of the chemotherapy drugs doxorubicin, cisplatin, etoposide, and cytarabine to cause cancer cell death. (pinestreetfoundation.org)
  • 2000) A second study, involving the chemotherapy drugs etoposide and calcimycin, confirms this finding: Human Burkitt's lymphoma cells were unable to die quickly by apoptosis in the presence of oxidative stress and instead died using the slower and messier method of necrosis. (pinestreetfoundation.org)
  • Background and importance Etoposide is widely used in paediatric chemotherapy treatment, although hypersensitivity can be severe and treatment limiting. (bmj.com)
  • Impact on survival of addition of etoposide to primary chemotherapy in diffuse large B-cell lymphoma: a Swedish Lymphoma Registry study. (lu.se)
  • OBJECTIVES: I. Determine the efficacy of prolonged oral etoposide (VP-16) in patients with advanced ovarian epithelial or cervical cancer. (knowcancer.com)
  • Purpose: The combination of cisplatin, ifosfamide, and oral etoposide (PlEo) given concurrently with accelerated hyperfractionated thoracic radiation was studied in patients with limited small-cell lung cancer in a phase II trial to assess response, survival, and toxicity. (psu.edu)
  • Previous studies had suggested a synergism between cisplatin and etoposide, and some authors had reported interesting response rates with either of the two combinations: etoposide/cisplatin (EP)[4] or etoposide/doxorubicin (Adriamycin)/cisplatin (EAP). (cancernetwork.com)
  • Liposomal Doxorubicin and Etoposide. (checkorphan.org)
  • Adjuvant or palliative treatment for adrenocortical carcinoma (AC) has been studied by using mitotane, cisplatin, etoposide, and doxorubicin. (medscape.com)
  • studies have focused on the regimen etoposide and cisplatin and on etoposide, doxorubicin, and cisplatin. (medscape.com)
  • 60 years, regimens such as rituximab plus etoposide , prednisone , vincristine (Oncovin), and doxorubicin (dose-adjusted R-EPOCH) are also commonly used with success. (msdmanuals.com)
  • A few years ago, we performed a phase II trial with the FLEP regimen, in which fluorouracil (5-FU) and leucovorin are combined with etoposide and cisplatin (Platinol). (cancernetwork.com)
  • In 1989, Preusser et al[3] reported a 57% response rate with the FLEP regimen-5-FU, leucovorin, etoposide, and cisplatin (Platinol). (cancernetwork.com)
  • The FLEP regimen we used consisted of leucovorin 300 mg/m 2 /day, followed by etoposide 100 mg/m 2 /day, 5-FU 500 mg/m 2 /day, and cisplatin 30 mg/m 2 /day, all given on days 1 through 3 and repeated every 28 days. (cancernetwork.com)
  • There were 24 patients that could be evaluated for efficacy of this combination regimen of Irinotecan and Etoposide. (addon.life)
  • We are offering optimum quality Etoposide Injection , which is used in combination with other medications to treat cancer of the testicles. (kdiamexim.com)
  • Due to its excellent quality and long shelf life, the offered Etoposide Injection is extremely valued by the clients. (kdiamexim.com)
  • Scholars@Duke publication: Dose-intense cyclophosphamide and etoposide for patients with refractory or high-risk non-Hodgkin's lymphoma. (duke.edu)
  • 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)
  • 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)
  • A Phase II Study of Irinotecan and Etoposide as Treatment for Refractory Metastatic Breast Cancer. (addon.life)
  • Both Irinotecan and Etoposide are natural, plant-derived compounds that are modulators of topoisomerase (TOP) enzyme isoforms. (addon.life)
  • Irinotecan is a TOP1 and Etoposide a TOP2 modulator. (addon.life)
  • Randomized phase-III study of low-dose cytarabine and etoposide? (cdc.gov)
  • tell your doctor and pharmacist if you are allergic to etoposide, any other medications, or any of the ingredients in etoposide capsules. (medlineplus.gov)
  • Here, we report on seven patients with recurrent medulloblastoma, most heavily pretreated with a variety of chemotherapeutic agents, including parenteral etoposide (VP-16), who showed responses to the administration of repeated courses of low-dose oral VP-16. (elsevierpure.com)
  • This study aimed to assess the efficacy and safety of apatinib combined with etoposide in patients with recurrent platinum-resistant EOC. (jcancer.org)
  • The efficacy of apatinib combined with etoposide is encouraging in patients with platinum-resistant EOC. (jcancer.org)
  • Etoposide is in the topoisomerase inhibitor family of medication. (wikipedia.org)
  • Etoposide forms a ternary complex with DNA and the topoisomerase II enzyme, which is an enzyme that aids in relaxing negative or positive supercoils in DNA. (wikipedia.org)
  • We have shown that colorectal cancer cell lines defective in DNA MMR exhibit an increased sensitivity to both camptothecin, a topoisomerase I inhibitor, and etoposide, a topoisomerase II inhibitor. (aacrjournals.org)
  • Etoposide is a glycosidic derivative of podophyllotoxin that exerts a cytotoxic effect by stabilizing the normally transient covalent intermediates formed between the DNA substrate and topoisomerase II. (medscape.com)
  • According to IMpower133 and CASPIAN, anti-PD-L1 blockades combined with etoposide and platinum (EP) were the conventional first-line therapy for extensive-stage small-cell lung cancer ( ES-SCLC). (physiciansweekly.com)
  • Etoposide / Etoposide is used for Small Cell Lung Cancer, Acute Leukemia, Bladder Cancer, Spread Of Cancer Cells, Cancer Of Testicles and other conditions. (actizapharma.com)
  • Etoposide is used to treat certain forms of lung cancer (such as small cell lung cancer). (oceanpharmaproducts.com)
  • Therapeutic effectiveness of anlotinib combined with etoposide in extensive-stage small-cell lung cancer: a single-arm, phase II trial. (bvsalud.org)
  • Etoposide / Etoposide improves the patient's condition by performing the following functions like Inhibiting the tumor cells from dividing, Inhibiting the tumor cells from dividing.The following is a list of possible side-effects that may occur in medicines that contain Etoposide / Etoposide. (actizapharma.com)
  • Etoposide does not influence phenotype of this sub-population of melanoma cells, while a combined treatment with Etoposide and Bevacizumab significantly abolished P1 sphere-forming ability, an effect associated with apoptosis of this subset of cells. (oncotarget.com)
  • Hypoxic melanoma cells sorted for VEGF-R2/CD133 positivity also undergo apoptosis when exposed to Etoposide and Bevacizumab. (oncotarget.com)
  • When Etoposide and Bevacizumab-treated hypoxic cells were injected intravenously into immunodeficient mice revealed a reduced capacity to induce lung colonies, which also appear with a longer latency period. (oncotarget.com)
  • Hence, our study indicates that a combined exposure to Etoposide and Bevacizumab targets melanoma cells endowed with stem-like properties and might be considered a novel approach to treat cancer-initiating cells. (oncotarget.com)
  • One cycle comprising bleomycin 30000 IU on days 1, 8, and 15, etoposide 165 mg/m 2 on days 1-3, and cisplatin 50 mg/m 2 on days 1-2, plus antibacterial and granulocyte colony stimulating factor prophylaxis. (nih.gov)
  • It is used in form of its salt etoposide phosphate. (wikipedia.org)
  • 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 is a semisynthetic derivative of podophyllotoxin from the rhizome of the wild mandrake (Podophyllum peltatum). (wikipedia.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)
  • Instead Klose Training is low CBD content, while high THC options a a mixed format course 75 hours Dec 21 2018 etoposide RealSelf members say the cost 200 on average but each treatment session of Emsculpt costs about 1 000 and a series of four initial sessions results so you might end up paying more. (annamariadadomo.com)
  • After successful primary etoposide -based therapy , anlotinib was administered at 12 mg/day on days 1 to 14 of 21-day cycles until disease progression or consent withdrawal. (bvsalud.org)
  • Etoposide is in a class of medications known as podophyllotoxin derivatives. (medlineplus.gov)
  • 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)
  • Etoposide may also be used for purposes not listed in this medication guide. (exportersindia.com)
  • Etoposide (Lastet (50 mg)) is an anti-cancer agent, prescribed for lung cancer and testicular cancer. (medindia.net)
  • Conclusion: Relative to conventional etoposide/cisplatin and concurrent AHTRT, chemoradiation with PlEo produced similar median and 2-year survival rates and a higher rate of acute esophageal toxicity. (psu.edu)
  • I was a 40+ pack year smoker until my dx in 01/07, at which time I quit preparatory to undergoing concurrent radiation and cisplatin/etoposide therapy. (lungevity.org)
  • Material and methods A retrospective observational study was conducted in paediatric patients treated with etoposide from June 2013 to September 2020. (bmj.com)
  • The six year old about school with your down on the ground and allows her ampicilina existence of both substances, just like flavones, flavonoids or terpenes, therefore their upside down underneath etoposide a seems to be unneeded. (annamariadadomo.com)
  • There are conflicting data in the literature regarding the incidence of etoposide hypersensitivity reactions in adults and children. (bmj.com)
  • Dr. Kagan investigated the interaction between dietary antioxidants, vitamins C and E, BHT and BHA, and etoposide VP-16, a widely used phenolic antitumor drug. (aicr.org)
  • and etoposide 100 mg/m2 IV on day 1 and then 200 mg/m2/day orally on days 2 and 3. (cancernetwork.com)
  • You should not become pregnant or breast-feed while you are taking etoposide. (medlineplus.gov)
  • If you become pregnant while taking etoposide, call your doctor. (medlineplus.gov)
  • Etoposide was first synthesized in 1966 and U.S. Food and Drug Administration approval was granted in 1983. (wikipedia.org)
  • Emergency Central , emergency.unboundmedicine.com/emergency/view/Davis-Drug-Guide/109244/11.0/etoposide. (unboundmedicine.com)
  • Grapefruit can affect the removal of etoposide from your body, which may affect how etoposide works. (rapid-medico.com)
  • In summary, UFT/leucovorin/etoposide is effective and moderately toxic in patients with advanced gastric cancer. (cancernetwork.com)
  • Etoposide can cause a severe decrease in the number of blood cells in your bone marrow. (medlineplus.gov)
  • apalutamide will decrease the level or effect of etoposide by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
  • enzalutamide will decrease the level or effect of etoposide by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
  • ivosidenib will decrease the level or effect of etoposide by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
  • Many other medications may also interact with etoposide, so be sure to tell your doctor about all the medications you are taking, even those that do not appear on this list. (medlineplus.gov)