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The Topo II inhibitor etoposide has been administered to women during pregnancy, with healthy babies born, although there are no data on the side-effects of etoposide on the reproductive system of these children, as none have yet reached puberty. Our results, using in vitro systems to assess the effects of etoposide, show that exposure of pre-follicular ovaries to etoposide results in a near-complete elimination of healthy follicles by the end of culture. This observed lack of follicles is a direct result of etoposide-treated pre-follicular germ cells failing to survive, with only a small proportion capable of forming follicles. Etoposide was used in concentrations considerably lower than those measured in the serum of patients, concentrations of 50-150 ng ml−1 being used, compared with 5-60 μg ml−1 in patient serum [38]. In contrast, exposure to oocytes once they were enclosed in follicles had no effect on total follicle numbers or health, the only effect seen on transitional follicles, ...
NOTE: *Patients who are unable to receive etoposide IV on day 2 may receive oral etoposide on days 2 and 3.. In both arms, chemotherapy (carboplatin and etoposide) repeats every 3 weeks for up to 6 courses. Patients receive thalidomide or placebo continuously for up to 2 years. Treatment continues in the absence of disease progression or unacceptable toxicity. Patients who experience disease progression may continue to receive thalidomide or placebo provided the patient is clinically and symptomatically stable.. Quality of life is assessed at baseline, during each course of chemotherapy, at 3-4 weeks after completion of chemotherapy, and at 6, 12, 18, and 24 months.. Patients are followed every 2 months for 2 years after the completion of chemotherapy and then every 3 months thereafter.. Peer Reviewed and Funded or Endorsed by Cancer Research UK. PROJECTED ACCRUAL: A total of 372 patients (186 per treatment arm) will be accrued for this study. ...
Etoposide may be at least as, or even more, effective and less myelotoxic when given in low doses over prolonged periods of time.. Patients receive low-dose oral etoposide on days 1 through 7 of every 2-week cycle. Patients who achieve a complete or partial response after two cycles and have no toxicity greater than grade 2 may have their dose escalated for subsequent cycles. If there are no responses to therapy among the first 14 evaluable patients, the study will close; if there is at least one objective response to therapy among the first 14 evaluable patients, enrollment will continue until all 41 patients are enrolled. Patients continue therapy until maximal tumor response (either stable disease or complete response) is achieved or disease progression occurs. ...
Etoposide Injection, USP by Hospira: Etoposide belongs to the group of cancer-fighting medications called antineoplastics. Etoposide kills cancer cells by interfering with the genetic material DNA, which is necessary for their growth and reproduction. Etoposide is used alone or in combination with other antineoplastic medications to treat many types of cancer. These include certain types of lung cancer, lymphoma (cancer of the lymph cells), and cancers of the testicles.
Etoposide Injection, USP by Mylan: Etoposide belongs to the group of cancer-fighting medications called antineoplastics. Etoposide kills cancer cells by interfering with the genetic material DNA, which is necessary for their growth and reproduction. Etoposide is used alone or in combination with other antineoplastic medications to treat many types of cancer. These include certain types of lung cancer, lymphoma (cancer of the lymph cells), and cancers of the testicles.
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Etoposide - Get up-to-date information on Etoposide side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about Etoposide
Etoposide is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Etoposide is used to treat small cell lung cancer. It is usually given in combination with other cancer medicines. Etoposide may also be used for purposes not listed in this medication guide.
Paclitaxel and etoposide are two chemotherapy agents with broad cytotoxic activity and different mechanisms of action and resistance. Preclinical studies of their combined cytotoxicity have yielded conflicting results. We performed two sequential Phase II trials using different sequence schedules of paclitaxel and etoposide as first-line treatment in advanced non-small cell lung cancer (NSCLC). Forty-four patients with stage IIIB or IV NSCLC were included between July 1995 and September 1996. All patients received etoposide at 100 mg/m2, given as an i.v. infusion on days 1, 2, and 3. The first 20 patients (part A) also received paclitaxel at 175 mg/m2 as a 3-h infusion on day 1, immediately prior to etoposide. The subsequent 24 patients (part B) were given the same paclitaxel dose, but on day 4. Grade 3-4 granulocytopenia was seen in 70% of the patients in part A and in 37% of those in part B (P = 0.04). Twenty-five % of the courses in part A and 4% of the courses in part B were associated with ...
Reduction of atherosclerotic lesions in rabbits treated with etoposide associated with cholesterol-rich nanoemulsions Elaine R Tavares1, Fatima R Freitas1, Jayme Diament1, Raul C Maranhão1,21Heart Institute of the Medical School Hospital (InCor), University of São Paulo, São Paulo, Brazil; 2Faculty of Pharmaceutical Sciences, University of São Paulo, São Paulo, BrazilObjectives: Cholesterol-rich nanoemulsions (LDE) bind to low-density lipoprotein (LDL) receptors and after injection into the bloodstream concentrate in aortas of atherosclerotic rabbits. Association of paclitaxel with LDE markedly reduces the lesions. In previous studies, treatment of refractory cancer patients with etoposide associated with LDE had been shown devoid of toxicity. In this study, the ability of etoposide to reduce lesions and inflammatory factors in atherosclerotic rabbits was investigated.Methods: Eighteen New Zealand rabbits were fed a 1% cholesterol diet for 60 days. Starting from day 30
Cisplatin, etoposide, and irinotecan may be clinically beneficial as a second-line chemotherapy for selected patients with small cell lung cancer (SCLC).
Our results are most consistent with a model for etoposide-induced gene rearrangement shown in Fig. 4C. In this model, etoposide induces DNA damage (Topo II-linked DSBs) somewhere in the chromsomes. Etoposide-induced DNA damage then activates the apoptotic signaling pathway, which leads to activation of caspase-3 followed by ICAD cleavage and activation of CAD. Activated CAD then cleaves DNA within the MLL bcr as well as within MLL partner genes. The repair of the DSB within the MLL bcr through NHEJ results in rearrangement of the MLL gene with one of its ,50 partner genes and hence t-AML.. The role of apoptotic nuclease in genome instability is a surprising finding. It is generally thought that apoptotic nucleases, such as CAD, play a role late in the apoptotic cell death program. Our results suggest that a population of apoptotic cells with activated CAD may escape cell death and survive with a few DSBs ( 15). A possible consequence of this escape is gene rearrangements. It should be pointed ...
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Etoposide Pharmaswiss is a medicine available in a number of countries worldwide. A list of US medications equivalent to Etoposide Pharmaswiss is available on the Drugs.com website.
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Before you begin using a medication, be sure to inform your doctor of any medical conditions or allergies you may have, any medications you are taking, whether you are pregnant or breast-feeding, and any other significant facts about your health. These factors may affect how you should use this medication.. Allergic reactions: Allergic reactions, including difficulty breathing and swelling of the throat and mouth, can occur with the use of this medication. Tell your doctor immediately if you experience any of these symptoms.. Blood clotting: This medication can reduce the number of platelet cells in the blood. Platelets help the blood to clot, and a shortage could make you bleed more easily. Tell your doctor of any signs that your blood is not clotting as quickly as usual. Such symptoms may include black and tarry stools, blood in the urine, easy bruising, or cuts that wont stop bleeding.. Infection: As well as killing cancer cells, etoposide can reduce the number of cells that fight infection ...
Both ATM and ATR display a preference for phosphorylating SQ/TQ motifs in their substrates (Kim et al., 1999; Traven and Heierhorst, 2005; Shiloh, 2006). ATR is predominantly activated by UV light and stalled replication forks, whereas ATM is specifically activated by DSBs of DNA, as seen after irradiation, etoposide, or oxidative stress (Abraham, 2001; Shiloh, 2006). In contrast, treatment with the ATP-competitive kinase inhibitor, staurosporine, does not activate ATM or affect the phosphorylation status of ATM-dependent substrates (Kamer et al., 2005). We show here that DNA-damaging agents, such as IR and etoposide, trigger MEF2D phosphorylation. Moreover, MEF2D phosphorylation only increased after etoposide exposure in wt-ATM cells but not in ATM-deficient cells. These results suggest that ATM mediates MEF2D phosphorylation in response to DSBs in DNA.. Furthermore, in the present study, RNA interference-mediated knockdown experiments in cerebellar granule cells indicate that endogenous MEF2D ...
Introduction: Vorinostat has been shown to potentiate DNA damage induced by topoisomerase II inhibitors in a sequence dependent fashion. A multi-center, open label phase I study with escalating doses of vorinostat in combination with etoposide was conducted to establish the safety of the combination in pediatric patients with refractory solid tumors to determine the maximum tolerated dose (MTD), dose limiting toxicity (DLT) and recommended phase II dose (RP2D) of this regimen.. Methods: Eligible patients were ≤21 years of age with relapsed/refractory solid tumors including central nervous system tumors. Study design consisted of a standard 3+3 dose escalation schema. Vorinostat was administered once daily for days 1-4 of the treatment cycle in escalating doses (125 mg/m2, 160 mg/m2, 210 mg/m2, and 270 mg/m2). Etoposide was administered at a fixed dose of 100 mg/m2/day on days 3-5 of the treatment cycle. Etoposide was administered 4 hours after administration of vorinostat. Each treatment cycle ...
Researchers studying etoposide (used in lung & testicular cancer, leukemias and brain tumors) showed that combining it with other compounds can improve outcomes.
Dose . BCCA Administration Guide : 0 . etoposide : 100 mg/m² . IV in 500 mL NS over 1 h (use non-DEHP equipment with in-line filter) 1 . mesna : 360 mg/m². ...
This study is investigating ibrutinib and immuno-chemotherapy using dose-adjusted-temozolomide, etoposide, doxil, dexamethasone, ibrutinib, rituximab
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For the second time this month, the FDA has given an approval to Genentechs PD-L1 inhibitor, Tecentriq.. On March 18, 2019, the FDA awarded the immunotherapy agent, Tecentriq (atezolizumab; Genentech), in combination with chemotherapy (carboplatin and etoposide), approval for the first-line treatment of adults with extensive-stage small-cell lung cancer (ES-SCLC).. As evidence of the rapidity with which the immunotherapy field is gaining ground in cancer treatment, this new approval comes only 10 days after the drug received an accelerated approval (in combination with nab-paclitaxel) for the treatment of triple-negative breast cancer. Not only is this the second approval for atezolizumab in close succession to the first, but it is the first novel treatment in 2 decades for ES-SCLC, an aggressive and deadly malignancy.. This latest approval was based on data from the phase 3 IMpower133 trial, which was the first study to show that initial treatment with the immunotherapy-based combination ...
Radiotherapy improves the survival of patients with extensive-disease small-cell lung cancer: a propensity score matched analysis of Surveillance, Epidemiology, and End Results database Rui Zhang,* Ping Li,* Qin Li, Yunfeng Qiao, Tangpeng Xu, Peng Ruan, Qibin Song, Zhenming Fu Cancer Center, Renmin Hospital of Wuhan University, Wuhan 430060, China *These authors contributed equally to this work Background: The survival advantage of radiotherapy for patients with extensive-disease small-cell lung cancer (ED-SCLC) has not been adequately evaluated.Methods: We analyzed stage IV SCLC patients enrolled from the Surveillance, Epidemiology, and End Results (SEER) registry through January 2010 and December 2012. Propensity score analysis with 1:1 matching was performed to ensure well-balanced characteristics of all comparison groups. Kaplan–Meier and Cox proportional hazardous model were used to evaluate the overall survival (OS), cancer-specific survival (CSS), and corresponding 95% CI.Results: Overall,
To determine the efficacy of the addition of ifosfamide to cisplatin plus etoposide (VIP), or vinblastine (VeIP), in patients with recurrent germ cell tumors. DESIGN: Nonrandomized, prospective phase II trial. SETTING: Tertiary referral university hospital. PATIENTS: Fifty-six of fifty-eight entered patients with measurable and progressive recurrent germ cell tumors of testicular (46 patients), ovarian (1 patient), and extragonadal (9 patients) origin were evaluable for response after not being cured with cisplatin, vinblastine, and etoposide regimens. INTERVENTIONS: Patients were administered cisplatin (20 mg/m2 body surface area daily for 5 days), ifosfamide (1.2 g daily for 5 days), plus either etoposide (75 mg daily for 5 days) or vinblastine (0.11 mg/kg body weight on days 1 and 2). In addition, vigorous intravenous hydration therapy with normal saline (100 to 125 mL/h) was administered during the treatment course. Uroepithelial protective agents, N-acetylcysteine (orally) or mesna ...
Tumors developed in BRCA1 mutation carriers show distinctive cytologic and molecular profiles compared with the sporadic tumor counterparts (1, 24). Nevertheless, at the moment, tailored treatments for this group of patients have only been partially investigated (12, 13). The rarity of human BRCA1-mutated cancer cell lines has further limited the exploitation of such approaches.. In the current study, we used the RNA interference technology to generate several isogenic BRCA1-silenced/nonsilenced breast cancer cell lines to assess whether a biological rational exists to implement therapeutic protocols specific for BRCA1 cancer patients. Our cell models were then challenged with several chemotherapeutics commonly used in breast cancer treatment.. We found no association between BRCA1 down-regulation and sensitivity to the topoisomerase II inhibitors etoposide and doxorubicin. Although differential response was observed in a few clones, this was not correlated to BRCA1 expression levels. ...
TY - JOUR. T1 - Chronic daily administration of oral etoposide - A phase I trial. AU - Hainsworth, J. D.. AU - Johnson, D. H.. AU - Frazier, S. R.. AU - Greco, F. A.. PY - 1989. Y1 - 1989. N2 - In this phase I study, we administered etoposide (VP-16) orally for 21 consecutive days to patients with advanced refractory cancers. All patients had received previous chemotherapy, and 50% of patients had received more than one combination regimen. When given for 21 consecutive days, the maximum-tolerated dose of oral VP-16 was 50 mg/m2/d. Myelosuppression was the dose-limiting toxicity, and occurred between days 21 and 28. In most patients, blood counts had recovered sufficiently by day 35 to begin another 3-week course. WBC count nadirs of , 1,000/μL occurred in four of 20 courses at this dose, and three patients required hospitalization for treatment of neutropenia and fever. Alopecia occurred in most patients; gastrointestinal (GI) and other toxicities were uncommon. Five of 16 patients with ...
Around 1 in 1,000 pregnant women are diagnosed with cancer, requiring consideration for the use of chemotherapy during pregnancy. However, little is known about the possible long-term detrimental effects of etoposide on the reproductive system of the unborn child. ...
This randomized phase II trial studies paclitaxel and carboplatin to see how well they work compared with bleomycin sulfate, etoposide phosphate, and cisplatin in treating patients with sex cord-ovarian stromal tumors that have spread to other places in the body and usually cannot be cured or controlled with treatment (advanced) or has returned (recurrent). Drugs used in chemotherapy work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Giving more than one drug (combination chemotherapy) may kill more tumor cells. It is not yet known which chemotherapy regimen is more effective in treating sex cord-ovarian stromal tumors. ...
The antitumor drug etoposide (ETO) is widely used in treating several cancers including adrenocortical tumor (ACT). the autophagy inhibitor reduced Take action cell growth and inhibited ETO-induced centrosome amplification. Chloroquine alleviated CDK2 and ERK but not Chk2 activation and thus inhibited centrosome amplification in either ETO- or hydroxyurea-treated ACT cells. In addition chloroquine also inhibited centrosome amplification in osteosarcoma U2OS cell lines when treated with ETO or hydroxyurea. In summary we have exhibited that chloroquine inhibited ACT cell growth and alleviated DNA damage-induced centrosome amplification by inhibiting CDK2 and ERK activity thus preventing genomic instability and recurrence of ACT. Introduction Adrenal gland which is composed of the cortex and medulla is the most important endocrine organ that lies on top of the kidney. Adrenocortex is the major site of steroidogenesis in response to adrenocorticotropic hormone stimulation and its abnormal growth ...
Dose escalation study of high-dose carboplatin and etoposide with autologous bone marrow support in patients with recurrent and refractory germ cell tumors.: Th
Background: In an attempt to reduce the toxicity of chemotherapy in good-risk testicular cancer patients the two drug combinations, cisplatin plus etoposide (EP) and carboplatin plus etoposide (EC), have been compared. Methods: Good risk was defined according to the MSKCC and IU criteria. 39 Patients have been treated with EP (cisplatin 20 mg/m2 i.v. and etoposide 100 mg/m2 i.v. on days 1 to 5), and 23 patients received EC (carboplatin 350 mg/m2 on day 1 and etoposide 100 mg/m2 on days 1 to 5). Four cycles of chemotherapy were given at 21- and 28-day intervals, respectively, with delays of up to 7 days in istances of leukocyte counts less than 3.0 x 10(9)/l or platelet counts less than 100 x 10(9)/l. Results: In the EP group 34 (87%) of 39 patients achieved CR (26 with chemotherapy alone, 8 with additional surgery). After a median follow-up of 26 (12-58) months 3 (9%) patients relapsed from CR. Currently 38 patients are alive, and 37 (94%) are NED. In the EC group 20 (87%) of 23 patients ...
The tumor suppressor gene HIC1 (Hypermethylated In Cancer 1) encodes a transcriptional repressor mediating the p53-dependent apoptotic response to irreparable DNA double-strand breaks (DSBs) through direct transcriptional repression of SIRT1. HIC1 is also essential for DSB repair as silencing of endogenous HIC1 in BJ-hTERT fibroblasts significantly delays DNA repair in functional Comet assays. HIC1 SUMOylation favours its interaction with MTA1, a component of NuRD complexes. In contrast with irreparable DSBs induced by 16-hours of etoposide treatment, we show that repairable DSBs induced by 1 h etoposide treatment do not increase HIC1 SUMOylation or its interaction with MTA1. Furthermore, HIC1 SUMOylation is dispensable for DNA repair since the non-SUMOylatable E316A mutant is as efficient as wt HIC1 in Comet assays. Upon induction of irreparable DSBs, the ATM-mediated increase of HIC1 SUMOylation is independent of its effector kinase Chk2. Moreover, irreparable DSBs strongly increase both the
Twenty three patients with paediatric soft tissue sarcomas who had relapsed or refractory disease were treated with a rapid schedule of intravenous etoposide (100 mg/m2 daily on three consecutive days, weekly over 3 weeks). The regimen was well tolerated with predictable myelotoxicity. In 19 patients with rhabdomyosarcoma, there was a response rate of 42%. This appears to be better than previously reported with conventional three weekly schedules. These data indicate that for rhabdomyosarcoma, as for some other tumours, a divided dose regimen may be the optimal schedule and is worthy of further evaluation ...
Transposase activity was thought to be extinct in humans because DNA movement can be deleterious in higher organisms, resulting in genomic instability and perha...
... cyclophosphamide and doxorubicin (DA-EPOCH-R) with traditional rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) regimens in CD5+ double-hit lymphoma (DHL) and to evaluate prognostic factors. PFS (85.7% vs 23.0%, em P /em =0.029), but there was no statistical difference in OS (87.7% vs 34.4.0%, em P /em =0.064). However, in DA-EPOCH-R protocol, there was no significant difference between CD5+ DHL (MYC/BCl2 and MYC/BCL6) and triple-hit lymphoma ( em buy IWP-2 P /em =0.776 for PFS; em P /em =0.728 for OS). Multivariate analysis showed that CD5+ treatment regimen and disease stage were independent prognostic factors. Conclusion Our retrospective study shows that CD5+ has a poorer prognosis than CD5? patients. Based on its improved lifetime and good tolerance on CD5+ patients, which is expected to become the first-line treatment for high-risk DLBCL types based on more ...
In this international, double-blind, phase 3 trial, adults with newly diagnosed ES-SCLC, ECOG PS ≤ 1, and no previous systemic therapy for SCLC are randomized 1:1 to receive either EP plus a 200-mg fixed dose of pembrolizumab intravenously (IV) once every 3 weeks (Q3W) or EP plus pbo IV Q3W. Randomization is stratified by the chosen platinum therapy (carboplatin vs cisplatin), ECOG PS (0 vs 1), and baseline lactate dehydrogenase concentration (≤ upper limit of normal [ULN] vs > ULN). Study treatment includes a total of 4 cycles of EP and 2 y of pembrolizumab/pbo and continues until documented PD, intolerable toxicity, or withdrawal of consent. Pts with a response after 4 cycles of EP plus pbo or pembrolizumab may receive prophylactic cranial irradiation. Pts who complete 2 y of pembrolizumab treatment or stop pembrolizumab for reasons other than PD/intolerability, but subsequently have documented PD, may receive an additional 1 y of pembrolizumab. Tumor response is assessed every 6 wk for 48 ...
Etoposide is a semisynthetic derivative of podophyllotoxin, which inhibits DNA synthesis via topoisomerase II inhibition activity.
The present invention provides amphiphilic prodrugs comprising a therapeutic compound conjugated to an PEG-oligomer/polymer and methods for using said prodrugs to enable oral drug delivery and/or delivery of drugs across the blood brain barrier into the central nervous system.
An etoposide-treated DU145 prostate cancer cell exploding into a cascade of apoptotic bodies. The sub images were extracted from a 61-hour time-lapse microscopy video, created using quantitative phase-contrast microscopy. The optical thickness is color-coded. With increasing thickness, color changes from gray to yellow, red, purple and finally black.[1] ...
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This is a multinational, multicenter, randomized controlled, open-label, adaptive study to evaluate the efficacy of PaCE chemotherapy in chemotherapy na