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 ...

TY - JOUR. T1 - Evaluation of the continuous infusion of etoposide plus cisplatin in metastatic breast cancer a collaborative north central cancer treatment group/mayo clinic phase ii study. AU - Krook, James E.. AU - Loprinzi, Charles L.. AU - Schaid, Daniel J.. AU - Kardinal, Carl G.. AU - Mailliard, James A.. AU - Pfeifle, Delano M.. AU - Ellison, Neil M.. AU - Reuter, Nicholas F.. AU - Nelimark, Robert A.. N1 - Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1990/2/1. Y1 - 1990/2/1. N2 - A prospective clinical trial was done to evaluate the efficacy and toxicity of cisplatin plus etoposide (VP‐16) in patients with breast cancer who failed one previous chemotherapy regimen for advanced disease or relapsed within 12 months of adjuvant chemotherapy. Partial responses occurred in 11 of 44 evaluable patients (25%; 95% confidence interval (CI), 13% to 40%). The median time to disease progression in responding patients was 4 months (range, 3 to 6+ months), whereas the median ...

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 ...

During B cell activation, the DNA lesions that initiate somatic hypermutation and class switch recombination are introduced by activation-induced cytidine deaminase (AID). AID is a highly mutagenic protein that is maintained in the cytoplasm at steady state, however AID is shuttled across the nuclear membrane and the protein transiently present in the nucleus appears sufficient for targeted alteration of immunoglobulin loci. AID has been implicated in epigenetic reprogramming in primordial germ cells and cell fusions and in induced pluripotent stem cells (iPS cells), however AID expression in non-B cells is very low. We hypothesised that epigenetic reprogramming would require a pathway that instigates prolonged nuclear residence of AID. Here we show that AID is completely re-localised to the nucleus during drug withdrawal following etoposide treatment, in the period in which double strand breaks (DSBs) are repaired. Re-localisation occurs 2-6 hours after etoposide treatment, and AID remains in the

Supplementary MaterialsSupplementary Table 1. prolonged lifespan of was associated with decreased levels of daf-16 which related to the insulin/insulin-like growth factor signaling pathway (IIS) activity and reactive air types (ROS), whereas heat surprise transcription aspect-1 (hsf-1) pathway had not been … Continue reading →. ...

Dive into the research topics of Phase II trial of cisplatin/etoposide and concurrent radiotherapy followed by paclitaxel/carboplatin consolidation for limited small-cell lung cancer: Southwest Oncology Group 9713. Together they form a unique fingerprint. ...

OBJECTIVES:. I. Determine the feasibility, tolerability, and toxicities, in terms of the maximum tolerated dose (MTD), of the sequential combination of vorinostat (SAHA) followed by cytarabine and etoposide in patients with relapsed and/or refractory acute leukemia or transforming myelodysplastic syndromes or myeloproliferative disorders.. II. Determine whether the addition of SAHA to cytarabine and etoposide chemotherapy improves outcome, in terms of complete response rate, duration of response, and overall survival, in these patients.. III. Determine the effects of SAHA on induction of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-death receptors DR4 and DR5 and other pro-apoptotic mediators in patient-derived cancer cells (leukemia blast cells) and somatic cells (buccal mucosa cells, using pre-SAHA and on SAHA treatment samples).. IV. Determine the ability of SAHA to block leukemia blast cells in the G1 phase of the cell cycle (leukemia blast cells, using pre-SAHA and on ...

OBJECTIVES:. I. Determine the feasibility, tolerability, and toxicities, in terms of the maximum tolerated dose (MTD), of the sequential combination of vorinostat (SAHA) followed by cytarabine and etoposide in patients with relapsed and/or refractory acute leukemia or transforming myelodysplastic syndromes or myeloproliferative disorders.. II. Determine whether the addition of SAHA to cytarabine and etoposide chemotherapy improves outcome, in terms of complete response rate, duration of response, and overall survival, in these patients.. III. Determine the effects of SAHA on induction of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-death receptors DR4 and DR5 and other pro-apoptotic mediators in patient-derived cancer cells (leukemia blast cells) and somatic cells (buccal mucosa cells, using pre-SAHA and on SAHA treatment samples).. IV. Determine the ability of SAHA to block leukemia blast cells in the G1 phase of the cell cycle (leukemia blast cells, using pre-SAHA and on ...

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. ...

Although histone deacetylases (HDACs) are involved in the carcinogenesis of solid tumors and HDAC inhibitors (HDACi) have already proved their efficacy in clinical trials, isoenzyme specific functions are still ill defined. In this thesis a high expression of HDAC2 in vivo in human and murine pancreatic ductal adenocarcinomas (PDAC) was demonstrated, suggesting an important role of HDAC2 in the pathogenesis of PDAC. In pancreatic cancer cell lines a HDAC2 dependent signaling pathway was discovered which resulted in resistance towards the topoisomerase II inhibitor etoposide by repression of the BH3-only protein NOXA. Targeting HDAC2 by HDACi will therefore be a promising strategy to overcome therapeutic resistance of PDAC against DNA damage inducing chemotherapeutics. « ...

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 ...

Etoposide injection is used in combination with other medications to treat cancer of the testicles that has ... after treatment with other medications or radiation therapy. Etoposide injection is also used in combination with other ...

DNA damage can be sensed as a danger-associated molecular pattern by the innate immune system. Here we find that keratinocytes and other human cells mount an innate immune response within hours of etoposide-induced DNA damage, which involves the DNA sensing adaptor STING but is independent of the cy …

Transposase activity was thought to be extinct in humans because DNA movement can be deleterious in higher organisms, resulting in genomic instability and perha...

Etoposide is a widely used anticancer drug successfully used for the treatment of many types of cancer in children and adults. Its use, however, is associated with an increased risk of development of secondary acute myelogenous leukemia involving the mixed-lineage leukemia (MLL) gene (11q23) translocations. Previous studies demonstrated that the phenoxyl radical of etoposide can be produced by action of myeloperoxidase (MPO), an enzyme found in developing myeloid progenitor cells, the likely origin for myeloid leukemias. We hypothesized, therefore, that one-electron oxidation of etoposide by MPO to its phenoxyl radical is important for converting this anticancer drug to genotoxic and carcinogenic species in human CD34+ myeloid progenitor cells. In the present study, using electron paramagnetic resonance spectroscopy, we provide conclusive evidence for MPO-dependent formation of etoposide phenoxyl radicals in growth factor-mobilized CD34+ cells isolated from human umbilical cord blood and ...

Objectives To compare the efficacy of rituximab, dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide and doxorubicin (DA-EPOCH-R) with traditional rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) regimens in CD5+ double-hit lymphoma (DHL) and to evaluate prognostic factors. PFS (85.7% vs 23.0%, em P /em =0.029), but there was no statistical difference in OS (87.7% vs 34.4.0%, em P /em =0.064). However, in DA-EPOCH-R protocol, there was no significant difference between CD5+ DHL (MYC/BCl2 and MYC/BCL6) and triple-hit lymphoma ( em buy IWP-2 P /em =0.776 for PFS; em P /em =0.728 for OS). Multivariate analysis showed that CD5+ treatment regimen and disease stage were independent prognostic factors. Conclusion Our retrospective study shows that CD5+ has a poorer prognosis than CD5? patients. Based on its improved lifetime and good tolerance on CD5+ patients, which is expected to become the first-line treatment for high-risk DLBCL types based on more ...

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] ...

Golf great Phil Mickelson has been finding it a struggle on the course in recent weeks so could have done without a freak occurrence which left his participation in the final round of the BMW Championship at Medinah in some doubt. Teenage girls have designed Africas first private satellite due to launch into space in 2017. Its hoped it can monitor and find answers to South Africas drought crisis. There are currently1277 DSP recipients who list their only medical condition asdrug or alcohol dependence, official figures have revealed. 1000 mg generic avamigran ...

This is a multinational, multicenter, randomized controlled, open-label, adaptive study to evaluate the efficacy of PaCE chemotherapy in chemotherapy na

Jack Yalowich, PhD, is a member of the Translational Therapeutics Program at OSUCCC - James, where his research focuses on therapeutic treatment and prevention of cancers. In particular, he is exploring how to improve ability of the clinically effective anticancer agent etoposide (VP-16) in

Just a quickie today. Erin had blood counts done yesterday. It was Day 11 of 21 days (hump day for this cycle). With all the chemos Erin has done in the past Day 11 was usually a pretty important day. It was the day Erin was most likely to have the lowest white blood counts and be the most susceptible to germs or infections. We tended to keep a low profile on Days 10 to Day 13 or so, just to be on the safe side. I knew that oral etoposide was supposed to be easy on the counts, but so was topo/cyclo. Even with neulasta support (the injection to build her white counts), with topo/cyclo her ANC would drop down under 1000 every time. [To refresh your memory, normal ANC is over 2000. Under 500 is considered neutropenic and requires her to stay home from school, etc. ] With the etoposide, she didnt have the benefit of neulasta (thats akin to saying she doesnt have the benefit of being beaten with a stick), and she has bone marrow that has faced down almost a year of toxic chemo. ...

Despite the premature end of her first chemotherapy cycle, Sadie remained remarkably stable. Between no etoposide and lots of dexamethasone, she was feeling great. We wondered if wed heard the doctors correctly on August 27th. Sadie didnt look like someone with only weeks to live.. Sadies second chemotherapy cycle should have started on September 18, but her bloodwork wasnt good enough. She did have an MRI that day, a month ahead of schedule. The MRI confirmed her prognosis: the tumor had grown dramatically since Sadies last MRI. What cisplatinum and etoposide shed gotten were having no effect. On September 22, the doctors recommended we stop treatment and enjoy the time Sadie had left. Sadie and we concurred.. We went home. Wed cried on August 27th, but today we were just numb. Her prognosis wasnt new, and despite the hard evidence in black-and-white MRI images, it still seemed unreal. I remember feeling mostly relieved that Sadie wouldnt be so miserably sick now that chemotherapy was ...

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5S,5aR,8aR,9R)-9-(4-hydroxy-3,5-dimethoxyphenyl)-8-oxo-5,5a,6,8,8a,9-hexahydrofuro[3,4:6,7]naphtho[2,3-d][1,3]dioxol-5-yl 4,6-O-[(1R)-ethylidene]-beta-D- ...

Background: IIIA T1N2M0 NSCL Lung Cancer. 10/2013 URL Removal followed up with chemoradiation; Radiation to Mediastinum and area of lobectomy. Carbo/Taxol concurrent with 35 radiation treatments; Chemo only 3 treatments - allergic reaction to Taxol replaced with 3 treatments of Cisplatin/Etoposide. 4 months post treatment, ER visit and Pulmonary DR visit follow-up for extreme

NU7441, also known as KU-57788, is a highly potent and selective DNA-PK inhibitor (IC50=14 nM), exhibiting ATP-competitive inhibition kinetics. NU7441 increased the cytotoxicity of ionizing radiation and etoposide in SW620, LoVo, and V3-YAC cells but not in V3 cells, confirming that potentiation was due to DNA-PK inhibition. NU7441 substantially retarded the repair of ionizing radiation-induced and etoposide-induced DSB.

Learn about the potential side effects of Toposar (etoposide). Includes common and rare side effects information for consumers and healthcare professionals.

Page 2 - Okay, this is really bugging me. My friend (and coworker) had to give Etoposide the other night. And like a good little doo-bee, she looked up the med on the hospitals computerized drug reference

TY - JOUR. T1 - Limited-stage small-cell lung cancer. T2 - Patterns of intrathoracic recurrence and the implications for thoracic radiotherapy. AU - Liengswangwong, V.. AU - Bonner, J. A.. AU - Shaw, E. G.. AU - Foote, R. L.. AU - Frytak, S.. AU - Eagan, R. T.. AU - Jett, J. R.. AU - Richardson, R. L.. AU - Creagan, E. T.. AU - Su, J. Q.. PY - 1994/3. Y1 - 1994/3. N2 - Purpose: This analysis was performed to determine the most appropriate volume that should be encompassed by thoracic radiation treatments (TRTs) for patients with limited-stage small-cell lung cancer (LSSCLC) who have responded to initial chemotherapy. Patients and Methods: A retrospective review of all patients (N = 67) with LSSCLC who were not entered onto a research protocol and were treated at our institution between the years of 1982 and 1990 was performed. Fifty-nine of 67 patients had adequate information regarding the size of the tumor before the start of chemotherapy (computed tomographic [CT] scan of chest or chest ...

This study evaluated the prognosis of patients with extensive-stage small-cell lung cancer (ES-SCLC) that may be associated with timing of thoracic radiotherapy (TRT). ES-SCLC patients (n = 232) without progression were retrospectively analyzed after first-line induction chemotherapy. Patients in the TRT group were stratified as early-TRT (ERT; ≤3 cycles of induction chemotherapy received prior to TRT, n = 65) or late-TRT (LRT; |3 cycles, n = 122). To avoid selection bias, we conducted Propensity Score Matching (PSM) for patients. Overall survival (OS), progression-free survival (PFS), and locoregional recurrence-free survival (LRRFS) were assessed and compared. Overall, the median survival time, PFS, and LRRFS were 13.2, 8.7, and 14.6 months, respectively. After matching by PSM, there were 45 patients total in the TRT/non-TRT groups, and 56 patients total in the ERT/LRT groups. OS, PFS, and LRRFS were significantly longer in the TRT group than the non-TRT group (P | 0.001, all). However, between the

This study evaluated the prognosis of patients with extensive-stage small-cell lung cancer (ES-SCLC) that may be associated with timing of thoracic radiotherapy (TRT). ES-SCLC patients (n = 232) without progression were retrospectively analyzed after first-line induction chemotherapy. Patients in the TRT group were stratified as early-TRT (ERT; ≤3 cycles of induction chemotherapy received prior to TRT, n = 65) or late-TRT (LRT; |3 cycles, n = 122). To avoid selection bias, we conducted Propensity Score Matching (PSM) for patients. Overall survival (OS), progression-free survival (PFS), and locoregional recurrence-free survival (LRRFS) were assessed and compared. Overall, the median survival time, PFS, and LRRFS were 13.2, 8.7, and 14.6 months, respectively. After matching by PSM, there were 45 patients total in the TRT/non-TRT groups, and 56 patients total in the ERT/LRT groups. OS, PFS, and LRRFS were significantly longer in the TRT group than the non-TRT group (P | 0.001, all). However, between the

The acquisition of resistance to anticancer drugs is a key obstacle to successful cancer therapy. An increasing number of studies have investigated the roles of microRNAs in drug resistance. We previously reported that the upregulation of miR-135b and miR-196b correlated positively with acquired drug resistance in the human T-cell leukemia cell line, CCRF-CEM (CEM), and that the elevation of expression of these two microRNAs in response to the DNA damaging agent etoposide appears to be histiotype-specific (T-T Ho et al, Proceedings of the 102nd Annual Meeting of the AACR 2011). To develop a mechanistic understanding of why these microRNAs are differentially expressed, we have studied miR-196b, which maps between the HoxA9 and HoxA10 genes on chromosome 7p15.2, suggesting that miR-196b and HoxA genes might be co-activated. Indeed, we found upregulation of HoxA9 mRNA after short-term (48 h) exposure of CEM cells to the topoisomerase II inhibitors etoposide and doxorubicin. Of note, we also found ...

TY - JOUR. T1 - Randomized phase II-III trial of combination beta and gamma interferons and etoposide and cisplatin in inoperable non-small cell cancer of the lung. AU - Schiller, Joan H.. AU - Storer, Barry. AU - Dreicer, Robert. AU - Rosenquist, Debra. AU - Frontiera, Michael. AU - Carbone, Paul P.. PY - 1989/11/15. Y1 - 1989/11/15. N2 - We observed major responses in two patients with adenocarcinoma of the lung who had received a combination of interferon (IFN)-β and IFN-γ, immediately followed by chemotherapy. To verify these observations, we initiated a prospective randomized phase II-III trial of etoposide and cisplatin, with or without IFN-β and IFN-γ, in patients with inoperable non-small cell lung cancer. Thirty-seven patients were randomized to receive either two cycles of chemotherapy or 6 weeks of IFN-β plus IFN-γ followed by two cycles of chemotherapy. Chemotherapy consisted of 60 mg of cisplation/m2 on day 1 and 120 mg of etoposide/m2 on days 4, 6, and 8, repeated every 21 ...

The therapeutic effectiveness of continuous infusion of 5-fluorouracil and cisplatin, and etoposide (FEP) for treatment of metastatic gastric cancer was examined. Studies were made on 17 patients with gastric cancer with distant metastases. 5-fluorouracil (300 mg/m(2)/day) and cisplatin (80 mg/m(2)/day) were administered by continuous intravenous infusion for 120 and 24 hours, respectively; etoposide (60 mg/m(2)/day) was injected intravenously over a 2 hour period on days 2, 3 and 4. These chemotherapy treatments were repeated every 28 days. Partial, but not complete, remission was seen in four patients (24%). The treatment increased the survival times of patients with differentiated or Borrmann 2 or 3 type cancer, but not significantly. In many cases the treatment caused myelosuppression, but side effects were usually mild or moderate. It is concluded that infusion of 5-fluorouracil, etoposide and cisplatin is effective and well tolerated ...

Background: Much research has confirmed the favorable effect of irinotecan/cisplatin (IP) and etoposide/cisplatin (EP) on extensive-stage small cell lung c

The UK Medical Research Council conducted this trial of carboplatin chemotherapy in advanced seminoma to compare single agent carboplatin with a standard combination of etoposide with cisplatin. The use of single agent carboplatin was expected to be associated with reduced toxicity. A total of 130 patients with advanced seminoma were randomly assigned to treatment with either single agent carboplatin (C) at a dose of 400 mg/m(2)to be corrected for glomerular filtration rate outside the range 81-120 ml min(-1)and to be administered on day 1 of a 21 day cycle to a total of 4 cycles or to etoposide + platinum (EP). The trial was designed as an equivalence study aiming to exclude a reduction in the 3-year progression-free survival in patients allocated to carboplatin of between 10 and 15%, requiring initially a target accrual of 250 patients (90% power significance level 5% (one-sided)). The trial closed after 130 patients had been randomized following recommendation by an independent data ...

As a dose-response relationship has been suggested for cisplatin, it appeared attractive to explore high-dose-intensity regimens in non-small-cell lung cancer. In a phase I study of weekly administration of cisplatin combined with oral etoposide we achieved a cisplatin dose intensity of 52.5-60 mg/m2 per week in most patients. We subsequently explored this regimen in advanced non-small-cell lung cancer. Patients were treated with cisplatin infused at 70 mg/m2 on days 1, 8, 15 and 29, 36, 43 in combination with oral etoposide given at 50 mg on days 1-15 and 29-43. Patients showing stable disease or a better response were continued on treatment with oral etoposide given at 50 mg/m2 per day on days 1-21 every 28 days for a maximum of four cycles. In all, 22 patients with stage III disease and 31 patients with stage IV disease entered the study. The median number of cisplatin administration was 6 per patient; 17 patients reached the planned cisplatin dose intensity of 60 mg/m2 per week, 11 patients ...

TY - JOUR. T1 - Phase I and pharmacologie study of the arotinoid Ro 40-8757 in combination with cisplatin and etoposide in patients with non-small cell lung cancer. AU - Van Zuylen, Lia. AU - Schellens, Jan H.M.. AU - Goey, Swan H.. AU - Pronk, Linda C.. AU - De Boer-Dennert, Maureen M.. AU - Loos, Walter J.. AU - Ma, Jianguo. AU - Stoter, Gerrit. AU - Verweij, Jaap. PY - 1999/1/1. Y1 - 1999/1/1. N2 - This phase I study was performed to assess the feasibility of combining cisplatin/etoposide (VP-16) with the arotinoid Ro 40-8757 and to determine the dose-limiting toxicity (DLT) of Ro 40-8757 in this combination. Patients with non-small cell lung cancer were eligible. Treatment consisted of Ro 40-8757 p.o. day 1-21, cisplatin 100 mg/m2 i.v. on day 2 and VP-16 100 mg/m2 i.v. on day 2-4, repeated every 3 weeks. Eighteen patients were évaluable for toxicity and response. The doses of Ro 40-8757 ranged from 84 mg/m2 once daily to 42 mg/m2 thrice daily (tid). DLT consisting of delayed nausea/vomiting ...

Read Epstein-Barr virus-mediated protection against etoposide-induced apoptosis in BJA-B B cell lymphoma cells: role of Bcl-2 and caspase proteins, Archives of Virology on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.

The authors evaluated the combination of etoposide/cyclophosphamide (VP/CY) as initial, presurgical therapy for patients with osteosarcoma and found an 88% response rate for the primary tumor and any metastases. After definitive, limb-salvage surgery and adjuvant chemotherapy with etoposide, cyclophosphamide, cisplatin, and doxorubicin, patients without metastases at diagnosis whose cases were followed for a median of 2 years from diagnosis achieved a relapse-free survival (RFS) probability of 78% +/- 9%. This result is equivalent to the best adjuvant chemotherapy results reported to date. Patients without metastases at diagnosis had significantly better RFS probability (78% +/- 9%) than those with metastases at diagnosis (0%). Transient, severe myelosuppression has been the only major toxicity of the VP/CY courses. No irreversible organ damage or toxic deaths have been seen in patients enrolled in this study. The authors conclude that the combination of VP/CY is effective treatment for ...

T-cell acute lymphoblastic leukemia (T-ALL) is a lymphoid disorder that results from an over proliferation of immature lymphocytes in the blood and bone marrow. It has been determined that 60% of patients stricken with T-ALL aberrantly express TAL-1 and have been shown to respond poorly to chemotherapy. This research sought to determine if TAL-1 influences the expression of the Bcl-2 family members Bcl-2 (anti-apoptotic), Bad and Bax (pro-apoptotic). TAL-1 and Bcl-2 levels were elevated while Bad and Bax levels were lower in etoposide-treated Jurkat cells as compared to TRAIL-treated and dual-treated Jurkat cells in which TAL-1 and Bcl-2 levels were lower while Bad and Bax levels were elevated. These results suggest TAL-1 up-regulates Bcl-2 and suppress Bad and Bax expression in response to etoposide treatment, thus inducing an anti-apoptotic response in the cell. These results also suggest that TRAIL and the dual treatment of etoposide and TRAIL down-regulates TAL-1 and Bcl-2 expression while ...

SCLC accounts for about 15% of all lung cancers, and it is strongly associated with tobacco use. SCLC is an aggressive cancer type, with a 5-year overall survival rate of about 6% to 7%. Although a number of combinations have been studied, until the recent advent of immune checkpoint inhibitors, standard first-line therapy for extensive-stage SCLC had remained etoposide/platinum for the preceding 30 years, Dr. Rudin noted. Although patients respond to etoposide/platinum, the median overall survival on this regimen is less than 1 year.. Pembrolizumab is currently U.S. Food and Drug Administration-approved for use as third-line or later therapy for metastatic SCLC. This study sought to explore its use in the first-line setting for SCLC.. Study Details. KEYNOTE-604 was conducted at 133 sites in 18 countries and randomly assigned 453 patients with previously untreated disease in a 1:1 ratio to pembrolizumab/etoposide/platinum or placebo/etoposide/platinum. Pembrolizumab was given as 200 mg once ...

article{c3ac9f80-11f8-4d66-9522-8c076ab60131, abstract = {Purpose: This trial of the German High-Grade Non-Hodgkins Lymphoma Study Group compares the use of high-dose therapy (HDT) as part of primary treatment with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus etoposide followed by involved-field (IF) radiotherapy in a randomized, multicenter, phase III study. Patients and Methods: Three hundred twelve patients with aggressive non-Hodgkins lymphoma aged greater than or equal to 60 years with elevated serum lactate dehydrogenase levels were included from 1990 to 1997. Patients with at least a minor response after two cycles of CHOEP (CHOP + etoposide 3 x 100 mg/m(2)) were to receive three further cycles of CHOEP followed by IF radiotherapy (arm A) or one further cycle of CHOEP followed by autologous stem-cell transplantation and IF radiotherapy (arm B). Results: Among 158 patients randomized to arm B, 103 (65%) received HDT. The complete remission rate at the end of ...

Bleomycin, vincristine, cisplatin/bleomycin, etoposide, cisplatin chemotherapy: an alternating, dose intense regimen producing promising results in untreated patients with intermediate or poor prognosis malignant germ-cell ...

This partially randomized phase III trial studies how well active surveillance, bleomycin, carboplatin, etoposide, or cisplatin work in treating pediatric and adult patients with germ cell tumors. Active surveillance may help doctors to monitor subjects with low risk germ cell tumors after their tumor is removed. Drugs

Doctors have reported that maintenance therapy using Sutent® (sunitinib) delays the time to cancer progression and improves survival in patients with extensive-stage small-cell lung cancer (SCLC). These encouraging results were recently reported in the online March 3, 2015 Journal of Clinical Oncology. Small-cell lung cancer is a fast-growing type of lung cancer and accounts for […]. ...

Previous reports have shown that Wee1 degradation can be suppressed by activation of the G2/M checkpoint in the presence of DNA damage (12) that also causes nucleolar disruption (6). Therefore, it is possible that depletion of NOL11, TIF-IA, or UBF induces DNA damage, which in turn causes nucleolar disruption as well as Wee1 accumulation via G2/M checkpoint activation. To test this hypothesis, we examined the levels of Chk1 phosphorylation at Ser317 (Chk1-pS317), a marker of G2/M checkpoint activation, and γH2A.X, a marker of DNA double-strand breaks. The Chk1-pS317 signal was undetectable for cells with nucleolar disruption caused by depletion of NOL11, TIF-IA, or UBF, whereas the signal was clear for cells treated with etoposide, which induces DNA damage and G2/M checkpoint activation (fig. S7A). Furthermore, NOL11, TIF-IA, or UBF depletion caused nucleolar disruption but did not increase γH2A.X signal, even though etoposide treatment increased it (fig. S7B). In addition, neither the ...

This study evaluates the use of carfilzomib in combination with cyclophosphamide and etoposide for children with relapsed/refractory solid tumors or leukemia.

patients treated with EP[23]. However, another two phase Ⅲ trials 8 Renshaw AA, Haja J, Lozano RL, et al. Distinguishing in United States showed no significant difference in RR and carcinoid tumor from small cell lung carcinoma of the OS between irinotecan combined with cisplatin and EP[24]. And lung: correlating cytologic features and performance in many other combination agents such as irinotecan plus CBP and, the College of American Pathologists Non-Gynecologic CBP plus oral etoposide, irinotecan plus platinum and etoposide Cytology Program. Arch Pathol Lab Med, 2005, 129(5): plus platinum were discovered to be effective in the treatment SCLC. However, it was also reported that paclitaxel combined 9 Castillo JJ, Vincent M, Justice E. Diagnosis and with either CBP or cisplation plus etoposide achieved promising management of hyponatremis in cancer patients. Oncologist, results in a study, which could not improve patients survival 2012, 17(6): 756-65. time due to the unacceptable adverse ...

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome comprising familial/genetic HLH (FHL) and secondary HLH. In the HLH-94 study, with an estimated 5-year probability of survival (pSu) of 54% (95% CI, 48-60%), systemic therapy included etoposide, dexamethasone and, from week nine, cyclosporine A (CSA). HSCT was indicated in patients with familial/genetic, relapsing, or severe and persistent disease. In HLH-2004, CSA was instead administered upfront, aiming to reduce pre-HSCT mortality and morbidity. During 2004-2011, 369 children aged ,18-years fulfilled the HLH-2004 inclusion criteria (5/8 diagnostic criteria, affected siblings, and/or molecular diagnosis in FHL-causative genes). At a median follow-up of 5.2 years, 230/369 (62%) patients were alive (5-year pSu 61%, 56-67%). The 5-year pSu in children with (n=168) and without (n=201) family history/genetically verified FHL was 59% (52-67%) and 64% (57-71%), respectively [familial occurrence (n=47): 58% ...

This dose-escalation trial is comparing the tolerability and efficacy of vorinostat + niacinamide, and vorinostat + niacinamide + etoposide, in patients with

As this eMedTV article explains, if someone uses too much etoposide, it may cause serious problems like low blood pressure and low blood cell counts. Descriptions of other possible overdose symptoms and treatment options are also given.

2The Institute of Physical and Chemical Research, RIKEN Genomic Sciences Center, Japan. We have established RIKEN full-length cDNA microarray containing 20K set of unique mouse genes. Using this microarray system, we examined to identify the target genes and the genetic pathways which could contribute to acquire the resistance against the exposure to an anti-cancer drug, etoposide in breast cancer cell lines of mice. The comparison of the expression profiles between FM3A cells and the etoposide-resistant Fvp^rB350 cells treated with etoposide or paclitaxel reveals that a large number of genes including apoptosis-related genes and other unknown genes were differentially expressed. The analysis of the gene expression relative to drug resistance may lead to the discovery of novel targets for cancer treatments.. ...

The major finding of the current study is that overexpression of a PKCδKD mutant protects INS-1 cells against apoptosis induced by both STZ and IL-1β. The corresponding PKCα mutant was without effect. Identical KD mutants have been widely used in functional studies to inhibit endogenous PKC in an isozyme-specific manner (12,31-34,36). The current results suggest for the first time that PKCδ plays a specific and important role in mediating apoptosis in pancreatic β-cells. Our findings also confirm and extend earlier studies in which pharmacological inhibitors of PKCδ inhibited spontaneous apoptosis in neutrophils (21), as well as the cytotoxic effects of ultraviolet radiation on keratinocytes (19) and of etoposide on salivary cells (20). However, the specificity of the pharmacological agents used in these earlier studies, and especially the use of rottlerin as a PKCδ inhibitor, is now open to doubt (37). Therefore, molecular approaches, such as those used here, are increasingly the methods ...

Chronic oral VP-16 and tamoxifen has modest activity and acceptable toxicity in far-advanced HCC, and is a useful palliative treatment in about a quarter of such patients.

If you or someone close to you has been diagnosed with cancer, we can help. Find out what to expect, get information, practical advice and support, hear from experts and read about other peoples experiences.

Reuters) - Immunogen Inc said it would discontinue a mid-stage trial of its experimental small-cell lung cancer drug following the death of a patient, sending its shares down 17 percent.. The company said an independent monitoring panel had recommended that all patients discontinue the treatment, noting an imbalance in the rate of infection and infection-related deaths between patients on the treatment and those receiving standard chemotherapy.. The trial was testing the benefits of the drug, code-named IMGN901, in combination with chemotherapy drugs carboplatin or etoposide, compared with chemotherapy alone.. This news is a negative for the stock and a setback for the company, since IMGN901 is one of four clinical programs that are wholly owned, and was the most advanced clinically, Cowen and Co analyst Simos Simeonidis wrote in a client note.. The company said there had been one infection-related death, possibly related to the drug, among 198 patients receiving the therapy.. Immunogen said ...

If you or someone close to you has been diagnosed with cancer, youre not alone. Find out what to expect, get information, practical advice and support, hear from experts and read about other peoples experiences.

Sometimes a treatment may be started at a lower dose or the dose needs to be changed during treatment. There may also be times when your treatment is delayed. This can happen if your doctor thinks you are likely to have severe side effects, if you get severe side effects, if your blood counts are affected and causing delays in treatment, or if you are finding it hard to cope with the treatment. This is called a dose reduction, dose change or treatment delay. Your doctor will explain if you need any changes or delays to your treatment and the reason why. ...

OncoLink, the Webs first cancer resource,provides comprehensive information on coping with cancer, cancer treatments, cancer research advances, continuing medical education, cancer prevention, and clinical trials

Within one week, I was experiencing pelvic pain, back pain, bloating, changes in bathroom habits, and feeling full quickly while eating. I really did not know what was wrong with me! Could I be gaining weight? That fast? That was my worry. Well, after visiting a gynecologist, it turned out I had Immature Teratoma (a rare type of ovarian cancer). Yes, I had cancer. Its a disease I always hear about but never in my life did it occur to me that it could happen to me, well at least not at this age. I was 25, recently married and a career-oriented woman.. After having gone through a surgery (tumor removal), all the tests showed I was cancer-free. Yet, because it was Grade III, I had to do chemotherapy to prevent it from recurring.. My husband and family decided that its best if I get my treatment at the Memorial Sloan Kettering Cancer Center in New York. Briefly, the chemotherapy that I needed was 3 cycles of BEP (Bleomycin, Etoposide & Cisplatin).. So I decided to look at this journey in a ...

Now Im back in the hospital for a few days, getting the VAC (Vincristine/Adriamycin/Cyclophosphamide). For some reason, every time I come in as an in-patient, it takes FOREVER to get the chemo actually started. Today we got to the patient ward around 11 and they didnt start the chemo until almost 4pm. I guess they need to wait for the orders to come through and the pharmacy to mix the drugs and such. Still, its kind of annoying that I come in here and have to sit around for hours. The nurse just hung my Adriamycin bag (around 5pm), so now Ive got 48 hours to wait til I get out of here. Luckily, after five of these VAC cycles, Ill stop getting Adriamycin and this set of drugs will only take one day. The other set (IE - Ifosfamide/Etoposide) will still take 4 days, but I may move to out-patient for that one eventually. The out-patient schedule is fairly grueling, though - you basically have to come in at 7am every day for 12 hours. Still, I suspect it might be better than staying in the ...

Ready-to-use high quality apoptosis inducers including actinomycin D, camptothecin, cycloheximide, dexamethasone, doxorubicin and etoposide.

For those of you following at home, this round is ye olde etoposide and ifosfamide, which cause the usual nausea, low blood counts, fatigue, etc. Since my counts were low last week, theyre only giving me 80% of the normal dose for this drug, which means ostensibly only 4 days instead of 5 in the hospital. Unfortunately, we got started late on Monday around 5pm, so Ill end up being here til Fri morning anyhow. Not a huge deal, since I have to be here for radiation at noon anyway, but it would have been nice to have a little less time in F-ground ...

The First Bancorp in Damariscotta ended 2011 with $12.4 million in net income, a 2% rise over 2010, despite a slide in the last quarter of the year. The companys year-end income was up $248,000 over