Search results for "Etoposide"
showing 10 items of 97 documents
The DNA damage-induced decrease of Bcl-2 is secondary to the activation of apoptotic effector caspases.
2003
Apoptosis induced by DNA-damaging agents or radiation mainly proceeds through death receptor-independent caspase activation. The release of mitochondrial apoptogenic proteins, such as cytochrome c, into the cytoplasm leading to Apaf1-dependent activation of caspase-9 is a key event in this pathway. The permeability of the mitochondrial outer membrane is regulated by the various pro- and antiapoptotic Bcl-2 family proteins, and it is thought that DNA damage triggers apoptosis through the downregulation of antiapoptotic Bcl-2. Using murine embryonic fibroblasts (MEF) deficient and proficient in Apaf1, we show that DNA-damaging agents and radiation lead to a decline in Bcl-2 protein only in wt…
Impact of Undernutrition on the Pharmacokinetics and Pharmacodynamics of Anticancer Drugs: A Literature Review
2017
The etiology of undernourishment in cancer patients is multifactorial: tumor-related mechanisms (such as obstruction, metabolic abnormalities, and functionality changes) in addition to the influence of anticancer therapies, which can induce or worsen undernutrition. The evident role of undernutrition in cancer treatment outcomes suggests the need of considering nutritional status when evaluating anticancer drugs. In order to merge the available data and offer researchers and clinicians a global view of this phenomenon, the present manuscript reviews on a drug-by-drug basis the undernutrition-related pharmacokinetic and pharmacodynamic aspects of anticancer treatments. This review notes inte…
The apoptotic effects of cisplatin and carboplatin in retinoblastoma Y79 cells.
1998
This study demonstrated that cisplatin and carboplatin stimulate apoptosis in human retinoblastoma Y79 cells, cisplatin being the most effective compound. The apoptotic effect appeared after 8 h and then increased in a time-dependent manner. Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2. The prolonged exposure of Y79 cells to cisplatin induced resistance to cisplatin, carboplatin and etoposide. The basal level of p53 was in resistant cells higher than in untreated cells, while Bcl-2 was not modified. p53 and Bcl-2 levels did not change after treating of resistant cells with cisplatin, carboplatin or etoposide. However…
Phase II study of mitomycin C, etoposide and vindesine in metastatic stage IV non-small-cell lung cancer.
1991
A total of 72 patients with metastatic stage IV non-small-cell lung cancer (NSCLC) were treated with combination chemotherapy comprising the MEV regimen (mitomycin C, 8 mg/m2 given i. v. on day 1; etoposide, 100 mg/m2 given i.v. on days 1–3; and vindesine, 3 mg/m2 given i.v. on day 1; treatment repeated every 3 weeks). In 64 evaluable patients, the objective response rate was 37% (complete responses, 4.7%; partial responses, 32.3%). The median survival was 7.6 months for all patients. The treatment was very well tolerated. MEV proved to be an active and non-toxic regimen for the treatment of metastatic NSCLC.
68 O - Maintenance low-dose (LD) oral idarubicin (oIDA) in elderly patients (pts) with acute myelogeneous leukemia (AML)
1996
IDA by i.v. route. especially in combination with cytosine arabinoside (Ara-C). proved quite effective for intensive chemotherapy of AML However, persisting controversies on aggressive/intensive versus “ottenvated” regimens for elderly AML pts emphasize the interest of olDA in this latter setting (ct M.R. Howard et al and M.J. Keating. Clin. Drug Invest. 1995; 9. Suppl. 2: 16–38) A 69% complete response (CR) rate was recentty reported (F. Leoni et al Br. J. Hoematol 1995; 90: 169–174) among 25 elderly AML pts (> 60 yrs old) with an “attenuated” dose of IDA, i.e. 8 mg/m2 i.v. d, 1. 3, and 5. plus Ara-C 200 mg/m2 by continuous i.v. infusion (ClV) d, 1–7, and etoposide (VP-16) 60 mg/m2 i.v. d,…
A randomized phase II study of estramustine phosphate versus estramustine phosphate plus etoposide in hormone refractory prostate cancer (HRPC)
2008
20632 Background: Docetaxel-based regimens represent the treatment of choice of HRPC. However, in some patients toxicity may be a concern and the quality of life may be compromised. The aim of this phase II randomized study is to investigate the efficacy and safety of low-dose chemotherapy regimen adopting a combination of EMP and VP16 in patients affected by HRPC. Methods: 54 HRPC patients were randomized between: arm A, daily oral standard dose EMP (10mg/kg) and arm B, low-dose EMP (3mg/kg) plus VP16 (25mg/mq) for 2 weeks followed by 2-weeks’rest. Systemic toxicity and hematologic exams were monitored every 2 weeks. Performance status, pain and analgesic use were evaluated according to WH…
Mitomycin C plus vindesine plus etoposide (MEV) versus mitomycin C plus vindesine plus cisplatin (MVP) in stage IV non-small-cell lung cancer: A phas…
1996
Purpose : To compare mitomycin C plus vindesine plus etoposide (MEV) vs. mitomycin C plus vindesine plus cisplatin (MVP) in the treatment of stage IV non-small-cell lung cancer. Patients and methods : 204 patients were entered in a phase III multicentre randomised trial from June 1990 to December 1994 and stratified according to the ECOG performance status (0-1 vs. 2). MVP was given in the following dosages : mitomycin C 8 mg/m 2 + vindesine 3 mg/m 2 + cisplatin 100 mg/m 2 i.v. day 1 and vindesine 3 mg/m 2 i.v. day 8 with cycles repeated every 4 weeks. MEV was given in the following dosages : mitomycin C 8 mg/m 2 + vindesine 3 mg/m 2 i.v. day I and etoposide 100 mg/m 2 i.v. days 1 to 3 with…
Thymosin α1 and α-Inteferon with Cisplatin and Etoposide in Advanced Non-Small-Cell Lung Cancer: A Phase II Study
1993
In recent years, biological response modifiers (BRMs) have emerged as an important new class of agents for treating cancer. Agents such as interferon (IFN) and interleukin 2 (IL-2) have been reported to induce significant tumor regression in various types of cancer usually resistant to chemotherapy (1,12), but their use in non-small-cell lung cancer (NSCLC) has received little attention.
The HMG-CoA reductase inhibitor lovastatin protects cells from the antineoplastic drugs doxorubicin and etoposide
2002
Ras-homologous GTPases are involved in the regulation of genotoxic stress-induced gene expression and cell death. Since they need C-terminal isoprenylation for correct intracellular localization and function, we investigated whether depletion of cells from isopren precursor moieties using the HMG-CoA reductase inhibitor lovastatin affects cellular sensitivity to DNA damaging drugs. Here we show that lovastatin renders cells highly resistant to the tumor-therapeutic compound doxorubicin. Desensitization by lovastatin was reverted by co-treatment with GGPP indicating that inhibition of protein geranylgeranylation is involved in acquired doxorubicin resistance. Lovastatin does not influence ce…
Unraveling the extracellular matrix-tumor cell interactions to aid better targeted therapies for neuroblastoma
2021
Treatment in children with high-risk neuroblastoma remains largely unsuccessful due to the development of metastases and drug resistance. The biological complexity of these tumors and their microenvironment represent one of the many challenges to face. Matrix glycoproteins such as vitronectin act as bridge elements between extracellular matrix and tumor cells and can promote tumor cell spreading. In this study, we established through a clinical cohort and preclinical models that the interaction of vitronectin and its ligands, such as αv integrins, are related to the stiffness of the extracellular matrix in high-risk neuroblastoma. These marked alterations found in the matrix led us to speci…