Oral treatment with etoposide in small cell lung cancer – dilemmas and solutions

Rezonja, Renata; Knez, Lea; Čufer, Tanja; Mrhar, Aleš

doi:10.2478/raon-2013-0008

Cited by 34 publications

(28 citation statements)

References 87 publications

(104 reference statements)

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“…Applied either sequentially or in a concurrent schedule, platinum-based chemotherapy with radical radiation therapy is the standard of care for locally advanced NSCLC as well as for small cell lung cancer (SCLC) 7,8. However, the optimal drugs, schedule, sequence and doses of chemotherapy have not been adequately defined.…”

Section: Introductionmentioning

confidence: 99%

Induction gemcitabine in standard dose or prolonged low-dose with cisplatin followed by concurrent radiochemotherapy in locally advanced non-small cell lung cancer: a randomized phase II clinical trial

Vrankar

Zwitter

Bavcar

et al. 2014

Radiology and Oncology

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Disclosure: No potential conflicts of interest were disclosed.Background. The optimal combination of chemotherapy with radiation therapy for treatment locally advanced non-small cell lung cancer (NSCLC) remains an open issue. This randomized phase II study compared gemcitabine in two different schedules and cisplatin -as induction chemotherapy, followed by radiation therapy concurrent with cisplatin and etoposid.Patients and methods. Eligible patients had microscopically confirmed inoperable non-metastatic non-small cell lung cancer; fulfilled the standard criteria for platin-based chemotherapy; and signed informed consent. Patients were treated with 3 cycles of induction chemotherapy with gemcitabine and cisplatin. Two different aplications of gemcitabine were compared: patients in arm A received gemcitabine at 1250 mg/m 2 in a standard half hour i.v. infusion on days 1 and 8; patients in arm B received gemcitabine at 250 mg/m 2 in prolonged 6-hours i.v. infusion on days 1 and 8. In both arms, cisplatin 75 mg/m 2 on day 2 was administered. All patients continued treatment with radiation therapy with 60-66 Gy concurrent with cisplatin 50 mg/m 2 on days 1, 8, 29 and 36 and etoposid 50 mg/m 2 on days 1-5 and 29-33. The primary endpoint was response rate (RR) after induction chemotherapy; secondary endpoints were toxicity, progression-free survival (PFS) and overall survival (OS).Results. From September 2005 to November 2010, 106 patients were recruited to this study. No statistically signifficant differences were found in RR after induction chemotherapy between the two arms (48.1% and 57.4%, p = 0.34).Toxicity profile was comparable and mild with grade 3/4 neutropenia as primary toxicity in both arms. One patient in arm B suffered from acute peripheral ischemia grade 4 and an amputation of lower limb was needed. With a median follow-up of 69.3 months, progression-free survival and median survival in arm A were 15.7 and 24.8 months compared to 18.9 and 28.6 months in arm B. The figures for 1-and 3-year overall survival were 73.1% and 30.8% in arm A, and 81.5 % and 44.4% in arm B, respectively.Conclusions. Among the two cisplatin-based doublets of induction chemotherapy for inoperable NSCLC, both schedules of gemcitabine have a comparable toxicity profile. Figures for RR, PFS and OS are among the best reported in current literature. While there is a trend towards better efficacy of the treament with prolonged infusion of gemcitabine, the difference between the two arms did not reach statistical significance.

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Section: Introductionmentioning

confidence: 99%

Induction gemcitabine in standard dose or prolonged low-dose with cisplatin followed by concurrent radiochemotherapy in locally advanced non-small cell lung cancer: a randomized phase II clinical trial

Vrankar

Zwitter

Bavcar

et al. 2014

Radiology and Oncology

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“…Etoposide is an anticancer drug used alone or in combination with other drugs in chemotherapy of testicular cancer, lung cancer, lymphoma, leukemia, neuroblastoma and ovarian cancer [1][2][3][4][5]. Side effects of treatment include, vomiting, neutropenia, myelosuppression and alopecia [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Amifostine against Etoposide-Induced Genotoxicity Evaluated By the Comet Assays

Shokrzadeh¹,

Ghassemi-Barghi²

2018

SOJPPS

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Etoposide is one of the most effective chemotherapeutic agents used for the treatment of number of neoplasia. However, as a topoisomerase inhibitor, during clinical use several side effects may occur. In addition in several in vivo and in vitro studies etoposide has shown a range of genotoxic effects including mutation induction and inhibition of DNA synthesis. Amifostine, an organic thiophosphate prodrug, has been shown to exert important cyto-protective effects in many tissues. The aim of this study was to explore whether amifostine protects against etoposide-induced genotoxicity in HepG2 cell line. HepG2 cells (25×10 4 cells/well) were cultured in 24-well plates: a control group and three 'amifostine etoposide groups (pre and co-treatment conditions). Our results show that etoposide induced a noticeable genotoxic effect in HepG2 cells. Amifostine reduced the effects of etoposide significantly in both type of experiment conditions, through reduced the level of DNA damage measured via comet andmicronucleus assay. Furthermore, amifostine decreased the intracellular ROS generation induced by etoposide. It increased also the intracellular GSH levels in HepG2 cells. Altogether, our results suggest a protective action of amifostine against etoposide cytotoxicity and genotoxicity via various pathways. The most protective effect was observed with amifostine when it was administrated 24 h before etoposide treatment.

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“…Furthermore, ERG is shown to be included in pathway aberrations of DNA repair mechanism [5]. Etoposide is an anticancer agent that has the ability to break the double stranded DNA and prevent repair mechanism through interaction with topoisomerase II [6]. Etoposide is widely used alone or in combination with other chemotherapeutic agents in different cancer types including lung cancer [7].…”

Section: Introductionmentioning

confidence: 99%

Effect of Etoposide Treatment on ERG Transfected H358 Cell Line

Kandemiş

Alkhatib

Sergi

et al. 2018

The 2nd International Cell Death Research Congress

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Lung cancer is listed as the most fatal type of cancer around the world. ERG, a transcription factor, is an ETS family member protein. It is involved in Epithelial Mesenchymal Transition (EMT), metastasis and DNA repair defects. Etoposide is a chemotherapeutic agent used in treatment of a variety of different cancer types, including lung cancer. Moreover, Etoposide has been tested alone and in combination with other drugs in order to inhibit DNA synthesis and exhibit antitumor activity. The purpose of this study is to examine the effect of Etoposide treatment on ERG transfected non-small cell lung cancer (NSCLC) cell line, H358.

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Oral treatment with etoposide in small cell lung cancer – dilemmas and solutions

Cited by 34 publications

References 87 publications

Induction gemcitabine in standard dose or prolonged low-dose with cisplatin followed by concurrent radiochemotherapy in locally advanced non-small cell lung cancer: a randomized phase II clinical trial

Induction gemcitabine in standard dose or prolonged low-dose with cisplatin followed by concurrent radiochemotherapy in locally advanced non-small cell lung cancer: a randomized phase II clinical trial

Protective Effect of Amifostine against Etoposide-Induced Genotoxicity Evaluated By the Comet Assays

Effect of Etoposide Treatment on ERG Transfected H358 Cell Line

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