Gefitinib Compared with Systemic Chemotherapy as First-line Treatment for Chemotherapy-naive Patients with Advanced Non-small Cell Lung Cancer: A Meta-analysis of Randomised Controlled Trials

Wang, F.; Wang, L.D.; Li, B.; Sheng, Zhixin

doi:10.1016/j.clon.2011.09.013

Cited by 10 publications

(6 citation statements)

References 16 publications

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“…a design in which only patients harbouring the predictive characteristic are eligible for the trial) have undoubtedly proven that patients with EGFR mutation benefit from TKIs in terms of progression-free survival although the benefit on overall survival is less clear. So, EGFR has become the first molecular target in advanced non-small cell lung cancer that is definitely of clinical usefulness in routine practice [47][48][49][50][51][52][53]; it is now a standard treatment to give patients with EGFR mutation a TKI as part of their first-line treatment although there still remains a role for chemotherapy [54].…”

Section: Egfr and Tkismentioning

confidence: 99%

Prognostic and predictive factors for lung cancer

Paesmans

2012

BRE

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Section: Egfr and Tkismentioning

confidence: 99%

Prognostic and predictive factors for lung cancer

Paesmans

2012

BRE

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“…This is particularly important as current first line regimes add little >2 months to the average survival ( Goldstraw et al , 2011 ). In addition, many therapies are less beneficial (or indeed more harmful) in squamous tumours, such as the antifolate agent pemetrexed ( Scagliotti et al , 2011 ), anti-vascular endothelial growth factor (VEGF) antibody bevacuzimab ( Johnson et al , 2004 ) and tyrosine kinase inhibitor (TKI) gefitinib ( Wang et al , 2012 ). Selection for the latter drug usually also involves testing for EGFR mutation ( Wang et al , 2012 ), meaning that the pool of patients in whom each drug works is increasingly small.…”

mentioning

confidence: 99%

Identification of novel vascular targets in lung cancer

et al. 2014

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Background:Lung cancer remains the leading cause of cancer-related death, largely owing to the lack of effective treatments. A tumour vascular targeting strategy presents an attractive alternative; however, the molecular signature of the vasculature in lung cancer is poorly explored. This work aimed to identify novel tumour vascular targets in lung cancer.Methods:Enzymatic digestion of fresh tissue followed by endothelial capture with Ulex lectin-coated magnetic beads was used to isolate the endothelium from fresh tumour specimens of lung cancer patients. Endothelial isolates from the healthy and tumour lung tissue were subjected to whole human genome expression profiling using microarray technology.Results:Bioinformatics analysis identified tumour endothelial expression of angiogenic factors, matrix metalloproteases and cell-surface transmembrane proteins. Predicted novel tumour vascular targets were verified by RNA-seq, quantitative real-time PCR analysis and immunohistochemistry. Further detailed expression profiling of STEAP1 on 82 lung cancer patients confirmed STEAP1 as a novel target in the tumour vasculature. Functional analysis of STEAP1 using siRNA silencing implicates a role in endothelial cell migration and tube formation.Conclusions:The identification of cell-surface tumour endothelial markers in lung is of interest in therapeutic antibody and vaccine development.

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“…Gefitinib, trade name Iressa ® , is a small molecule that inhibits EGFR tyrosine kinase activity, and is the first molecular-targeted agent registered to treat advanced non-small cell lung cancer (NSCLC). Gefitinib trials have demonstrated that there is an overall response rate of 10-20% in patients with advanced NSCLC, which could be as high as 70% in patients with EGFR gene mutations when used as a first-line treatment (8,9). There are two biomarkers, the presence of the EGFR gene mutations and an increase in gene copy number, known to be potent predictors of the response to gefitinib (10,11).…”

Section: Introductionmentioning

confidence: 99%

The enhanced tumor inhibitory effects of gefitinib and L-ascorbic acid combination therapy in non-small cell lung cancer cells

et al. 2017

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Abstract. Despite documentation of successful therapy with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in patients with lung cancer, the response rate of patients treated with this therapy remains low. The present study investigated whether L-ascorbic acid serves an adjuvant role in vitro when combined with the EGFR tyrosine kinase inhibitor gefitinib (Iressa ® ) in lung cancer cell lines. A total of three human lung cancer cell lines were used. The antiproliferative effects and changes in the cell cycle and expression of intracellular signaling molecules, including extracellular signal-regulated kinases (Erk), signal transducer and activator of transcription 3 (Stat3) and protein kinase B (Akt), were measured in cells treated with gefitinib and/or L-ascorbic acid at various concentrations. When combined with gefitinib, L-ascorbic acid exhibited an additive effect on cell proliferation in all gefitinib-sensitive and gefitinib-resistant cell lines. A decrement of ~40% was observed with a low dose 0.5 mM L-ascorbic acid and gefitinib in the relatively gefitinib-resistant A549 cell line (85.6±5.4% with gefitinib alone vs. 52.7±7.3% with combination therapy; P=0.046). The downregulation of intracellular signaling cascades, including EGFR, Akt, Erk and Stat3, was also observed. L-Ascorbic acid serves an adjuvant role when administered in combination with gefitinib; however, the degree of inhibition of cell proliferation differs between lung cancer cell lines.

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Gefitinib Compared with Systemic Chemotherapy as First-line Treatment for Chemotherapy-naive Patients with Advanced Non-small Cell Lung Cancer: A Meta-analysis of Randomised Controlled Trials

Cited by 10 publications

References 16 publications

Prognostic and predictive factors for lung cancer

Prognostic and predictive factors for lung cancer

Identification of novel vascular targets in lung cancer

The enhanced tumor inhibitory effects of gefitinib and L-ascorbic acid combination therapy in non-small cell lung cancer cells

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