EGFR mutations are associated with prognosis but not with the response to front-line chemotherapy in the Chinese patients with advanced non-small cell lung cancer

Wu, Meina; Zhao, Jun; Song, Shalei; Zhuo, Minglei; Wang, Xin; Bai, Hua; Wang, Shuhang; Yang, Lu; An, Tongtong; Zhang, Yan; Duan, Jianchun; Wang, Yuyan; Guo, Qingzhi; Liu, Xuyi; Liu, Ninghong; Wang, Jie

doi:10.1016/j.lungcan.2009.04.011

Cited by 47 publications

(39 citation statements)

References 22 publications

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“…Also, patients of non-squamous cell carcinoma, never smoking status and female showed a significantly longer PFS and OS after receiving second-line chemotherapy in the univariate analysis, while female patients did not remain a predictor for longer PFS and OS in the multi-variate analysis. The EGFR mutation distribution in different subgroup might attribute to this result (Wu et al, 2010). As we all knows, it were histological type and smoking status but not gender significantly affect the incidence of EGFR mutation.…”

Section: Discussionmentioning

confidence: 79%

Efficacy of First-line Chemotherapy Affects the Second-Line Setting Response in Patients with Advanced Non-Small Cell Lung Cancer

Cao

Li²,

Ren³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 79%

Efficacy of First-line Chemotherapy Affects the Second-Line Setting Response in Patients with Advanced Non-Small Cell Lung Cancer

Cao

Li²,

Ren³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Because of the strong association to the non-smoking status, EGFR mutationpositive lung adenocarcinoma and lung cancer in neversmokers as such are nowadays considered as distinct biological tumor subsets in the view of molecular pathogenesis [25]. Affected patients appear to have a better prognosis even when they are treated with cytotoxic chemotherapy [26][27][28]. In contrast to patients with EGFR wild-type tumors, they benefit from EGFR TKI treatment in terms of higher objective response rates (ORR), longer progression-free Köhler/Schuler survival (PFS), and/or longer median overall survival (OS) times [17,21,22,29].…”

Section: Egfr Mutation-positive Lung Adenocarcinoma -A Distinct Subsementioning

confidence: 99%

Afatinib, Erlotinib and Gefitinib in the First-Line Therapy of EGFR Mutation-Positive Lung Adenocarcinoma: A Review

Köhler

Schüler

2013

Oncol Res Treat

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Non-small cell lung cancer (NSCLC) consists of several histomorphologically defined phenotypes that display an enormous genetic variability. In recent years, epidermal growth factor receptor (EGFR) mutation-positive lung adenocarcinoma has emerged as a unique subset of NSCLC in terms of etiopathogenesis and tumor biology. Since the introduction of the reversible EGFR tyrosine kinase inhibitors (TKIs) erlotinib and gefitinib, patients with metastatic EGFR mutation-positive lung cancer can be offered a therapeutic alternative that has proven its superiority over standard platinum-based chemotherapy. However, primary or acquired resistance limits the therapeutic success of these targeted agents. Irreversible inhibitors targeting all ErbB family receptor tyrosine kinases, such as afatinib and dacomitinib, have been developed to confer sustained disease control in ErbB-dependent cancers. The large LUX-Lung 3 phase III trial recently reported afatinib to be clearly superior over the most effective platinum doublet in patients with EGFR mutation-positive lung cancer. To fully exploit the clinical activity of afatinib, proactive management of its gastrointestinal and dermatologic toxicities is advised.

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“…Although surgical operation is the most effective therapy for NSCLC, many cases with advanced stage are unresectable [2,3]. Even in patients diagnosed at an early stage, however, the reported relapse rate is as high as 15-35 % after surgical resection.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of eIF3d inhibits cell proliferation through G2/M phase arrest in non-small cell lung cancer

2015

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Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and remains the leading cause of cancer-related death worldwide. Eukaryotic translation initiation factor 3, subunit d (eIF3d) has been recognized recently in several human cancers. In this paper, we attempt to evaluate the functional role of eIF3d in NSCLC cells. Lentivirus-mediated RNA interference (RNAi) was applied to silence eIF3d in the human NSCLC cell lines A549 and 95D. Cell viability was measured by MTT. Cell colony-forming ability was measured by colony formation. Cell cycle progression was determined by propidium iodide staining and flow cytometry. Intracellular signaling molecules were detected using a PathScan(®) intracellular signaling array kit. In this study, we firstly proved that lentivirus-mediated RNAi specifically suppressed the expression of eIF3d both at the mRNA and protein levels in A549 and 95D cell lines. Further investigations revealed that eIF3d knockdown significantly inhibited cell proliferation and colony formation. Moreover, the cell cycle of A549 cells was arrested at G2/M phase after eIF3d knockdown. Furthermore, the activations of AKT, HSP27 and SAPK/JNK were suppressed by eIF3d knockdown. This study highlights the crucial role of eIF3d in promoting NSCLC cell proliferation, and provides a foundation for further study into the clinical potential of lentiviral-mediated delivery of eIF3d RNAi therapy for treatment of NSCLC.

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EGFR mutations are associated with prognosis but not with the response to front-line chemotherapy in the Chinese patients with advanced non-small cell lung cancer

Cited by 47 publications

References 22 publications

Efficacy of First-line Chemotherapy Affects the Second-Line Setting Response in Patients with Advanced Non-Small Cell Lung Cancer

Efficacy of First-line Chemotherapy Affects the Second-Line Setting Response in Patients with Advanced Non-Small Cell Lung Cancer

Afatinib, Erlotinib and Gefitinib in the First-Line Therapy of EGFR Mutation-Positive Lung Adenocarcinoma: A Review

Knockdown of eIF3d inhibits cell proliferation through G2/M phase arrest in non-small cell lung cancer

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