Chemotherapy influence EGFR mutation status for Chinese patients with regionally advanced non-small cell lung cancer.

Wang, J.; Chen, K.; Bai, Hongwei; Wang, Z.; Zhuo, M L; An, T.; Duan, Jian; Yang, Lian; Wu, Mei‐Mei; Guo, Qian; Liu, X.; Wang, S.; Wang, Y.

doi:10.1200/jco.2011.29.15_suppl.7031

Cited by 3 publications

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“…After acquiring resistance to cytotoxic agents, there were several changes in cancer cells, including gene amplification, gene rearrangements, epigenetic changes, and microRNA changes [40]. Apart from one conference poster demonstrating that chemotherapy could influence EGFR mutation status [41], no drug resistance through gene mutation induced by cytotoxic drugs has been documented. Comparing paired cancer cells before and after chemotherapy from MPEs, we found that cytotoxic chemotherapy did not alter EGFR mutation status.…”

Section: Discussionmentioning

confidence: 99%

Survival of lung adenocarcinoma patients with malignant pleural effusion

Tsai

et al. 2012

Eur Respir J

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In the era of targeted therapy, the association between lung adenocarcinoma patient survival and malignant pleural effusions (MPEs) remains unclear. This study investigated the clinical characteristics, survival and epidermal growth factor receptor (EGFR) gene (EGFR) mutation status of lung adenocarcinoma patients with MPE.From June 2005 to December 2010, consecutive pleural effusions were collected prospectively. Patient clinical characteristics, EGFR mutation status, and overall survival were analysed.We collected MPEs from 448 patients in stage IV lung adenocarcinoma at initial diagnosis. Median overall survival for patients with MPEs at initial diagnosis and following disease progression were 14.3 months and 21.4 months, respectively (p50.001). There were 296 (66.1%) patients harbouring EGFR mutations, the mutation rates among patients with an MPE at initial diagnosis and one following disease progression were 68.2% and 56.6%, respectively (p50.044); the L858R mutation rate was also higher among the former (32.6% versus 18.1%; p50.009). Multivariate analysis revealed that patients who: developed MPEs following disease progression, harboured EGFR mutations, and received EGFR-tyrosine kinase inhibitor therapy, had longer overall survival. Patients in stage IV lung adenocarcinoma with MPEs at initial diagnosis have shorter overall survival and higher EGFR mutation rate, especially for L858R, than patients who develop MPEs following disease progression.

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Section: Discussionmentioning

confidence: 99%

Survival of lung adenocarcinoma patients with malignant pleural effusion

Tsai

et al. 2012

Eur Respir J

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Mirror Mirror on the Wall, Who Is the Fairest of Them All

Mok

2014

Journal of Thoracic Oncology

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C linical application of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) as first-line treatment of advanced stage non-small-cell lung cancer with EGFR mutation is based on vigorous science. 1,2 Multiple randomized studies have independently confirmed gefitinib and erlotinib to be superior to platinum-based doublet chemotherapy. 3-6 Thus, it is natural to ask if gefitinib is better than erlotinib or vice versa. Lim et al. 7 addressed this question with a relatively large case-control study of 121 matched pairs of gefitinib-treated and erlotinib-treated patients. The pair-matching was appropriately based on gender, smoking history, performance status, and type of EGFR mutations. Authors reported similar tumor response rate (76.9% versus 74.4%, p = 0.58) and median progression-free survival (PFS) (11.7 versus 9.6 months; p = 0.056) between the gefitiniband erlotinib-treated groups. Based on the data, Lim et al. 7 concluded equal effectiveness between the two EGFR TKIs. In short of a randomized comparative study, this report provides a relatively fair picture on the choice between gefitinib and erlotinib.But how "fair" is this fair comparison? Limited by retrospective nature of this study, authors can only take on the required action of patient-pairing to assure similar characteristics between two groups. However, they have ignored one important factor, which is the number of prior treatment(s). As a result, there are significantly more patients receiving firstline gefitinib than patients with first-line erlotinib. Authors may argue that PFS on first-line EGFR TKI is not different from second-/third-line EGFR TKI. 8 Truth is that this remains assumptive. There are data suggesting that chemotherapy may have significant impact on EGFR mutation status. 9 Sequential intercalation of chemotherapy and EGFR TKI may also potentially improve PFS and overall survival of patients with EGFR mutations. 10 Authors have also taken the required action of performing contrasted computed tomography scan every 8 weeks for assessment of tumor status. But it is unclear how they have followed the progress of 83 patients (34% of the 242 enrolled patients) with bone metastasis, knowing well that computed tomography scan is not a reliable method of assessment for bone metastasis. Thus, their comparison is fairly fair but not convincingly fair.We should also address the basic question of why we want to compare gefitinib with erlotinib? Both drugs are anilinoquinazolines with similar molecular structure ( Figure 1) and both drug share similar mechanism of action in binding to EGFR ATP binding pocket. Pharmacokinetics of the two drugs is not dramatically different. Main difference between the two compounds is the maximum tolerated dose of erlotinib being estimated at 150 mg daily while maximum tolerated dose of gefitinib at 700 mg daily (which is much higher than the standard prescription dose). 11 A network meta-analysis of multiple phase II and III studies indicated potential longer PFS associated with erlotinib. 12 Va...

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Treating Patients With EGFR-Sensitizing Mutations: First Line or Second Line—Is There a Difference?

Mok

Yang

Lam

2013

JCO

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First-line epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) is a standard treatment for patients with activating EGFR mutations. Six randomized studies have demonstrated consistent improvement in tumor response rate and progression-free survival over platinum-based combination chemotherapy. The only reason to consider EGFR TKI as second-line therapy is that none of the six comparative studies has shown improvement in overall survival, which can be explained by the high proportion of patients from the chemotherapy arm crossing over to the EGFR TKI arm on progression. It is true that patients with EGFR mutations may benefit from second-line EGFR TKI therapy, but we cannot conclude that the benefit is either equal to or inferior to first-line EGFR TKI therapy. To date, there are no direct comparative data between first- and second-line EGFR TKI in patients with activating EGFR mutations. Tumor response rates to second-line EGFR TKI have been inconsistent, which could potentially be explained by the impact of first-line chemotherapy on the abundance of tumor cells with activating EGFR mutations. However, numerous arguments, including assurance on drug exposure, improvement in quality of life, better tolerance by patients with poor performance status, and deferral of whole-brain radiation therapy for patients with brain metastasis, support the general application of first-line EGFR TKI.

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Chemotherapy influence EGFR mutation status for Chinese patients with regionally advanced non-small cell lung cancer.

Cited by 3 publications

References 0 publications

Survival of lung adenocarcinoma patients with malignant pleural effusion

Survival of lung adenocarcinoma patients with malignant pleural effusion

Mirror Mirror on the Wall, Who Is the Fairest of Them All

Treating Patients With EGFR-Sensitizing Mutations: First Line or Second Line—Is There a Difference?

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