Gefitinib versus vinorelbine plus cisplatin as adjuvant treatment for stage II–IIIA (N1–N2) EGFR-mutant NSCLC (ADJUVANT/CTONG1104): a randomised, open-label, phase 3 study

Zhong, Wen‐Zhao; Wang, Qun; Mao, Weimin; Xu, Songtao; Wu, Lin; Shen, Yi; Liu, Yong‐Yu; Chen, Chun; Cheng, Ying; Xu, Lin; Wang, Jun; Fei, Ke; Li, Xiaofei; Li, Jian; Huang, Cheng; Liu, Zhidong; Xu, Shun; Chen, Ke-Neng; Xu, Shidong; Liu, Lunxu; Yu, Ping; Wang, Buhai; Ma, Haitao; Yan, Hong‐Hong; Yang, Xue‐Ning; Zhou, Qing; Wu, Yi‐Long; Wang, Siyu; Hu, Jian; Liu, Wei; Li, Wei; Shi, Jianhua

doi:10.1016/s1470-2045(17)30729-5

Cited by 466 publications

(477 citation statements)

References 23 publications

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“…The strength of the current study was the examination of EGFR ‐mutant lung ADCs naive in terms of targeted therapy, after complete resection, thereby identifying the molecular backgrounds of potential candidates for adjuvant EGFR TKI treatment. Although initial randomized trial had proved that adjuvant EGFR TKI could prolong DFS in node‐positive NSCLCs with EGFR mutation, routine use of TKI in adjuvant setting is currently under debate because of its insufficient evidence of overall survival benefit . Nevertheless, the findings in this study could help determine the appropriate adjuvant TKI therapy for patients in future trials.…”

Section: Discussionmentioning

confidence: 84%

Mutation Profile of ResectedEGFR-Mutated Lung Adenocarcinoma by Next-Generation Sequencing

Zhao

Lin

et al. 2019

The Oncologist

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Background The efficacy of adjuvant targeted therapy for operable lung cancer is still under debate. Comprehensive genetic profiling is needed for detecting co‐mutations in resected epidermal growth factor receptor (EGFR)‐mutated lung adenocarcinoma (ADC), which may interfere the efficacy of adjuvant tyrosine kinase inhibitor (TKI) treatment. Materials and Methods Mutation profiling of 416 cancer‐relevant genes was conducted for 139 resected stage I–IIIa lung ADCs with EGFR mutations using targeted next‐generation sequencing. Co‐mutation profiles were systematically analyzed. Results Rare EGFR alterations other than exon 19 deletion and L858R, such as L861Q (∼3%) and G719A (∼2%), were identified at low frequencies. Approximately 10% of patients had mutations in EGFR exon 20 that could confer resistance to first‐generation TKIs. Ninety‐one percent of patients harbored at least one co‐mutation in addition to the major EGFR mutation. TP53 was the top mutated gene and was found more frequently mutated at later stage. Markedly, NF1 mutations were found only in stage II–III ADCs. Conversely, RB1 mutations were more frequent in stage I ADCs, whereas APC mutations were observed exclusively in this group. Thirty‐four percent of patients with EGFR TKI‐sensitizing mutations had genetic alterations involving EGFR downstream effectors or bypass pathways that could affect the response to EGFR TKIs, such as PIK3CA, BRCA1, and NOTCH1. Conclusion Operable lung ADCs with EGFR TKI‐sensitizing mutations are associated with a high proportion of co‐mutations. Mutation profiling of these resected tumors could facilitate in determining the applicability and efficacy of adjuvant EGFR TKI therapeutic strategy. Implications for Practice The efficacy of adjuvant epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy for lung cancer harboring EGFR mutation after surgical resection is still under debate. Next‐generation sequencing of 416 cancer‐relevant genes in 139 resected lung cancers revealed the co‐mutational landscape with background EGFR mutation. Notably, the study identified potential EGFR TKI‐resistant mutations in 34.71% of patients with a drug‐sensitizing EGFR mutation and who were naive in terms of targeted therapy. A comprehensive mutation profiling of these resected tumors could facilitate in determining the applicability and efficacy of adjuvant EGFR TKI therapeutic strategy for these patients.

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Section: Discussionmentioning

confidence: 84%

Mutation Profile of ResectedEGFR-Mutated Lung Adenocarcinoma by Next-Generation Sequencing

Zhao

Lin

et al. 2019

The Oncologist

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“…On the basis of the molecular knowledge of lung cancer, specifically targeted treatments besides traditional surgery or radiotherapy, promote positive therapeutic outcomes [7]. For example, various small molecule drugs have been designed to tackle all possible situations, such as gefitinib and erlotinib [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Peptide 17, an inhibitor of YAP/TEAD4 pathway, mitigates lung cancer malignancy

Zhang¹,

Pan²,

Liao³

et al. 2018

Trop. J. Pharm Res

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“…In a randomised trial of patients with lung cancer who had their tumours resected (ADJUVANT), the drug improved the time till disease recurrence or death (hazard ratio=0.60; 95% CI 0.42 to 0.87; P=0.005) 7. Overall survival was virtually identical between the arms, with 34.2% of patients in the trial dying, whereas in previous studies of non-small cell lung cancer, improvements in disease recurrence strongly predicted improvements in overall survival 8…”

Section: Trials With Discordant Resultsmentioning

confidence: 99%

Diagnostic expansion in clinical trials: myocardial infarction, stroke, cancer recurrence, and metastases may not be the hard endpoints you thought they were

Nishikawa

Prasad

2018

BMJ

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Gefitinib versus vinorelbine plus cisplatin as adjuvant treatment for stage II–IIIA (N1–N2) EGFR-mutant NSCLC (ADJUVANT/CTONG1104): a randomised, open-label, phase 3 study

Cited by 466 publications

References 23 publications

Mutation Profile of ResectedEGFR-Mutated Lung Adenocarcinoma by Next-Generation Sequencing

Mutation Profile of ResectedEGFR-Mutated Lung Adenocarcinoma by Next-Generation Sequencing

Peptide 17, an inhibitor of YAP/TEAD4 pathway, mitigates lung cancer malignancy

Diagnostic expansion in clinical trials: myocardial infarction, stroke, cancer recurrence, and metastases may not be the hard endpoints you thought they were

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