Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, open-label, randomised, phase 3 study

Zhou, Caicun; Wu, Yi‐Long; Chen, Gongyan; Feng, Jifeng; Liu, Xiao Qing; Wang, Changli; Zhang, Shucai; Wang, Jie; Zhou, Shunhua; Ren, Shengxiang; Lü, Shun; Zhang, Li; Hu, Chengping; Hu, Chunhong; Luo, Yi; Chen, Lei; Ye, Ming; Huang, Jianan; Zhi, Xiao; Zhang, Yiping; Xiu, Qingyu; Ma, Jun; You, Changxuan

doi:10.1016/s1470-2045(11)70184-x

Cited by 3,618 publications

(2,638 citation statements)

References 17 publications

Supporting

Mentioning

2,448

Contrasting

Unclassified

Order By: Relevance

“…Molecular therapy has become a newly emerging regimen over the last decade 4. With lesser toxicity, patients with sensitive molecular alterations could benefit more from an inhibitor therapy than traditional chemotherapy 5, 6, 7, 8, 9, 10.…”

Section: Introductionmentioning

confidence: 99%

Mutation and prognostic analyses of PIK3CA in patients with completely resected lung adenocarcinoma

Song

Zhang

2016

Cancer Medicine

Self Cite

View full text Add to dashboard Cite

PIK3CA mutation represents a clinical subset of diverse carcinomas. We explored the status of PIK3CA mutation and evaluated its genetic variability, treatment, and prognosis in patients with lung adenocarcinoma. A total of 810 patients with completely resected lung adenocarcinoma were recruited between 2008 and 2013. The status of PIK3CA mutation and other three genes, that is, EGFR mutation, KRAS mutation and ALK fusion were examined by reverse transcription‐polymerase chain reaction (RT‐PCR). Survival curves were plotted with the Kaplan–Meier method and log‐rank for comparison. Cox proportional hazard model was performed for multivariate analysis. Among the 810 patients, 23 cases of PIK3CA mutation were identified with a frequency of 2.8%. There were 14 men and 9 women with a median age of 61 years. Seventeen tumors revealed concurrent gene abnormalities of EGFR mutation (n = 12), KRAS mutation (n = 3), and ALK fusion (n = 2). Seven patients with EGFR & PIK3CA mutations recurred and administrated of EGFR‐TKIs yielded a median progression free‐survival of 6.0 months. Among four eviromous‐treated patients, stable disease was observed in three patients with a median Progression‐free survival (PFS) of 3.5 months. Patients with and without PIK3CA mutation had different overall survivals (32.2 vs. 49.6 months, P = 0.003). Multivariate analysis revealed that PIK3CA mutation was an independent predictor of poor overall survival (HR = 2.37, P = 0.017). The frequency of PIK3CA mutation was around 2.8% in the Chinese patients of lung adenocarcinoma. PIK3CA mutation was associated with reduced PFS of EGFR‐TKIs treatment and shorter overall survival.

show abstract

Section: Introductionmentioning

confidence: 99%

Mutation and prognostic analyses of PIK3CA in patients with completely resected lung adenocarcinoma

Song

Zhang

2016

Cancer Medicine

Self Cite

View full text Add to dashboard Cite

show abstract

“…5,28,29,[37][38][39] Recent studies have provided more compelling evidence of the clinical benefits of anti-EGFR treatment in the appropriate setting. 13,15,22,38,[40][41][42][43][44][45][46][47][48] Evidence from the large phase III randomized Iressa Pan-Asia Study trial and other phase III trials have prompted the American Society of Clinical Oncology to issue a provisional clinical opinion recommending the testing of EGFR mutational status in patients being considered for first line EGFR TKI therapy owing to their demonstrated benefit on progression-free survival. 22,41 Of note, they caution that no definitive benefit has been shown in patients treated with first-line TKIs in regards to overall survival.…”

mentioning

confidence: 99%

Molecular pathology of lung cancer: key to personalized medicine

et al. 2012

View full text Add to dashboard Cite

The majority of lung adenocarcinoma patients with epidermal growth factor receptor-(EGFR) mutated or EML4-ALK rearrangement-positive tumors are sensitive to tyrosine kinase inhibitors. Both primary and acquired resistance in a significant number of those patients to these therapies remains a major clinical problem. The specific molecular mechanisms associated with tyrosine kinase inhibitor resistance are not fully understood. Clinicopathological observations suggest that molecular alterations involving so-called 'driver mutations' could be used as markers that aid in the selection of patients most likely to benefit from targeted therapies. In this review, we summarize recent developments involving the specific molecular mechanisms and markers that have been associated with primary and acquired resistance to EGFR-targeted therapy in lung adenocarcinomas. Understanding these mechanisms may provide new treatment avenues and improve current treatment algorithms.

show abstract

“…Since the approval of the first EGFR-TKI gefitinib in clinical setting, several other compounds have been developed by pharma, which may be classified as first, second, and third-generation EGFR-TKIs. About eight phase III randomized clinical trials compared EGFR-TKI Gefitinib, Erlotinib, or Afatinib vs platinum-based chemotherapy as first-line treatment for EGFR-mutated NSCLC patients (Reis-Filho and Pusztai, 2011;Mitsudomi et al, 2010;Maemondo et al, 2010;Paz-Ares et al, 2017a;Network CGA, 2012;Zhou et al, 2011;Sequist et al, 2011;Wu et al, 2014). The results of all such studies convincingly and consistently demonstrated a significant superiority of EGFR-TKIs over standard platinum-chemotherapy, improving both response rate (RR), progression free survival (PFS) and quality of life (QoL) of EGFR-mutated NSCLC patients.…”

Section: Introductionmentioning

confidence: 99%

EGFR inhibition in NSCLC: New findings…. and opened questions?

Passiglia

Listì

Castiglia

et al. 2017

Critical Reviews in Oncology/Hematology

View full text Add to dashboard Cite

The targeted inhibition of epidermal growth factor receptor (EGFR) has represented a milestone in the treatment of lung cancer. Several studies convincingly and consistently demonstrated a significant superiority of EGFR-TKIs over standard platinum-chemotherapy in EGFR-mutated NSCLC patients, leading to the sequential approval of gefitinib, erlotinib and afatinib as new standard first-line clinical treatment. To date we are witnessing a second revolution in the management of EGFR-positive NSCLC thanks to the development of new treatment strategies aiming to overcome acquired resistance to TKIs and ultimately improve patients’ outcomes. In this review we summarize the most important recent findings regarding EGFR-inhibition in NSCLC, highlighting the current unsolved questions on the selection of the best TKI in first-line, which therapy can be combined with upfront EGFR-TKIs, how to overcome acquired resistance, and which are the clinical applications of liquid biopsy

show abstract

Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, open-label, randomised, phase 3 study

Cited by 3,618 publications

References 17 publications

Mutation and prognostic analyses of PIK3CA in patients with completely resected lung adenocarcinoma

Mutation and prognostic analyses of PIK3CA in patients with completely resected lung adenocarcinoma

Molecular pathology of lung cancer: key to personalized medicine

EGFR inhibition in NSCLC: New findings…. and opened questions?

Contact Info

Product

Resources

About