Impact of Systematic EGFR and KRAS Mutation Evaluation on Progression-Free Survival and Overall Survival in Patients with Advanced Non–Small-Cell Lung Cancer Treated by Erlotinib in a French Prospective Cohort (ERMETIC Project—Part 2)

Cadranel, Jacques; Mauguen, Audrey; Faller, M; Zalcman, Gérard; Buisine, Marie‐Pierre; Westeel, Virginie; Longchampt, Élisabeth; Wislez, Marie; Coudert, Bruno; Daniel, Catherine; Chetaille, Bruno; Michiels, Stefan; Blons, Hélène; Solassol, Jérôme; Fraipont, Florence de; Foucher, Pascal; Urban, T.; Lacroix, Ludovic; Poulot, Virginie; Quoix, Élisabeth; Antoine, Martine; Danton, Guillaume; Morin, Franck; Chouaïd, C.; Pignon, Jean-Pierre

doi:10.1097/jto.0b013e318265b2b5

Cited by 68 publications

(55 citation statements)

References 26 publications

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“…In a landmark trial, erlotinib improved OS and quality of life when compared with the best supportive care, with a median OS benefit of 2 months relative to the placebo arm [6]. The rates of response to erlotinib were higher in some patient subgroups, including patients of Asian origin, females, neversmokers and patients with adenocarcinoma [6][7][8]. However, never-smoker status was the only clinical factor associated with improved OS in multivariable analysis.…”

mentioning

confidence: 99%

Cost-effectiveness of three strategies for second-line erlotinib initiation in nonsmall-cell lung cancer: the ERMETIC study part 3

Borget¹,

Cadranel²,

Pignon³

et al. 2011

Eur Respir J

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Several clinical and biological parameters are known to influence the efficacy of second-line erlotinib therapy for nonsmall cell lung cancer (NSCLC), but their medico-economic impact has not been evaluated. The objective of this study was to compare the incremental costeffectiveness ratios of strategies for second-line erlotinib initiation in NSCLC: clinically guided initiation (nonsmoking females with adenocarcinoma received erlotinib; all other patients received docetaxel) and biologically guided selection (patients with epidermal growth factor receptor (EGFR) mutation received erlotinib; patients with wild-type EGFR or unknown status received docetaxel), compared with initiation with no patient selection (strategy reference).A Markov model was constructed. Outcomes (overall and progression-free survival), transition probabilities and direct medical costs (from the French third-party payer's perspective) were prospectively collected for individual patients treated with either erlotinib or docetaxel, from treatment initiation to disease progression. Published data were used to estimate utilities and post-progression costs. Sensitivity analyses were performed.The biologically and clinically guided strategies were both more efficient (incremental qualityadjusted life-yrs equal to 0.080 and 0.081, respectively) and less expensive (cost decrease equal to J5,020 and J5,815, respectively) than the no-selection strategy, and the biologically guided strategy was slightly less expensive than the clinically guided strategy. Sensitivity analyses confirmed the robustness of the results.The cost-effectiveness of second-line NSCLC treatment is improved when patients are selected on either clinical or biological grounds.

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confidence: 99%

Cost-effectiveness of three strategies for second-line erlotinib initiation in nonsmall-cell lung cancer: the ERMETIC study part 3

Borget¹,

Cadranel²,

Pignon³

et al. 2011

Eur Respir J

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“…In the meantime, based on eight studies (Felip et al, 2008;Schneider et al, 2008;Marchetti et al, 2009;O'Byrne et al, 2011;Sequist et al, 2011;Cadranel et al, 2012;Metro et al, 2012;Milella et al, 2012), the pooled HR for PFS was 1.33 (95%CI: 1.05-1.69, P=0.019 heterogeneity test P=0.10, I 2 =61.9%), shown in Figure 3B. The result suggested that patients with K-ras mutation had a shorter PFS than did wild-type K-ras patients.…”

Section: Predictive and Prognostic Value Of K-ras Mutationmentioning

confidence: 84%

“…Furthermore, EGFR-TKIs were more sensitive than anti-EGFR MoAbs to K-ras gene status. Eleven studies (Endoh et al, 2006;Ichihara et al, 2007;Felip et al, 2008;Schneider et al, 2008;Marchetti et al, 2009;O'Byrne et al, 2011;Sequist et al, 2011;Cadranel et al, 2012;Ludovini et al, 2012;Milella et al, 2012;Johnson et al, 2013) showed the correlation between OS and the K-ras status. Available HRs from the 11 studies were combined to get the pooled HR, shown in Figure 3A.…”

Section: Predictive and Prognostic Value Of K-ras Mutationmentioning

confidence: 99%

Predictive and Prognostic Biomarkers for Patients Treated with Anti-EGFR Agents in Lung Cancer: A Systemic Review and Meta-Analysis

Wang¹,

Qu²,

Shen³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: Several studies have investigated predictive and prognostic biomarkers for patients treated with anti-epidermal growth factor receptor (EGFR) agents in lung cancer. However, the conclusion is controversial. Materials and Methods: A meta-analysis was conducted to evaluate the associations of mutant K-ras, PIK3CA and PTEN deficiency with the efficacy of anti-EGFR agents in lung cancer. The primary endpoint was objective response rate (ORR). The secondary endpoints were overall survival (OS) and progression-free survival (PFS). Results: A total of 61 studies were included in the final meta-analysis. The result showed that K-ras mutation was a good predictor for ORR (RR=0.

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“…Sensitizing mutations and rearrangements in the EGFR and ALK genes, respectively, are responsible for the constitutively activated kinase, and render tumors exquisitely sensitive to TKIs. In the case of EGFR and ALK inhibitors, response rates and progression-free survival are dramatically improved compared with standard chemotherapy (6). Although TKIs are initially very effective in the majority of patients whose tumors harbor the genetic alteration, acquired resistance invariably occurs.…”

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confidence: 99%

Next-Generation Sequencing: Targeting Targeted Therapies

McCutcheon

Giaccone

2015

Clinical Cancer Research

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Next-generation sequencing (NGS) has given new perspective in oncology. With the ongoing development of targeted therapies, NGS is evolving molecular diagnostics by providing comprehensive interrogation of clinically actionable genomic aberrations in tumors. Having this assay as the primary testing method produces clinically beneficial results. See related article by Drilon et al., p. 3631 In this issue of Clinical Cancer Research, Drilon and colleagues (1) demonstrate the significant role of next-generation sequencing (NGS) as the primary testing method in molecular diagnostics. Thirty one previously tested lung adenocarcinoma patients assessed by single non-NGS molecular tests, such as fluorescence in situ hybridization (FISH), multiplex mass spectrometry, and sizing assays, produced "negative" results for known lung adenocarcinoma genomic alterations in the genes EGFR, ERBB2, KRAS, NRAS, BRAF, MAP2K1, PIK3CA, AKT1, ALK, ROS1, and RET. By retesting these patients with a broad, hybrid capturebased NGS assay, Drilon and colleagues (1) revealed actionable genomic alterations present in 65% of the patients that were formerly deemed "driver negative." NGS technologies are rapidly evolving and are being increasingly used in research settings as well as clinical settings, to replace older and less-sensitive technologies. As opposed to classic Sanger sequencing, NGS technology uses clonally amplified or singlemolecule templates that are sequenced in a massively parallel fashion, allowing examination of numerous amounts of large protein coding regions, which makes NGS assays suitable for a comprehensive interrogation of cancer drivers (2). Whereas current non-NGS tests mostly examine only one variant type, NGS technology allows the patient's tumor to be tested in a single run for all types of variants, including single-nucleotide variations (SNV), insertions, deletions, exon duplications, gene copy number changes, and known translocations (3).In recent years, the advancement of NGS technology in the clinical setting has been rapidly progressing and will soon likely replace older technologies. Lung cancer, the leading cause of cancer-related death in the world, comprises a complex mutational spectrum, and the discoveries of many oncogenic drivers in the tumors have led to the development and evolution of targeted therapy, especially in the adenocarcinoma of the lung, the most prevalent type of lung cancer (4, 5). Among these targeted therapies are the tyrosine kinase inhibitors (TKI); the FDA approved TKIs in lung adenocarcinoma treatment to target EGFR and ALK. Sensitizing mutations and rearrangements in the EGFR and ALK genes, respectively, are responsible for the constitutively activated kinase, and render tumors exquisitely sensitive to TKIs. In the case of EGFR and ALK inhibitors, response rates and progression-free survival are dramatically improved compared with standard chemotherapy (6). Although TKIs are initially very effective in the majority of patients whose tumors harbor the genetic alteration, acquired...

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Impact of Systematic EGFR and KRAS Mutation Evaluation on Progression-Free Survival and Overall Survival in Patients with Advanced Non–Small-Cell Lung Cancer Treated by Erlotinib in a French Prospective Cohort (ERMETIC Project—Part 2)

Cited by 68 publications

References 26 publications

Cost-effectiveness of three strategies for second-line erlotinib initiation in nonsmall-cell lung cancer: the ERMETIC study part 3

Cost-effectiveness of three strategies for second-line erlotinib initiation in nonsmall-cell lung cancer: the ERMETIC study part 3

Predictive and Prognostic Biomarkers for Patients Treated with Anti-EGFR Agents in Lung Cancer: A Systemic Review and Meta-Analysis

Next-Generation Sequencing: Targeting Targeted Therapies

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