Afatinib for the First-Line Treatment of
            <i>EGFR</i>
            Mutation-Positive NSCLC in China: a Review of Clinical Data

Tu, Hai‐Yan; Wu, Yi‐Long

doi:10.2217/fon-2020-0320

Cited by 2 publications

(3 citation statements)

References 83 publications

(143 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For T790M-negative patients, combination strategies involving targeted therapies hold the potential to overcome drug resistance. 24 Consistent with the published case report, the present study showed that one patient with EGFR uncommon mutation and MET amplification could obtain benefits from the combination of afatinib and crizotinib. 32 Our study suggested that afatinib plus anlotinib showed potent efficacy in one patient with EGFR G719X and FGFR1 amplification.…”

Section: Discussionsupporting

confidence: 92%

“…Our results suggested that EGFR T790M (11%) and FGFR1 amplification (11%), MET amplification (11%), following by were CDK4 amplification (7%), PI3KCA activation (7%), RET fusions (4%), and BRAF mutations (4%) may be the main resistance mechanisms of afatinib in patients with EGFR G719X/L861Q/S768I. Meanwhile, given that afatinib was a type of pan‐ERBB inhibitor, ERBB2 amplification is less likely to be the major resistance mechanism 24 . Notably, the resistance mechanisms remained unclear in approximately 42% of patients.…”

Section: Discussionmentioning

confidence: 99%

“…Meanwhile, given that afatinib was a type of pan-ERBB inhibitor, ERBB2 amplification is less likely to be the major resistance mechanism. 24 Notably, the resistance mechanisms remained unclear in approximately 42% of patients.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Efficacy and potential resistance mechanisms of afatinib in advanced non–small cell lung cancer patients with EGFR G719X/L861Q/S768I

Pang

Gan

Tan

et al. 2022

Cancer

View full text Add to dashboard Cite

BACKGROUND: Afatinib is the only currently approved EGFR-tyrosine kinase inhibitors for advanced non-small cell lung cancer (NSCLC) patients with EGFR G719X/L861Q/S768I. However, there are limited real-world data concerning the benefits and resistance mechanisms of afatinib in patients with these nonclassical mutations. To fill this gap, the present study was conducted. METHODS: All NSCLC patients treated with afatinib were screened, and patients with EGFR G719X/L861Q/S768I were enrolled into the analysis. Either tumor tissue or blood specimens were detected by the commercial next-generation sequencing (NGS) panels or amplification-refractory mutation system (ARMS)-polymerase chain reaction (PCR) to figure out the mutation genotype. RESULTS: A total of 106 advanced NSCLC patients with EGFR G719X/L861Q/S768I received afatinib treatment. The benefits of afatinib exhibited heterogeneity in different mutation genotypes. Notably, at baseline, NGS testing was performed in 59 patients, and TP53 was the most frequently coexisting mutation. Patients with TP53 mutations obtained fewer survival benefits than those with TP53 wild-type. A total of 68 patients ultimately experienced progression, and 27 patients received NGS testing to clarify the potential resistance mechanisms. EGFR-T790M, CDK4 amplification, FGFR1 amplification, PIK3CA, MET amplification, RET fusions, HER2, and BRAF mutations were identified in three (11.1%), three (11.1%), three (11.1%), three (11.1%), three (11.1%), one (3.7%), one (3.7%), and one (3.7%) of the cases, respectively. Five patients underwent ARMS-PCR testing for detecting EGFR-T790M mutation, and only one patient was T790M-positive. CONCLUSIONS: The present study elucidated the differential benefits of afatinib within different mutation genotypes and first revealed the spectrum of potential resistance mechanisms in patients with EGFR G719X/L861Q/S768I. The results of this study may provide practical clinical information that can guide optimal treatment in this setting. Cancer 2022;128:3804-3814.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Efficacy and potential resistance mechanisms of afatinib in advanced non–small cell lung cancer patients with EGFR G719X/L861Q/S768I

Pang

Gan

Tan

et al. 2022

Cancer

View full text Add to dashboard Cite

show abstract

Biomarker Subset Analysis of a Phase IIIb, Open-Label Study of Afatinib in EGFR Tyrosine Kinase Inhibitor-Naive Patients with EGFR m+ Non-Small-Cell Lung Cancer

et al. 2022

View full text Add to dashboard Cite

Aim: To explore the relationship between mutations in cfDNA and response to afatinib. Patients & methods: In total, 64 patients from one Chinese site with locally advanced/metastatic EGFRm+ non-small-cell lung cancer, who received afatinib 40 mg once daily, were included. Results: Overall, 33 (82.5%) patients became EGFRm- by visit 3; median progression-free survival was longer in these patients vs those who did not (11.0 vs 5.5 months). Progression-free survival was shorter in 42 (45.2%) patients with non- EGFR co-mutations at baseline vs those without (8.1 vs 12.5 months). Neither difference was significant. Conclusion: Afatinib provided clinical benefit for patients with EGFRm+ non-small-cell lung cancer across all subgroups. EGFRm status assessment in plasma cfDNA is a useful method of monitoring treatment.

show abstract

Afatinib for the First-Line Treatment of EGFR Mutation-Positive NSCLC in China: a Review of Clinical Data

Cited by 2 publications

References 83 publications

Efficacy and potential resistance mechanisms of afatinib in advanced non–small cell lung cancer patients with EGFR G719X/L861Q/S768I

Efficacy and potential resistance mechanisms of afatinib in advanced non–small cell lung cancer patients with EGFR G719X/L861Q/S768I

Biomarker Subset Analysis of a Phase IIIb, Open-Label Study of Afatinib in EGFR Tyrosine Kinase Inhibitor-Naive Patients with EGFR m+ Non-Small-Cell Lung Cancer

Contact Info

Product

Resources

About