ArticleBMC cancer2016
Metastatic EML4-ALK fusion detected by circulating DNA genotyping in an EGFR-mutated NSCLC patient and successful management by adding ALK inhibitors: a case report.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Cross-Cancer Detectability of ctDNA Biomarkers in Asian Populations: Implications for Pan-Cancer Detection.Cancer management and research · 2026Review
- Article
- Detection of oncogenic fusions in colorectal cancer using a partner-agnostic next-generation sequencing approach.BMC cancer · 2025Article
- Therapeutic strategies to overcomeFrontiers in oncology · 2024Article
- Osimertinib and Selpercatinib Efficacy, Safety, and Resistance in a Multicenter, Prospectively Treated Cohort of EGFR-Mutant and RET Fusion-Positive Lung Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Case report: ConcomitantFrontiers in pharmacology · 2023Article
- ALK rearrangements as mechanisms of acquired resistance to osimertinib in EGFR mutant non-small cell lung cancer.Thoracic cancer · 2021Article
- [Gene Fusions as Acquired Resistance Mechanisms of EGFR-TKI].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020Review
- Detection ofCancer research · 2019Review
- Crizotinib-induced acute fatal liver failure in an AsianWorld journal of clinical cases · 2019Article
- Identification of Actionable Fusions as an Anti-EGFR Resistance Mechanism Using a Circulating Tumor DNA Assay.JCO precision oncology · 2019Article
- Frequency, clinical features and differential response to therapy of concurrentDrug design, development and therapy · 2019Article
- Clinical applications of liquid biopsies for early lung cancer detection.American journal of cancer research · 2019Review
- Clinical Utility of Cell-Free DNA for the Detection ofClinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Baicalin hydrate inhibits cancer progression in nasopharyngeal carcinoma by affecting genome instability and splicing.Oncotarget · 2018Article
- Targeted error-suppressed quantification of circulating tumor DNA using semi-degenerate barcoded adapters and biotinylated baits.Scientific reports · 2017Article
- Emergence of FGFR3-TACC3 fusions as a potential by-pass resistance mechanism to EGFR tyrosine kinase inhibitors in EGFR mutated NSCLC patients.Lung cancer (Amsterdam, Netherlands) · 2017Article
- Liquid biopsy genotyping in lung cancer: ready for clinical utility?Oncotarget · 2017Review
- Detection of circulating tumor DNA in patients with advanced non-small cell lung cancer.Oncotarget · 2017Article
- Prospective Feasibility Study for Using Cell-Free Circulating Tumor DNA-Guided Therapy in Refractory Metastatic Solid Cancers: An Interim Analysis.JCO precision oncology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRebiopsy is highly recommended to identify the mechanism of acquired resistance to EGFR-TKIs in advanced lung cancer. Recent advances in multiplex genotyping based on circulating tumor DNA (ctDNA) provide a strong and non-invasive alternative for detection of the resistance mechanism. CASE PRESENTATION: Here we report a multiple metastatic NSCLC patient who was detected to have pure EGFR 19 exon deletion (negative for EML4-ALK and ROS1 in both IHC-based and sequencing assay) in the primary lesion and responded to first-line and second-line EGFR-TKI treatments (erlotinib then HY-15772). At 8 months, most lesions remained well controlled except for the liver metastases which presented dramatic progression. Considering the high risk of bleeding in rebiopsy of hepatic lesions, we conducted a multiplex genomic profiling with ctDNA. Results reported coexistence of EGFR mutation and EML4-ALK gene translocation in plasma which heavily indicated that ALK was the primary reason for progression of the liver lesions. This deduction was supported by the repeated response to ALK inhibitors (crizotinib then AP26113) of the hepatic metastases.
conclusionsThis is the first report of the existence of ALK rearrangement in metastatic lesions in an EGFR mutated patient. It highlighted the feasibility and advantages of using ctDNA multiplex genotyping in identifying the heterogeneity across lesions and the resistance mechanism of targeted treatments.
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