Targeted Sequencing of Circulating Cell Free DNA Can Be Used to Monitor Therapeutic Efficacy of Tyrosine Kinase Inhibitors in Non-small Cell Lung Cancer Patients
| Autor: | How-Wen Ko, Chih-Liang Wang, Ji-Dung Luo, Chiuan-Chian Chiou, Chien-Ying Liu, Cheng-Ta Yang |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Adult
Male Cancer Research Lung Neoplasms Mutant Case Report medicine.disease_cause Biochemistry Circulating Tumor DNA chemistry.chemical_compound Carcinoembryonic antigen Carcinoma Non-Small-Cell Lung Antineoplastic Combined Chemotherapy Protocols Genetics Biomarkers Tumor Tumor Cells Cultured Medicine Humans Epidermal growth factor receptor Lung cancer Molecular Biology Protein Kinase Inhibitors Aged Aged 80 and over Mutation biology business.industry High-Throughput Nucleotide Sequencing Middle Aged medicine.disease Prognosis Circulating Cell-Free DNA respiratory tract diseases Tumor Burden ErbB Receptors Gene Expression Regulation Neoplastic chemistry biology.protein Cancer research Disease Progression Female business Tyrosine kinase DNA Follow-Up Studies |
| Zdroj: | Cancer Genomics Proteomics |
| Popis: | Background/aim Circulating tumor DNA (ctDNA) bears specific mutations derived from tumor cells. The amount of mutant ctDNA may reflect tumor burden. In this study, we detected epidermal growth factor receptor (EGFR) mutations in ctDNA as a monitoring marker for the response of non-small cell lung cancer (NSCLC) patients to tyrosine kinase inhibitors (TKIs). Patients and methods Serial plasma samples from eight NSCLC patients during TKI treatment were collected. Libraries with barcoded adapters were constructed from ctDNA of these plasma samples using a PCR-based targeted DNA panel. The libraries were then sequenced for measuring EGFR mutations. In addition, carcinoembryonic antigen (CEA) was also measured in these patients. Results In six patients who suffered disease progression (PD), five had elevated EGFR mutation reads before PD. In the two patients who did not develop PD, EGFR mutations remained undetectable in their plasma. The CEA levels were higher than the cutoff value in most samples and had a poor correlation with disease status. Conclusion The mutation count of tumor-specific mutations can be a monitoring marker of TKI treatment in NSCLC patients. |
| Databáze: | OpenAIRE |
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