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Tytuł pozycji:

Barcode sequencing identifies resistant mechanisms to epidermal growth factor receptor inhibitors in circulating tumor DNA of lung cancer patients.

Tytuł:
Barcode sequencing identifies resistant mechanisms to epidermal growth factor receptor inhibitors in circulating tumor DNA of lung cancer patients.
Autorzy:
Kitazono S; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Sakai K; Department of Genome Biology, Kindai University Faculty of Medicine, Osaka, Japan.
Yanagitani N; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Ariyasu R; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yoshizawa T; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Dotsu Y; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Koyama J; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Saiki M; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Sonoda T; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Nishikawa S; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Uchibori K; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Horiike A; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Nishio K; Department of Genome Biology, Kindai University Faculty of Medicine, Osaka, Japan.
Nishio M; Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Źródło:
Cancer science [Cancer Sci] 2019 Oct; Vol. 110 (10), pp. 3350-3357. Date of Electronic Publication: 2019 Aug 19.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: 2005- : Oxford : Wiley Publishing on behalf of the Japanese Cancer Association
Original Publication: Tokyo : Japanese Cancer Association, c2003-
MeSH Terms:
Drug Resistance, Neoplasm*
Carcinoma, Non-Small-Cell Lung/*genetics
Circulating Tumor DNA/*genetics
High-Throughput Nucleotide Sequencing/*methods
Lung Neoplasms/*genetics
Aged ; Carcinoma, Non-Small-Cell Lung/pathology ; DNA Copy Number Variations ; ErbB Receptors/genetics ; Female ; Humans ; Lung Neoplasms/pathology ; Male ; Middle Aged ; Neoplasm Staging ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-met/genetics ; Sequence Analysis, DNA
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Grant Information:
14525177 Japan Agency for Medical Research and Development
Contributed Indexing:
Keywords: circulating tumor DNA; droplet digital PCR; epidermal growth factor receptor; molecular barcode sequencing; non-small cell lung cancer
Substance Nomenclature:
0 (Circulating Tumor DNA)
0 (Protein Kinase Inhibitors)
EC 2.7.10.1 (EGFR protein, human)
EC 2.7.10.1 (ErbB Receptors)
EC 2.7.10.1 (MET protein, human)
EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
Entry Date(s):
Date Created: 20190731 Date Completed: 20191011 Latest Revision: 20210110
Update Code:
20240105
PubMed Central ID:
PMC6778626
DOI:
10.1111/cas.14153
PMID:
31361375
Czasopismo naukowe
Most patients with epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) will inevitably develop acquired resistance induced by treatment with EGFR tyrosine kinase inhibitors (EGFR-TKI). The mechanisms of resistance to EGFR-TKI are multifactorial, and the detection of these mechanisms is critical for treatment choices in patients who have progressed after EGFR-TKI therapy. We evaluated the feasibility of a molecular barcode method using next-generation sequencing to detect multifactorial resistance mechanisms in circulating tumor DNA and compared the results with those obtained using other technologies. Plasma samples were collected from 25 EGFR mutation-positive NSCLC patients after the development of EGFR-TKI resistance. Somatic mutation profiles of these samples were assessed using two methods of next-generation sequencing and droplet digital PCR (ddPCR). The positive rate for EGFR-sensitizing mutations was 18/25 (72.0%) using ddPCR, 17/25 (68.0%) using amplicon sequencing, and 19/25 (76.0%) using molecular barcode sequencing. Rate of the EGFR T790M resistance mutation among patients with EGFR-sensitizing mutations was shown to be 7/18 (38.9%) using ddPCR, 6/17 (35.3%) using amplicon sequencing, and 8/19 (42.1%) using molecular barcode sequencing. Copy number gain in the MET gene was detected in three cases using ddPCR. PIK3CA, KRAS and TP53 mutations were detected using amplicon sequencing. Molecular barcode sequencing detected PIK3CA, TP53, KRAS, and MAP2K1 mutations. Results of the three assays were comparable; however, in cell-free DNA, molecular barcode sequencing detected mutations causing multifactorial resistance more sensitively than did the other assays.
(© 2019 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.)

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