抄録
Patients with EGFR-mutated non-small cell lung cancer (NSCLC) exhibit resistance to EGFR-tyrosine kinase inhibitors (TKIs) within 9–14 months of therapy. Recently, EGFR-mutated NSCLC has demonstrated the potential for heterogeneity; therefore, the manner of clonal heterogeneity may impact the duration of progression-free and overall survival and other parameters affecting EGFR-TKI treatment efficacy. However no predictive biomarker of these favorable treatment efficacies has been identified to date. The exosome-focused translational research for afatinib (EXTRA) study aims to identify a novel predictive biomarker and a resistance marker for afatinib by analyzing data from association studies of the clinical efficacy of afatinib and four “OMICs” (genomics, proteomics, epigenomics, and metabolomics) using peripheral blood from patients treated with afatinib. This study aims to: (i) conduct comprehensive multi-OMIC analyses in a prospective clinical trial, and (ii) focus on both sera/plasma and exosome as a source for OMIC analyses to identify a novel predictor of the efficacy of a specific drug. To eliminate the carryover bias of prior treatment, systemic treatment-naïve patients were enrolled. The candidates to be screened for biomarkers comprise a discovery cohort of 60 patients and an independent validation cohort of 40 patients. The EXTRA study is the first trial to screen novel biomarkers of longer treatment efficacy of EGFR-TKIs using four-OMICs analyses, focusing on both “naked or free” molecules and “capsulated” exosomal components in serially collected peripheral blood.
| 元の言語 | English |
|---|---|
| ジャーナル | Thoracic Cancer |
| DOI | |
| 出版物ステータス | Accepted/In press - 2018 1 1 |
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ASJC Scopus subject areas
- Oncology
- Pulmonary and Respiratory Medicine
これを引用
Prospective exosome-focused translational research for afatinib study of non-small cell lung cancer patients expressing EGFR (EXTRA study). / Okuma, Yusuke; Morikawa, Kei; Tanaka, Hisashi; Yokoyama, Takuma; Itani, Hidetoshi; Horiuchi, Kazuya; Nakagawa, Hideyuki; Takahashi, Nobumasa; Bessho, Akihiro; Soejima, Kenzo; Kishi, Kazuma; Togashi, Akira; Kanai, Yae; Ueda, Koji; Horimoto, Katsuhisa; Matsutani, Noriyuki; Seki, Nobuhiko.
：: Thoracic Cancer, 01.01.2018.研究成果: Article
}
TY - JOUR
T1 - Prospective exosome-focused translational research for afatinib study of non-small cell lung cancer patients expressing EGFR (EXTRA study)
AU - Okuma, Yusuke
AU - Morikawa, Kei
AU - Tanaka, Hisashi
AU - Yokoyama, Takuma
AU - Itani, Hidetoshi
AU - Horiuchi, Kazuya
AU - Nakagawa, Hideyuki
AU - Takahashi, Nobumasa
AU - Bessho, Akihiro
AU - Soejima, Kenzo
AU - Kishi, Kazuma
AU - Togashi, Akira
AU - Kanai, Yae
AU - Ueda, Koji
AU - Horimoto, Katsuhisa
AU - Matsutani, Noriyuki
AU - Seki, Nobuhiko
PY - 2018/1/1
Y1 - 2018/1/1
N2 - Patients with EGFR-mutated non-small cell lung cancer (NSCLC) exhibit resistance to EGFR-tyrosine kinase inhibitors (TKIs) within 9–14 months of therapy. Recently, EGFR-mutated NSCLC has demonstrated the potential for heterogeneity; therefore, the manner of clonal heterogeneity may impact the duration of progression-free and overall survival and other parameters affecting EGFR-TKI treatment efficacy. However no predictive biomarker of these favorable treatment efficacies has been identified to date. The exosome-focused translational research for afatinib (EXTRA) study aims to identify a novel predictive biomarker and a resistance marker for afatinib by analyzing data from association studies of the clinical efficacy of afatinib and four “OMICs” (genomics, proteomics, epigenomics, and metabolomics) using peripheral blood from patients treated with afatinib. This study aims to: (i) conduct comprehensive multi-OMIC analyses in a prospective clinical trial, and (ii) focus on both sera/plasma and exosome as a source for OMIC analyses to identify a novel predictor of the efficacy of a specific drug. To eliminate the carryover bias of prior treatment, systemic treatment-naïve patients were enrolled. The candidates to be screened for biomarkers comprise a discovery cohort of 60 patients and an independent validation cohort of 40 patients. The EXTRA study is the first trial to screen novel biomarkers of longer treatment efficacy of EGFR-TKIs using four-OMICs analyses, focusing on both “naked or free” molecules and “capsulated” exosomal components in serially collected peripheral blood.
AB - Patients with EGFR-mutated non-small cell lung cancer (NSCLC) exhibit resistance to EGFR-tyrosine kinase inhibitors (TKIs) within 9–14 months of therapy. Recently, EGFR-mutated NSCLC has demonstrated the potential for heterogeneity; therefore, the manner of clonal heterogeneity may impact the duration of progression-free and overall survival and other parameters affecting EGFR-TKI treatment efficacy. However no predictive biomarker of these favorable treatment efficacies has been identified to date. The exosome-focused translational research for afatinib (EXTRA) study aims to identify a novel predictive biomarker and a resistance marker for afatinib by analyzing data from association studies of the clinical efficacy of afatinib and four “OMICs” (genomics, proteomics, epigenomics, and metabolomics) using peripheral blood from patients treated with afatinib. This study aims to: (i) conduct comprehensive multi-OMIC analyses in a prospective clinical trial, and (ii) focus on both sera/plasma and exosome as a source for OMIC analyses to identify a novel predictor of the efficacy of a specific drug. To eliminate the carryover bias of prior treatment, systemic treatment-naïve patients were enrolled. The candidates to be screened for biomarkers comprise a discovery cohort of 60 patients and an independent validation cohort of 40 patients. The EXTRA study is the first trial to screen novel biomarkers of longer treatment efficacy of EGFR-TKIs using four-OMICs analyses, focusing on both “naked or free” molecules and “capsulated” exosomal components in serially collected peripheral blood.
KW - Afatinib
KW - epidermal growth factor receptor
KW - exosome
KW - OMIC
KW - translational research
UR - http://www.scopus.com/inward/record.url?scp=85058164168&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85058164168&partnerID=8YFLogxK
U2 - 10.1111/1759-7714.12923
DO - 10.1111/1759-7714.12923
M3 - Article
C2 - 30536780
AN - SCOPUS:85058164168
JO - Thoracic Cancer
JF - Thoracic Cancer
SN - 1759-7706
ER -