TY - JOUR
T1 - Propensity score analysis of overall survival between first- and second-generation EGFR-TKIs using real-world data
AU - Ito, Kentaro
AU - Murotani, Kenta
AU - Kubo, Akihito
AU - Kunii, Eiji
AU - Taniguchi, Hirokazu
AU - Shindoh, Joe
AU - Asada, Kazuhiro
AU - Imaizumi, Kazuyoshi
AU - Takahashi, Kosuke
AU - Karayama, Masato
AU - Okuno, Motoyasu
AU - Inui, Naoki
AU - Hataji, Osamu
AU - Morikawa, Sayako
AU - Hayai, Shunsaku
AU - Suda, Takafumi
AU - Abe, Takashi
AU - Tsuda, Takeshi
AU - Yamagichi, Teppei
AU - Kimura, Tomoki
AU - Oya, Yuko
AU - Yoshida, Tatsuya
AU - Hida, Toyoaki
N1 - Funding Information:
K Ito received research funding from Boehringer, Chugai, Novartis, Ono Pharma, Daiichi‐Sankyo, GSK, Byer, Kyorin, and lecture fees from Boehringer Ingelheim, Chugai Pharm, Eli Lily Japan, MSD, AstraZeneca, Ono Pharm, Pfizer. K Murotani received lecture fees from Boehringer Ingelheim, Chugai Pharm, MSD, Taiho Pharm. A Kubo received research funding from Boehringer Ingelheim, Chugai, Novartis, Ono Pharma, Lilly, and lecture fees from Boehringer Ingelheim, Chugai, Lilly, MSD, Novartis, AstraZeneca, Ono Pharm. H Taniguchi received lecture fees from Boehringer Ingelheim, Chugai Pharm, MSD, AstraZeneca, GSK, Daiichi‐Sankyo, Kyorin, Kyouwahakko‐kirin. J Shindoh received lecture fees from Boehringer Ingelheim, Chugai Pharm, AstraZeneca, Ono Pharm, Eli Lilly Japan, MSD, Bristol‐Myers Squibb. Kazuhiro Asada received lecture fees from Boehringer, Chugai, Novartis, Ono Pharma, Taiho, MSD, Eli Lily, Mochida. K Imaizumi received research funding from Boehringer, MSD, Taiho. K Takahashi received lecture fees from AstraZeneca, Boehringer Ingelheim, Chugai Pharm, Eli Lily Japan, MSD, Taiho Pharma. Naoki Inui received research funding from Chugai, and lecture fees from Boehringer Ingelheim, Chugai Pharm, AstraZeneca, Ono Pharm, Taiho Pharma. Osamu Hataji received research funding from Boehringer, Chugai, Novartis, Ono Pharma, Daiichi‐Sankyo, GSK, Byer, Kyorin, and lecture fees from Boehringer Ingelheim, Chugai Pharm, Novartis, MSD, AstraZeneca, Ono Pharm, Pfizer, Kyorin. Takafumi Suda received research funding from Boehringer, Ono Pharm, and lecture fees from Boehringer Ingelheim, MSD, AstraZeneca. Teppei Yamaguchi received lecture fees from Nippon Boehringer Ingelheim, Chugai Pharm, Eli Lily Japan, MSD, AstraZeneca, Taiho Pharmaceutical, Novartis Pharma, and Bristol‐Meyers Squibb. Tomoki Kimura received lecture fees from Boehringer Ingelheim, Chugai Pharm, Novartis, MSD, AstraZeneca, Ono Pharm, Pfizer, Kyorin. Toyoaki Hida received the research fund from Chugai Pharmaceutical, MSD, Eli Lilly, Ono Pharmaceutical, Novartis, Taiho Pharmaceutical, AstraZeneca, Nippon Boehringer Ingelheim, Bristol‐Meyers Squibb, Clovis Oncology, Eisai, Takeda Bio, Dainippon Sumitomo Pharma, Abbvie, Merck Serono, Ignyta, Kissei, Kyowa Hakko Kirin, Daiichi‐Sankyo, Servier, Astellas, Bayer, Janssen, and Pfizer, and lecture fees from Chugai Pharmaceutical, MSD, Eli Lilly, Ono Pharmaceutical, Novartis, Taiho Pharmaceutical, AstraZeneca, Kissei, Nippon Boehringer Ingelheim, Pfizer, Bristol‐Meyers Squibb, and Clovis Oncology. The other co‐authors have no disclosure. This work was supported through funding from Boehringer Ingelheim Japan.
PY - 2020/10/1
Y1 - 2020/10/1
N2 - We constructed a data set of EGFR-mutant non–small-cell lung carcinoma (NSCLC) patients, and compared the overall survival of first-generation (1G), and second-generation (2G) EGFR-tyrosine kinase inhibitors (TKIs) in clinical practice using a propensity score. We reviewed the clinical data of consecutive EGFR-mutated NSCLC patients who received EGFR-TKI therapy between January 2008 and August 2017 at 11 institutions in Japan. The primary endpoint was overall survival (OS). When comparing OS between 1G and 2G EGFR-TKIs, propensity score analyses were performed using 2 methods: matching and inverse probability of treatment weighting (IPTW). (Clinical Trial information: UMIN000030121) In total, 1400 patients from 11 institutions were enrolled in this study, and the data from the 1366 patients who received only EGFR-TKI therapy were analyzed (gefitinib [GEF], N = 732; erlotinib [ERL], N = 416; afatinib, N = 218). Median OS times (months [95%CI]) were 29.7 [27.5-33.5] in the 1G group (gefitinib, 32.0 [28.1-35.8]; erlotinib, 27.5 [23.9-31.7]), and 38.6 [32.2-NR] in the 2G group (afatinib), respectively. The trend of longer OS for afatinib against 1G EGFR-TKIs remained, even after adjusted by propensity score. (unadjusted, hazard ratio [HR] 0.676, P =.0023; adjusted by IPTW, HR 0.685 P <.0001; adjusted by matching, HR 0.725, P =.0418). Exploratory analysis showed that OS using the 2G EGFR-TKI was superior to that of the 1G EGFR-TKIs, suggesting the potential of sequential therapy of 2G EGFR-TKI followed by osimertinib. (HR 0.419, P =.0519) Real-world data analysis using 1354 data records, using propensity scoring, indicated that 2G EGFR-TKI had a trend of longer OS compared with 1G EGFR-TKIs.
AB - We constructed a data set of EGFR-mutant non–small-cell lung carcinoma (NSCLC) patients, and compared the overall survival of first-generation (1G), and second-generation (2G) EGFR-tyrosine kinase inhibitors (TKIs) in clinical practice using a propensity score. We reviewed the clinical data of consecutive EGFR-mutated NSCLC patients who received EGFR-TKI therapy between January 2008 and August 2017 at 11 institutions in Japan. The primary endpoint was overall survival (OS). When comparing OS between 1G and 2G EGFR-TKIs, propensity score analyses were performed using 2 methods: matching and inverse probability of treatment weighting (IPTW). (Clinical Trial information: UMIN000030121) In total, 1400 patients from 11 institutions were enrolled in this study, and the data from the 1366 patients who received only EGFR-TKI therapy were analyzed (gefitinib [GEF], N = 732; erlotinib [ERL], N = 416; afatinib, N = 218). Median OS times (months [95%CI]) were 29.7 [27.5-33.5] in the 1G group (gefitinib, 32.0 [28.1-35.8]; erlotinib, 27.5 [23.9-31.7]), and 38.6 [32.2-NR] in the 2G group (afatinib), respectively. The trend of longer OS for afatinib against 1G EGFR-TKIs remained, even after adjusted by propensity score. (unadjusted, hazard ratio [HR] 0.676, P =.0023; adjusted by IPTW, HR 0.685 P <.0001; adjusted by matching, HR 0.725, P =.0418). Exploratory analysis showed that OS using the 2G EGFR-TKI was superior to that of the 1G EGFR-TKIs, suggesting the potential of sequential therapy of 2G EGFR-TKI followed by osimertinib. (HR 0.419, P =.0519) Real-world data analysis using 1354 data records, using propensity scoring, indicated that 2G EGFR-TKI had a trend of longer OS compared with 1G EGFR-TKIs.
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U2 - 10.1111/cas.14560
DO - 10.1111/cas.14560
M3 - Article
C2 - 32639668
AN - SCOPUS:85088943431
VL - 111
SP - 3705
EP - 3713
JO - Cancer Science
JF - Cancer Science
SN - 1347-9032
IS - 10
ER -