Association of Tumor PD-L1 Expression with the T790M Mutation and Progression-Free Survival in Patients with EGFR-Mutant Non-Small Cell Lung Cancer Receiving EGFR-TKI Therapy
Minehiko Inomata,
Kenji Azechi,
Naoki Takata,
Kana Hayashi,
Kotaro Tokui,
Chihiro Taka,
Seisuke Okazawa,
Kenta Kambara,
Shingo Imanishi,
Toshiro Miwa,
Ryuji Hayashi,
Shoko Matsui,
Kazuyuki Tobe
Affiliations
Minehiko Inomata
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Kenji Azechi
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Naoki Takata
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Kana Hayashi
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Kotaro Tokui
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Chihiro Taka
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Seisuke Okazawa
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Kenta Kambara
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Shingo Imanishi
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Toshiro Miwa
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Ryuji Hayashi
Department of Medical Oncology, Toyama University Hospital, Toyama 930-0194, Japan
Shoko Matsui
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Kazuyuki Tobe
First Department of Internal Medicine, Toyama University Hospital, Toyama 930-0194, Japan
Background: Among patients with non-small cell lung cancer (NSCLC), we compared the progression-free survival (PFS) and proportion of acquisition of T790M mutation of the epidermal growth receptor gene (EGFR) after first-line treatment with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) in patient groups with and without tumor expression of programmed death ligand-1 (PD-L1). Methods: Data of patients with EGFR-mutant NSCLC were retrospectively analyzed. Tumor PD-L1 expression was evaluated by immunohistochemistry using the 22C3 antibody. T790M gene mutation was evaluated by Cobas EGFR assay using tissues or humoral specimens. Results: Data of 47 patients with EGFR-mutant NSCLC were analyzed. The median (95% confidence interval) PFS in the PD-L1-negative and -positive patient groups were 12.9 (9.7–15.4) months and 9.0 (5.1–12.3) months, respectively (p = 0.029). T790M gene mutation was analyzed in 27 patients. The proportion of acquisition of T790M mutation of EGFR after first-line treatment with an EGFR-TKI was higher in the PD-L1-negative patient group than in the PD-L1-positive patient group (8/11 patients (72.7%) vs. 4/16 patients (25.0%); p = 0.022). Conclusions: Patients with negative tumor PD-L1 expression showed longer PFS and a higher proportion of acquisition of T790M mutation of EGFR after first-line treatment with an EGFR-TKI.