Surgically Resected Second Primary Lung Adenocarcinoma After Pembrolizumab Administration
ANNALS OF THORACIC SURGERY
Authors: Takamori, Shinkichi; Matsubara, Taichi; Haratake, Naoki; Miura, Naoko; Yamaguchi, Masafumi; Toyozawa, Ryo; Seto, Takashi; Taguchi, Kenichi; Takenoyama, Mitsuhiro
Abstract
Non-small cell lung cancer (NSCLC) patients are sometimes referred for thoracic surgical consultation to address the possibility of resecting second primary lung cancer. We report a case of pulmonary resection for second primary lung adenocarcinoma after 3 cycles of pembrolizumab under circumstances in which the primary metastatic lung adenocarcinoma was controlled. The tumor statuses, including programmed death-ligand 1, epidermal growth factor receptor, and CD8+ tumor-infiltrating lymphocytes, were different between the surgically resected specimen and the previously biopsied sample. Surgery should be considered for second primary NSCLC in cases in which the primary NSCLC are well controlled with immune checkpoint inhibitors. (C) 2020 by The Society of Thoracic Surgeons
p38 alpha MAP kinase inhibitors to overcome EGFR tertiary C797S point mutation associated with osimertinib in non-small cell lung cancer (NSCLC): emergence of fourth-generation EGFR inhibitor
JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS
Authors: Ahmad, Iqrar; Shaikh, Matin; Surana, Sanjay; Ghosh, Arabinda; Patel, Harun
Abstract
The third-generation EGFR (epidermal growth factor receptor) inhibitors selectively and irreversibly target EGFR-T790M and other activating EGFR mutations. Osimertinib is the only FDA-approved third-generation inhibitor, which has a good potency against the EGFR-T790M mutant with minimal toxicities and excellent selectivity for wild-type EGFR. EGFR tertiary Cys797 to Ser797 (C797S) point mutation emanate rapidly after the treatment of osimertinib, which is an undruggable mutation to all three existing generation drugs. Recently, trisubstituted imidazoles were reported based on an off-target hit of a p38 alpha MAPK (mitogen-activated protein kinase) inhibitor as the fourth-generation EGFR-TKIs to overcome the C797S resistance by inhibiting the clinically relevant triple mutant kinase L858R/T790M/C797 EGFR. Here, we are reporting the clinical trial p38 alpha MAPK kinase inhibitors SD-06, Amgen 16, RWJ67657 and SCIO-323 as L858R/T790M/C797S EGFR TK inhibitors to overcome the problem of drug resistance in non-small cell lung cancer (NSCLC). Communicated by Ramaswamy H. Sarma
COA
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