Adjuvant Treatments for Surgically Resected Non–Small Cell Lung Cancer Harboring EGFR Mutations

Abstract

ImportanceThe use of adjuvant chemotherapy for stage IB-IIIA resected non–small cell lung cancer (NSCLC) has limited benefit for improving cure rates. The proportion of epidermal growth factor receptor (EGFR) alterations among patients with resected NSCLC is comparable to that observed in patients with advanced disease, and the use of EGFR tyrosine kinase inhibitors (TKIs) has been demonstrated to prolong disease-free survival (DFS). With recent approval of osimertinib in this context, a focus on the rapidly evolving scenario and future perspective in clinical practice is needed and was the aim of the current review.ObservationsRandomized phase 3 clinical trials demonstrated DFS benefit with adjuvant EGFR TKI therapy in patients with resected EGFR mutation–positive NSCLC. The most recent trial (ADAURA) assessed 3-year adjuvant osimertinib and showed consistent DFS benefit and a significant role of the intervention in preventing the occurrence of brain metastasis. However, the role of adjuvant chemotherapy, the appropriate duration of treatment, the management of disease relapse, and the effective cure rate remain undetermined. A deeper investigation on molecular biomarkers, covariant patterns, and dynamic monitoring of postsurgical circulating DNA would be helpful for the implementation of future strategies to further improve survival rates after adjuvant therapy for EGFR mutation–positive NSCLC.Conclusions and RelevanceAdjuvant osimertinib revolutionized the treatment algorithm for patients with stage IB-IIIA resected EGFR mutation–positive NSCLC. Further evidence driven by clinical issues will be key for further optimization of the goals of adjuvant treatment in these patients.

Clinical significance of TMEM229A Q200del mutation in lung adenocarcinoma

“…Moreover, the inhibitory of TMEM229A Q200del was more obvious than that of TMEM229A wide type. Once EGFR gene was presented mutations, EGFRassociated signaling pathways could be activated [50,51]. Therefore, we speculated that TMEM229A Q200del mutation probably affects the cancer-associated signaling pathways, such as extracellular signal-regulated kinase (ERK).…”