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Introduction: TP53 is a strong tumor suppressor gene; its deactivation contributes to carcinogenesis and influences clinical outcomes. However, the prognostic influence of p53 deactivation on early relapse in patients with surgically resected non–small cell lung cancer remains unclear. Materials and methods: A cohort of 170 patients with primary stage I through III lung adenocarcinoma (LADC) and lung squamous cell carcinoma who underwent complete resection at Tokyo Medical and Dental University was screened for TP53 mutations using panel testing, and association studies between TP53 mutations and clinical data, including histology and postoperative recurrence, were performed. The association between TP53 mutations and postoperative recurrence was validated using data from 604 patients with MSK-IMPACT from The Cancer Genome Atlas. Additional immunohistochemistry for p53 was performed on some subsets of the Tokyo Medical and Dental University population. Results: Mutations in TP53 were recurrently observed (35.9%; 61 out of 170) in the Tokyo Medical and Dental University cohort. In the histology-stratified analysis, patients with LADC histology showed TP53 mutations that were associated with poor relapse-free survival (log-rank test; P = .020), whereas patients with lung squamous cell carcinoma histology showed TP53 mutations that were not (P = .99). The poor prognosis of TP53 mutation-positive LADCs was validated in The Cancer Genome Atlas-LADC cohort (log-rank test; P = .0065). Additional immunohistochemistry for p53 in patients with LADC histology in the Tokyo Medical and Dental University cohort showed a significant correlation between TP53 mutations and abnormal IHC pattern of p53 (Cramer's correlation coefficient V = 0.67). Conclusions: TP53 mutation is a potential marker for worse prognosis in surgically resected LADC; immunohistochemistry for p53 could be a surrogate method to identify patients with LADC with a worse prognosis.

Introduction: The aim of this study is to evaluate the clinical backgrounds, including driver mutations, of those patients with early stage NSCLC who experienced recurrence beyond 5 years after complete resection. Methods: We used a cohort of 512 consecutive cases of surgically resected NSCLC without other malignances from 2006 to 2011 in Aichi Cancer Center Hospital. The inclusion criteria for this cohort were patients with primary NSCLC who underwent a surgically curable operation. Results: A total of 172 patients (32.8%) had recurrence after the surgery. Among the recurrent cases, 17 patients (3.3%) had a relapse more than 5 years after the surgery, and all except one (16 of 17, 94.1%) had driver mutations, including gene rearrangements. Conclusions: Even in early stage NSCLC after complete resection, it was found that some cases had a relapse more than 5 years after the surgery. Most of these cases had some kind of driver mutations; so more than 5 years of postoperative surveillance may be beneficial, especially in those with driver gene mutants.