Journal
JOURNAL OF THORACIC ONCOLOGY
Volume 5, Issue 8, Pages 1175-1184Publisher
ELSEVIER SCIENCE INC
DOI: 10.1097/JTO.0b013e3181e2f4d6
Keywords
EGFR; KRAS; Lung cancer; Mutation; Survival; Copy number; Chemotherapy
Categories
Funding
- National Health Research Institutes (NHRI) [96-A1-MG-PP-04, NHRI-A1-MG-98-PP04]
- National Science Council, Taiwan [NSC97-2320-B-400-006-MY3]
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Introduction: The prognostic role of epidermal growth factor receptor (EGFR) mutations in patients with surgically resectable non-small cell lung cancer (NSCLC) without EGFR tyrosine kinase inhibitor treatment has not been well established, because the reports are still few. Materials and Methods: We analyzed the survival data of 164 patients with surgically resectable (stages I to IIIA) NSCLC of two year groups (1996-1998 and 2002-2004), and compared with EGFR mutations, KRAS mutations, and EGFR gene copy numbers. Results: Comparing the survival of wild-type patients and patients having L858R mutations or exon 19 deletion, the median survival was much longer for patient with EGFR mutations (54.7 months) than wild type (34.9 months). The difference was not statistically significant by univariate analysis (p = 0.1981) but had borderline significance by multivariate analyses (p = 0.0506). In addition, the 3-year survival rates of patients with EGFR mutations were also significantly higher than wild type (p = 0.0232). After exclusion of 18 patients treated by EGFR-tyrosine kinase inhibitor for tumor recurrence, the trends were still the same. Patients with KRAS mutations had shorter median survival (21 months) than wild type (44.4 months). Patients with EGFR polysomy (>= copies) also had longer median survival (56.2 months) than wild type (53.4 months). But the survival differences of these two genetic markers were all not significant statistically. Conclusion: It is intriguing that patients with NSCLC with EGFR mutations had better survival than wild type. Such a tumor biology may confound the survival data in a study without the stratification by EGFR mutation.
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