PURPOSE: This study retrospectively assessed the mutations of the epidermal growth factor receptor (EGFR) and K-ras genes and their clinical significance in patients with resected stage I adenocarcinomas. METHODS: A total of 354 patients with resected lung adenocarcinomas were included, and 256 patients with stage I disease were analyzed for the prognostic and predictive value of these mutations. RESULTS: Mutations of EGFR and K-ras genes were detected in 149 (41.1 %) and 23 (6.4 %) of all tumors, and in 122 (47.6 %) and 14 (5.5 %) of stage I tumors, respectively. There were no significant differences in the disease-free survival (DFS) and overall survival (OS) between the EGFR-mutant and wild-type groups. However, the DFS and OS were significantly shorter in patients with K-ras mutations than in those without (5-year DFS: 50.8 vs. 76.9 %, 5-year OS: 70.0 vs. 86.6 %, p < 0.01). A multivariate analysis showed that K-ras mutations were an independent poor prognostic factor. Twenty-four of the 41 patients with recurrent disease after surgery were treated with an EGFR-TKI. Fifteen EGFR-mutant patients treated with an EGFR-TKI had a better prognosis than did the nine EGFR-wild-type patients. CONCLUSION: The presence of an EGFR gene mutation was a predictive factor for the response to EGFR-TKI treatment in patients with resected stage I adenocarcinoma, but was not a prognostic factor. The presence of a K-ras gene mutation was a poor prognostic factor.
PURPOSE: This study retrospectively assessed the mutations of the epidermal growth factor receptor (EGFR) and K-ras genes and their clinical significance in patients with resected stage I adenocarcinomas. METHODS: A total of 354 patients with resected lung adenocarcinomas were included, and 256 patients with stage I disease were analyzed for the prognostic and predictive value of these mutations. RESULTS: Mutations of EGFR and K-ras genes were detected in 149 (41.1 %) and 23 (6.4 %) of all tumors, and in 122 (47.6 %) and 14 (5.5 %) of stage I tumors, respectively. There were no significant differences in the disease-free survival (DFS) and overall survival (OS) between the EGFR-mutant and wild-type groups. However, the DFS and OS were significantly shorter in patients with K-ras mutations than in those without (5-year DFS: 50.8 vs. 76.9 %, 5-year OS: 70.0 vs. 86.6 %, p < 0.01). A multivariate analysis showed that K-ras mutations were an independent poor prognostic factor. Twenty-four of the 41 patients with recurrent disease after surgery were treated with an EGFR-TKI. Fifteen EGFR-mutant patients treated with an EGFR-TKI had a better prognosis than did the nine EGFR-wild-type patients. CONCLUSION: The presence of an EGFR gene mutation was a predictive factor for the response to EGFR-TKI treatment in patients with resected stage I adenocarcinoma, but was not a prognostic factor. The presence of a K-ras gene mutation was a poor prognostic factor.
Authors: R Rosell; J Gómez-Codina; C Camps; J Maestre; J Padille; A Cantó; J L Mate; S Li; J Roig; A Olazábal Journal: N Engl J Med Date: 1994-01-20 Impact factor: 91.245
Authors: K Sugio; H Uramoto; K Ono; T Oyama; T Hanagiri; M Sugaya; Y Ichiki; T So; S Nakata; M Morita; K Yasumoto Journal: Br J Cancer Date: 2006-03-27 Impact factor: 7.640
Authors: Neil R Parikh; Anna Likhacheva; Chelsea Pinnix; Pamela K Allen; Sujit S Prabhu; Nandita Guha-Thakurta; James W Welsh; Paul D Brown; Eric L Chang Journal: J Radiosurg SBRT Date: 2015
Authors: Ulrich C Lalji; Joachim E Wildberger; Axel Zur Hausen; Matyas Bendek; Anne-Marie C Dingemans; Monique Hochstenbag; Marco Das Journal: Cardiovasc Intervent Radiol Date: 2015-05-13 Impact factor: 2.740
Authors: Luka Brcic; Marko Jakopovic; Marija Misic; Fran Seiwerth; Izidor Kern; Silvana Smojver-Jezek; Franz Quehenberger; Miroslav Samarzija; Sven Seiwerth Journal: Diagn Pathol Date: 2016-09-21 Impact factor: 2.644