The Impact of Clinical Outcomes According to EGFR Mutation Status in Patients with Locally Advanced Lung Adenocarcinoma Who Recieved Concurrent Chemoradiotherapy

2014 ◽  
Vol 37 (2) ◽  
pp. 144-147 ◽  
Author(s):  
Hiroaki Akamatsu ◽  
Kyoichi Kaira ◽  
Haruyasu Murakami ◽  
Masakuni Serizawa ◽  
Yasuhiro Koh ◽  
...  
2016 ◽  
Vol 57 (5) ◽  
pp. 449-459 ◽  
Author(s):  
Satoru Ochiai ◽  
Yoshihito Nomoto ◽  
Yui Watanabe ◽  
Yasufumi Yamashita ◽  
Yutaka Toyomasu ◽  
...  

Abstract The purpose of this review was to evaluate the impact of epidermal growth factor receptor (EGFR) mutation status on disease recurrence in patients treated with chemoradiotherapy (CRT) for locally advanced non–small cell lung cancer (NSCLC). A literature search was conducted and a total of three studies were analyzed. There was no significant difference in the objective response rate between the EGFR mutation group and the EGFR wild-type group (odds ratios [OR] 1.46, 95% CI, 0.79–2.70, P = 0.228), and there was no significant difference in the incidence of disease recurrence (OR 1.37, 95% CI, 0.68–2.75, P = 0.379) between the two groups. There were significant difference in the incidence of local/locoregional progression (LP) (OR 0.35, 95% CI, 0.18–0.71, P = 0.003) and distant progression (DP) (OR 2.97, 95% CI, 1.59–5.54, P < 0.001). Brain metastasis (BM) was one of the main recurrence patterns of DP, and the incidence was significantly higher in the EGFR mutant group (OR 2.75, 95% CI, 1.43–5.31, P = 0.003). There were no statistically significant heterogeneities in these pooled analyses. The patterns of recurrence after CRT for locally advanced NSCLC were different according to EGFR mutation status. LP after CRT in patients with EGFR mutation was less frequent, but the high incidence of DP, especially BM, continued to be the major problem. On the other hand, LP continued to be the major problem in EGFR wild-type patients. In multimodality treatment for inoperable locally advanced NSCLC, we may need to consider different treatment strategies according to EGFR mutation status.


2017 ◽  
Vol 12 (11) ◽  
pp. S2351
Author(s):  
K. Hyun ◽  
S. Park ◽  
H.J. Lee ◽  
I.K. Park ◽  
Y. Kim ◽  
...  

2017 ◽  
Vol 14 (1) ◽  
pp. 885-890 ◽  
Author(s):  
Mikiko Ishihara ◽  
Satoshi Igawa ◽  
Jiichiro Sasaki ◽  
Sakiko Otani ◽  
Tomoya Fukui ◽  
...  

2019 ◽  
Vol 16 (9) ◽  
pp. 1199-1206 ◽  
Author(s):  
Kenichi Mizutani ◽  
Xin Guo ◽  
Akihiro Shioya ◽  
Jing Zhang ◽  
Jianbo Zheng ◽  
...  

2020 ◽  
Vol 28 (5) ◽  
pp. 502-506
Author(s):  
Wencheng Li ◽  
Angela G. Niehaus ◽  
Stacey S. O’Neill

Significant advances in targeted therapy have been made in recent years for patients with lung adenocarcinoma. These targeted therapies have made molecular testing of paramount importance to drive therapeutic decisions. Material for testing is often limited, particularly in cytology specimens and small core biopsies. A reliable screening tool is invaluable in triaging limited tissue and selection for epidermal growth factor receptor ( EGFR) mutation testing. We hypothesized that the immunohistochemistry (IHC) profile of lung adenocarcinoma predicts EGFR mutation status. In this retrospective study, we evaluated the thyroid transcription factor-1 (TTF-1)/napsin A IHC profile and EGFR mutation status in 339 lung adenocarcinomas at our academic institution. In our cohort, we found that 92.3% of cases were positive for TTF-1 and/or napsin A by IHC with an EGFR positivity rate of 17.3%. Importantly, 7.7% of the cases were dual TTF-1/napsin A negative, and none of these cases contained EGFR mutations. This finding supports the use of TTF-1 and napsin A IHC to identify cases where EGFR mutation status will be negative, thus preserving limited tissue for other ancillary testing.


2018 ◽  
Vol 7 (11) ◽  
pp. 419 ◽  
Author(s):  
Sophia Subat ◽  
Kentaro Inamura ◽  
Hironori Ninomiya ◽  
Hiroko Nagano ◽  
Sakae Okumura ◽  
...  

The EGFR gene was one of the first molecules to be selected for targeted gene therapy. EGFR-mutated lung adenocarcinoma, which is responsive to EGFR inhibitors, is characterized by a distinct oncogenic pathway in which unique microRNA (miRNA)–mRNA interactions have been observed. However, little information is available about the miRNA–mRNA regulatory network involved. Both miRNA and mRNA expression profiles were investigated using microarrays in 155 surgically resected specimens of lung adenocarcinoma with a known EGFR mutation status (52 mutated and 103 wild-type cases). An integrative analysis of the data was performed to identify the unique miRNA–mRNA regulatory network in EGFR-mutated lung adenocarcinoma. Expression profiling of miRNAs and mRNAs yielded characteristic miRNA/mRNA signatures (19 miRNAs/431 mRNAs) in EGFR-mutated lung adenocarcinoma. Five of the 19 miRNAs were previously listed as EGFR-mutation-specific miRNAs (i.e., miR-532-3p, miR-500a-3p, miR-224-5p, miR-502-3p, and miR-532-5p). An integrative analysis of miRNA and mRNA expression revealed a refined list of putative miRNA–mRNA interactions, of which 63 were potentially involved in EGFR-mutated tumors. Network structural analysis provided a comprehensive view of the complex miRNA–mRNA interactions in EGFR-mutated lung adenocarcinoma, including DUSP4 and MUC4 axes. Overall, this observational study provides insight into the unique miRNA–mRNA regulatory network present in EGFR-mutated tumors. Our findings, if validated, would inform future research examining the interplay of miRNAs and mRNAs in EGFR-mutated lung adenocarcinoma.


Medicine ◽  
2015 ◽  
Vol 94 (42) ◽  
pp. e1784 ◽  
Author(s):  
Tetsuya Isaka ◽  
Tomoyuki Yokose ◽  
Hiroyuki Ito ◽  
Masashi Nagata ◽  
Hideyuki Furumoto ◽  
...  

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