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The Association of EGFR Mutations with Stage at Diagnosis in Lung Adenocarcinomas.

ABSTRACT: BACKGROUND:The prognostic role of epidermal growth factor receptor (EGFR) mutations in patients with lung adenocarcinomas remains controversial and the association between EGFR mutations and stage at the time of the initial diagnosis is debatable. In this study, we evaluated the association of EGFR mutations with stage at diagnosis in lung adenocarcinomas. MATERIALS AND METHODS:We retrospectively analyzed 1004 consecutive patients who were diagnosed with lung adenocarcinomas and tested for EGFR mutations between June 2011 and December 2014. RESULTS:EGFR mutations were detected in 49.2% of 1004 patients with lung adenocarcinomas. In multivariable analysis, EGFR mutations were significantly associated with early stage disease (stage I to II) at diagnosis (odds ratio [OR], 0.65; 95% confidence interval [CI], 0.49-0.87; P = 0.003). When adjusted for age, sex, smoking status, and screening, the adjusted proportion of EGFR mutations significantly decreased according to stage. The adjusted proportions of EGFR mutations were 57.6% (95% CI, 51.7%-63.3%) for stage I, 47.9% (95% CI, 36.9%-59.0%) for stage II, 47.5% (95% CI, 39.6%-55.5%) for stage III, and 43.4% (95% CI, 38.3%-48.6%) for stage IV (P = 0.0082). CONCLUSIONS:The presence of EGFR mutations is significantly associated with early stage disease at initial diagnosis in lung adenocarcinomas after adjusting for age, sex, smoking status, and screening. This finding implies that EGFR mutations may play a role as a positive prognostic marker.

SUBMITTER: Cho J

PROVIDER: S-EPMC5115811 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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The Association of EGFR Mutations with Stage at Diagnosis in Lung Adenocarcinomas.

Cho Jaeyoung J Choi Sun Mi SM Lee Jinwoo J Lee Chang-Hoon CH Lee Sang-Min SM Yim Jae-Joon JJ Chung Doo Hyun DH Yoo Chul-Gyu CG Kim Young Whan YW Han Sung Koo SK Park Young Sik YS

PloS one 20161118 11

<h4>Background</h4>The prognostic role of epidermal growth factor receptor (EGFR) mutations in patients with lung adenocarcinomas remains controversial and the association between EGFR mutations and stage at the time of the initial diagnosis is debatable. In this study, we evaluated the association of EGFR mutations with stage at diagnosis in lung adenocarcinomas.<h4>Materials and methods</h4>We retrospectively analyzed 1004 consecutive patients who were diagnosed with lung adenocarcinomas and t ...[more]

PMID: 27861565

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Project description:Epidermal growth factor receptor EGFR major driver mutations may affect downstream molecular networks and pathways, which would influence treatment outcomes of non-small cell lung cancer (NSCLC). This study aimed to unveil profiles of mutant proteins expressed in lung adenocarcinomas of 36 patients harboring representative driver EGFR mutations (Ex19del, nine; L858R, nine; no Ex19del/L858R, 18). Surprisingly, the orthogonal partial least squares discriminant analysis performed for identified mutant proteins demonstrated the profound differences in distance among the different EGFR mutation groups, suggesting that cancer cells harboring L858R or Ex19del emerge from cellular origins different from L858R/Ex19del-negative cells. Weighted gene coexpression network analysis, together with over-representative analysis, identified 18 coexpressed modules and their eigen proteins. Pathways enriched differentially for both the L858R and Ex19del mutations included carboxylic acid metabolic process, cell cycle, developmental biology, cellular responses to stress, mitotic prophase, cell proliferation, growth, epithelial to mesenchymal transition (EMT), and immune system. The IPA causal network analysis identified the highly activated networks of PARPBP, HOXA1, and APH1 under the L858R mutation, whereas those of ASGR1, APEX1, BUB1, and MAPK10 were highly activated under the Ex19del mutation. Interestingly, the downregulated causal network of osimertinib intervention showed the highest significance in overlap p-value among most causal networks predicted under the L858R mutation. We also identified the causal network of MAPK interacting serine/threonine kinase 1/2 (MNK1/2) highly activated differentially under the L858R mutation. Tumor-suppressor AMOT, a component of the Hippo pathways, was highly inhibited commonly under both L858R and Ex19del mutations. Our results could identify disease-related protein molecular networks from the landscape of single amino acid variants. Our findings may help identify potential therapeutic targets and develop therapeutic strategies to improve patient outcomes.

Dataset Information

The Association of EGFR Mutations with Stage at Diagnosis in Lung Adenocarcinomas.

Publications

The Association of EGFR Mutations with Stage at Diagnosis in Lung Adenocarcinomas.

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