ArticleOncotarget2016
Gene status and clinicopathologic characteristics of lung adenocarcinomas with mediastinal lymph node metastasis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Predictors of occult lymph node metastasis in clinical T1 lung adenocarcinoma: a retrospective dual-center study.BMC pulmonary medicine · 2025Article
- Clinical characteristics of patients withTranslational cancer research · 2020Article
- Targeting non-small cell lung cancer: driver mutation beyond epidermal growth factor mutation and anaplastic lymphoma kinase fusion.Therapeutic advances in medical oncology · 2020Review
- Metastasis manners and the underlying mechanisms of ALK and ROS1 rearrangement lung cancer and current possible therapeutic strategies.RSC advances · 2019Review
- PD-L1 expression indicates favorable prognosis for advanced lung adenocarcinoma patients treated with pemetrexed.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer with mediastinal lymph node metastasis is more likely to develop recurrence and metastasis after complete resection and targeted therapy is a promising treatment strategy. We performed amplification refractory mutation system (ARMS) fluorescence quantitative PCR to detect the gene status of EGFR, ALK, ROS1 and RET in resected samples from 280 patients who were confirmed to have primary lung adenocarcinomas with N1-N2 lymph node metastasis. Of the 280 patients enrolled, the frequency of EGFR mutations, ALK fusions, ROS1 fusions, RET fusions and no mutations was 42.9%, 10.7%, 1.8%, 3.6% and 42.9%, respectively. Five patients exhibited the coexistence of the EGFR and ALK alterations. ALK, ROS1 and RET fusions were mutually exclusive. The frequency of EGFR mutation was significantly lower among patients with poor differentiation, while the rates of ALK and ROS1 fusions were the opposite. RET fusions also tended to be more prevalent in poorly differentiated patients. EGFR and ALK double positive tumors were characterized by significantly smaller size compared with those had single gene alteration. Our study comprehensively analyzed the distinct and common clinicopathologic characteristics according to genotypes of the cohort, which should help in categorizing patients for efficient screening.
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Registered trials
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