ArticleOncology letters2019
Predicting the survival of patients with lung adenocarcinoma using a four-gene prognosis risk model.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 13 citations in OpenAlex.
- Review
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- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- miR-17-5p/Frontiers in neurology · 2022Article
- Involvement of MicroRNA-1-FAM83A Axis Dysfunction in the Growth and Motility of Lung Cancer Cells.International journal of molecular sciences · 2020Article
- ERO1L promotes IL6/sIL6R signaling and regulates MUC16 expression to promote CA125 secretion and the metastasis of lung cancer cells.Cell death & disease · 2020Article
- Uncovering Prognosis-Related Genes and Pathways by Multi-Omics Analysis in Lung Cancer.Biomolecules · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LAD) is difficult to diagnose as it tends to be small in size and metastasize early. The aim of the present study was to investigate prognostic factors for patients with LAD and establish a prognosis risk model. A training set consisting of clinical and RNA sequencing data from 503 patients with LAD, as well as expression data from a further 59 LAD and adjacent tissues, was obtained from The Cancer Genome Atlas. Additionally, a validation dataset was acquired from the Gene Expression Omnibus database (GSE26939), which included clinical and gene expression data from 115 patients. Using the DESeq2 package to compare expression between LAD and adjacent tissues, differentially expressed genes (DEGs) were identified. On the basis of survival and the random forests for survival, regression and classification package, genes for constructing the prognosis risk model were selected. The prognosis risk model was constructed and validated using the survival package. Subsequently, high- and low-risk groups were compared using the Limma package to identify DEGs, and enrichment analysis was performed using the web-based gene set analysis toolkit. A protein-protein interaction network was visualized using Cytoscape software. There were 18,567 DEGs between the LAD samples and the adjacent tissues, and 363 DEGs between the high- and low-risk groups. Of these, four genes were selected for constructing the prognosis risk model, myosin IE (
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