ArticleBMC medical genomics2013
Whole transcriptome sequencing identifies tumor-specific mutations in human oral squamous cell carcinoma.
Article in BMC medical genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Genetics and Molecular Mechanisms in Oral Squamous Cell Carcinoma: A Narrative Review.Medicina (Kaunas, Lithuania) · 2026Review
- Identification of novel biomarkers involved in oral squamous cell carcinoma by whole transcriptome sequencing and bioinformatics analysis.Cancer cell international · 2025Article
- Role of transcriptomics in the study of oral cancer.Frontiers in oral health · 2025Review
- Review
- p53 target ANKRA2 cooperates with RFX7 to regulate tumor suppressor genes.Cell death discovery · 2024Article
- NUP37 promotes the proliferation and invasion of glioma cells through DNMT1-mediated methylation.Cell death discovery · 2024Article
- Identification of the Antigens Recognised by Colorectal Cancer Patients Using Sera from Patients Who Exhibit a Crohn's-like Lymphoid Reaction.Biomolecules · 2022Article
- Molecular drivers of oral cavity squamous cell carcinoma in non-smoking and non-drinking patients: what do we know so far?Oncology reviews · 2022Article
- Identification of Co-Expression Modules and Genes Associated With Tumor Progression in Oral Squamous Cell Carcinoma.Pathology oncology research : POR · 2022Article
- Nucleoporin 37 promotes the cell proliferation, migration, and invasion of gastric cancer through activating the PI3K/AKT/mTOR signaling pathway.In vitro cellular & developmental biology. Animal · 2021Article
- Significantly high expression of NUP37 leads to poor prognosis of glioma patients by promoting the proliferation of glioma cells.Cancer medicine · 2021Article
- Next-generation sequencing reveals novel mutations in a collision tumor of glioblastoma and meningioma.CNS oncology · 2021Article
- Article
- TAF1L promotes development of oral squamous cell carcinoma via decreasing autophagy-dependent apoptosis.International journal of biological sciences · 2020Article
- Overexpression ofJournal of Cancer · 2019Article
- Biomarkers: paving stones on the road towards the personalized precision medicine for oral squamous cell carcinoma.BMC cancer · 2018Review
- NUP37, a positive regulator of YAP/TEAD signaling, promotes the progression of hepatocellular carcinoma.Oncotarget · 2017Article
- Contribution of LATS1 and LATS2 promoter methylation in OSCC development.Journal of cell communication and signaling · 2017Article
- Article
- Phenotype specific analyses reveal distinct regulatory mechanism for chronically activated p53.PLoS genetics · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe accumulation of somatic mutations in genes and molecular pathways is a major factor in the evolution of oral squamous cell carcinoma (OSCC), which sparks studies to identify somatic mutations with clinical potentials. Recently, massively parallel sequencing technique has started to revolutionize biomedical studies, due to the rapid increase in its throughput and drop in cost. Hence sequencing of whole transcriptome (RNA-Seq) becomes a superior approach in cancer studies, which enables the detection of somatic mutations and accurate measurement of gene expression simultaneously.
methodsWe used RNA-Seq data from tumor and matched normal samples to investigate somatic mutation spectrum in OSCC.
resultsBy applying a sophisticated bioinformatic pipeline, we interrogated two tumor samples and their matched normal tissues and identified 70,472 tumor somatic mutations in protein-coding regions. We further identified 515 significantly mutated genes (SMGs) and 156 tumor-specific disruptive genes (TDGs), with six genes in both sets, including ANKRA2, GTF2H5, STOML1, NUP37, PPP1R26, and TAF1L. Pathway analysis suggested that SMGs were enriched in cell adhesion pathways, which are frequently indicated in tumor development. We also found that SMGs tend to be differentially expressed between tumors and normal tissues, implying a regulatory role of accumulation of genetic aberrations in these genes.
conclusionsOur finding of known tumor genes proves of the utility of RNA-Seq in mutation screening, and functional analysis of genes detected here would help understand the molecular mechanism of OSCC.
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