ArticleOncotarget2015
Nuclear localization of epidermal growth factor receptor (EGFR) in ameloblastomas.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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, 16 citations in OpenAlex.
- Extracellular cell matrix stiffness-driven drug resistance of breast cancer cells via EGFR activation.Mechanobiology in medicine · 2023Article
- Significance of EGFR investigation in odontogenic keratocyst: a narrative review.Molecular biology reports · 2023Review
- Epidermal Growth Factor Receptor and Its Role in Pancreatic Cancer Treatment Mediated by Nanoparticles.International journal of nanomedicine · 2019Review
- Translocation of Epidermal Growth Factor (EGF) to the nucleus has distinct kinetics between adipose tissue-derived mesenchymal stem cells and a mesenchymal cancer cell lineage.Journal of structural biology · 2018Article
- Analysis of origin and protein-protein interaction maps suggests distinct oncogenic role of nuclear EGFR during cancer evolution.Journal of Cancer · 2017Article
- Laser-emission imaging of nuclear biomarkers for high-contrast cancer screening and immunodiagnosis.Nature biomedical engineering · 2017Article
- Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis.Current oral health reports · 2016Article
- Inner nuclear membrane localization of epidermal growth factor receptor (EGFR) in spontaneous canine model of invasive micropapillary carcinoma of the mammary gland.Pathology, research and practice · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAmeloblastoma is a locally invasive neoplasm often associated with morbidity and facial deformities, showing increased Epidermal Growth Factor Receptor (EGFR) expression. Inhibition of EGFR was suggested as a treatment option for a subset of ameloblastomas. However, there are resistance mechanisms that impair anti-EGFR therapies. One important resistance mechanism for EGFR-inhibition is the EGFR nuclear localization, which activates genes responsible for its mitogenic effects, such as Cyclin D1.
methodsWe assessed EGFR nuclear localization in encapsulated (unicystic, n = 3) and infiltrative (multicystic, n = 11) ameloblastomas and its colocalization with Cyclin D1 by using anti-EGFR and anti-lamin B1 double labeling immunofluorescence analyzed by confocal microscopy. Oral inflammatory fibrous hyperplasia and oral squamous cell carcinoma samples were used for comparison.
resultsTwelve cases of ameloblastoma exhibited nuclear EGFR colocalization with lamin B1. This positive staining was mainly observed in the ameloblast-like cells. The EGFR nuclear localization was also observed in control samples. In addition, nuclear EGFR colocalized with Cyclin D1 in ameloblastomas.
conclusionsNuclear EGFR occurs in ameloblastomas in association with Cyclin D1 expression, which is important in terms of tumor biology clarification and raises a concern about anti-EGFR treatment resistance in ameloblastomas.
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Registered trials
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