ArticleCell cycle (Georgetown, Tex.)2014
Activating FGFR3 mutations cause mild hyperplasia in human skin, but are insufficient to drive benign or malignant skin tumors.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Human papillomavirus and the landscape of secondary genetic alterations in oral cancers.Genome research · 2019Trial
- Identification of activating hotspot mutations in acrochordons through next-generation sequencing.JAAD international · 2025Article
- Inflammatory Mediators Suppress FGFR2 Expression in Human Keratinocytes to Promote Inflammation.Molecular and cellular biology · 2024Article
- Higher rates of non-skeletal complications and greater healthcare needs in achondroplasia compared to the general UK population: a matched cohort study using the CPRD database.Orphanet journal of rare diseases · 2023Article
- Leser-Trelat sign: Eruptive seborrheic keratoses and primary lung adenocarcinomas with an epidermal growth factor receptor mutation.JAAD case reports · 2023Article
- Targeting receptor tyrosine kinase signaling: Avenues in the management of cutaneous squamous cell carcinoma.iScience · 2023Review
- Transcriptomic Analysis of Human Keratinocytes Treated withJournal of clinical medicine · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- AhRR methylation contributes to disease progression in urothelial bladder cancer.Cancer biomarkers : section A of Disease markers · 2022Article
- Mouse genetics identifies unique and overlapping functions of fibroblast growth factor receptors in keratinocytes.Journal of cellular and molecular medicine · 2020Article
- Review
- Seborrheic keratosis evolution into squamous cell carcinoma: A truly modified sun-related tumor? A case report and review of the literature.Dermatology reports · 2019Article
- Single-Cell Transcriptomics Reveals Spatial and Temporal Turnover of Keratinocyte Differentiation Regulators.Frontiers in genetics · 2019Article
- Genomic Characterization of Upper-Tract Urothelial Carcinoma in Patients With Lynch Syndrome.JCO precision oncology · 2018Article
- Kinase Activity of Fibroblast Growth Factor Receptor 3 Regulates Activity of the Papillomavirus E2 Protein.Journal of virology · 2017Article
- Genetic alterations in seborrheic keratoses.Oncotarget · 2017Article
- Computational identification of microRNAs associated to both epithelial to mesenchymal transition and NGAL/MMP-9 pathways in bladder cancer.Oncotarget · 2016Article
- Evaluation of FGFR3 as a Therapeutic Target in Head and Neck Squamous Cell Carcinoma.Targeted oncology · 2016Article
- Article
- Fibroblast growth factor receptor 3 protein is overexpressed in oral and oropharyngeal squamous cell carcinoma.Cancer medicine · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor receptor 3 (FGFR3) activating mutations are drivers of malignancy in several human tissues, including bladder, lung, cervix, and blood. However, in skin, these mutations are associated predominantly with benign, common epidermal growths called seborrheic keratoses (SKs). How epidermis resists FGFR3 mediated transformation is unclear, but previous studies have suggested that FGFR3 activation in skin keratinocytes may serve a tumor-suppressive role by driving differentiation and antagonizing Ras signaling. To define the role of FGFR3 in human normal and neoplastic epidermis, and to directly test the hypothesis that FGFR3 antagonizes Ras, we engineered human skin grafts in vivo with mutant active FGFR3 or shRNA FGFR3 knockdown. We show that FGFR3 active mutants drive mild hyperproliferation, but are insufficient to support benign or malignant tumorigenesis, either alone, or in combination with G 1-S checkpoint release. This suggests that additional cell-intrinsic or stromal cues are required for formation of benign SKs with FGFR3 mutations. Further, FGFR3 activation does not alter the growth kinetics or differentiation status of engineered human epidermal SCCs driven by Ras, and FGFR3 protein itself is dispensable for Ras-driven SCC. To extend these findings to patients, we examined a uniquely informative human tumor in which SCC developed in continuity with a SK, raising the hypothesis that one of the tumors evolved from the other. However, mutational analysis from each tumor indicates that the overlapping SK and SCC evolved independently and supports our conclusion that FGFR3 activation is insufficient to drive SCC.
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Registered trials
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