ArticleOncogene2001
Loss of heterozygosity at 4p16.3 and mutation of FGFR3 in transitional cell carcinoma.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 107 citations in OpenAlex.
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- Validation of a Novel, Sensitive, and Specific Urine-Based Test for Recurrence Surveillance of Patients With Non-Muscle-Invasive Bladder Cancer in a Comprehensive Multicenter Study.Frontiers in genetics · 2019Article
- Systematic Review: Characteristics and Preclinical Uses of Bladder Cancer Cell Lines.Bladder cancer (Amsterdam, Netherlands) · 2018Article
- TACC3 transcriptionally upregulates E2F1 to promote cell growth and confer sensitivity to cisplatin in bladder cancer.Cell death & disease · 2018Article
- Kavalactone yangonin induces autophagy and sensitizes bladder cancer cells to flavokawain A and docetaxel via inhibition of the mTOR pathway.Journal of biomedical research · 2017Article
- A place for precision medicine in bladder cancer: targeting the FGFRs.Future oncology (London, England) · 2016Review
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- Muscle-invasive urothelial bladder cancer: an update on systemic therapy.Therapeutic advances in urology · 2015Review
- Is 5´-AMP-Activated Protein Kinase Both Jekyll and Hyde in Bladder Cancer?International neurourology journal · 2015Review
- Activating FGFR3 mutations cause mild hyperplasia in human skin, but are insufficient to drive benign or malignant skin tumors.Cell cycle (Georgetown, Tex.) · 2014Article
- FGFR3 has tumor suppressor properties in cells with epithelial phenotype.Molecular cancer · 2013Article
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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
4p16.3 has previously been identified as a region of non-random LOH in transitional cell carcinoma, suggesting the presence of a tumour suppressor gene. One candidate within this region is fibroblast growth factor receptor 3 (FGFR3). Germline mutations in FGFR3 are known to cause several autosomal dominant skeletal dysplasias, the severity of which depends on the position and nature of the mutation in the protein. We investigated the frequency and nature of FGFR3 mutations in a panel of transitional cell carcinomas and cell lines and studied the possible link between mutation and loss of heterozygosity (LOH) on 4p16.3. FGFR3 coding sequence from 63 transitional cell carcinomas (TCC) of various stages and grades, and 18 cell lines was analysed by fluorescent SSCP. Samples with abnormal migration patterns were sequenced to identify the mutation or polymorphism. Thirty-one of the 63 tumours had previously been assessed to have LOH at 4p16.3. Twenty-six of the 63 tumours (41%) and 4/18 (22%) of the cell lines had missense mutations in FGFR3. All mutations detected in our panel have been reported in the germline where all apart from one cause lethal conditions. One tumour contained K652Q which has recently been identified in less severe cases of skeletal dysplasia. Tumours with and without LOH at 4p16.3 had mutations in FGFR3 suggesting that these two events are not causally linked. The frequency of FGFR3 mutation indicates that this protein plays an important role in TCC.
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