Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/6102
Title: Incidence of fibroblast growth factor receptor 3 gene (FGFR3) A248C, S249C, G372C, and T375C mutations in bladder cancer
Authors: Dodurga, Yavuz
Tataroglu, C.
Kesen, Z.
Satiroglu-Tufan, Naciye Lale
Keywords: Bladder carcinoma
DNA sequencing
Fibroblast growth factor receptor 3
Mutation
PCR
Transitional cell carcinoma
fibroblast growth factor receptor 3
adult
aged
article
bladder cancer
bladder carcinogenesis
bladder carcinoma
cancer incidence
codon
controlled study
DNA sequence
exon
female
heterozygosity
human
major clinical study
male
missense mutation
polymerase chain reaction
restriction fragment length polymorphism
thanatophoric dysplasia mutation
transitional cell carcinoma
Adult
Aged
Aged, 80 and over
Carcinoma, Transitional Cell
Codon
Exons
Female
Genetic Association Studies
Genotype
Humans
Incidence
Male
Middle Aged
Neoplasm Staging
Receptor, Fibroblast Growth Factor, Type 3
Thanatophoric Dysplasia
Urinary Bladder Neoplasms
Abstract: Bladder cancer is the most frequent cancer of the urinary system. Fibroblast growth factor receptors (FGFR) belong to the tyrosine kinase family and have important roles in cell differentiation and proliferation and embryogenesis. FGFR3 is located on chromosome 4p16.3, and missense mutations of FGFR3 are associated with autosomal dominant human skeletal disorders and have some oncogenic effects. We examined the incidence of FGFR3 thanatophoric dysplasia mutations located in exon 7, A248C and S249C, and in exon 10, G372C and T375C, and their correlation with clinical-pathological parameters in bladder carcinoma patients. Fifty-six paraffin-embedded specimens of transitional cell carcinoma of the urinary bladder were included in this study. Analysis of FGFR3 thanatophoric dysplasia mutations located in exon 7, A248C and S249C, and in exon 10, G372C and T375C, was performed by PCR- restriction fragment length polymorphism (RFLP) analysis and DNA sequencing. FGFR3 thanatophoric dysplasia mutations located in exon 7, A248C and S249C, and in exon 10, G372C and T375C, were detected in 33 of the 56 patients (heterozygous mutant). Among the 56 transitional cell carcinomas, missense point mutations were detected in seven of them at codon A248C, 28 of them at codon S249C, and three of them at codon T375C, similar to data from previous reports. When the results of the FGFR3 thanatophoric dysplasia mutations located in exon 7, A248C and S249C and in exon 10, G372C and T375C, were analyzed one by one or as a group, despite the findings of previous research reports, our data suggest that these mutations are detected homogenously regardless of the tumor classification and tumor grade. © FUNPEC-RP.
URI: https://hdl.handle.net/11499/6102
https://doi.org/10.4238/vol10-1gmr923
ISSN: 1676-5680
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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