赫拉
神经母细胞瘤RAS病毒癌基因同源物
生物
突变
成纤维细胞生长因子受体3
癌症研究
基因
突变体
MAPK/ERK通路
癌变
分子肿瘤学
遗传学
克拉斯
成纤维细胞生长因子
信号转导
受体
作者
Adel Jebar,Carolyn D. Hurst,Darren C. Tomlinson,C.F. Johnston,Claire Taylor,Margaret A. Knowles
出处
期刊:Oncogene
[Springer Nature]
日期:2005-05-09
卷期号:24 (33): 5218-5225
被引量:313
标识
DOI:10.1038/sj.onc.1208705
摘要
Fibroblast growth factor receptor 3 (FGFR3) mutations are frequent in superficial urothelial cell carcinoma (UCC). Ras gene mutations are also found in UCC. As oncogenic activation of both FGFR3 and Ras is predicted to result in stimulation of the mitogen-activated protein kinase (MAPK) pathway, we hypothesized that these might be mutually exclusive events. HRAS mutation has been widely studied in UCC, but all three Ras gene family members have not been screened for mutation in the same sample series. We screened 98 bladder tumours and 31 bladder cell lines for mutations in FGFR3, HRAS, NRAS and KRAS2. FGFR3 mutations were present in 54 tumours (55%) and three cell lines (10%), and Ras gene mutations in 13 tumours (13%) and four cell lines (13%). These included mutations in all three Ras genes; ten in HRAS, four in KRAS2 and four in NRAS and these were not associated with either tumour grade or stage. In no cases were Ras and FGFR3 mutation found together. This mutual exclusion suggests that FGFR3 and Ras gene mutation may represent alternative means to confer the same phenotype on UCC cells. If these events have biological equivalence, Ras mutant invasive UCC may represent a novel subgroup.
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