Amplification and overexpression of E2F3 in human bladder cancer

被引:135
作者
Feber, A
Clark, J
Goodwin, G
Dodson, AR
Smith, PH
Fletcher, A
Edwards, S
Flohr, P
Falconer, A
Roe, T
Kovacs, G
Dennis, N
Fisher, C
Wooster, R
Huddart, R
Foster, CS
Cooper, CS [1 ]
机构
[1] Inst Canc Res, Sect Mol Carcinogenesis & Male Urol Canc Res, Sutton SM2 5NG, Surrey, England
[2] Univ Liverpool, Dept Pathol & Mol Genet, Liverpool L69 3GA, Merseyside, England
[3] Royal Marsden NHS Trust, Sutton SM2 5PT, Surrey, England
[4] Heidelberg Univ, Heidelberg Klinikum, D-69120 Heidelberg, Germany
[5] Royal Marsden NHS Trust, London SW3 6JJ, England
[6] Sanger Ctr, Cambridge CB10 1SA, England
基金
英国医学研究理事会;
关键词
E2F3; gene; bladder cancer; 6p22; amplicon;
D O I
10.1038/sj.onc.1207274
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We demonstrate that, in human bladder cancer, amplification of the E2F3 gene, located at 6p22, is associated with overexpression of its encoded mRNA transcripts and high levels of expression of E2F3 protein. Immunohistochemical analyses of E2F3 protein levels have established that around one-third (33/101) of primary transitional cell carcinomas of the bladder overexpress nuclear E2F3 protein, with the proportion of tumours containing over-expressed nuclear E2F3 increasing with tumour stage and grade. When considered together with the established role of E2F3 in cell cycle progression, these results suggest that the E2F3 gene represents a candidate bladder cancer oncogene that is activated by DNA amplification and overexpression.
引用
收藏
页码:1627 / 1630
页数:4
相关论文
共 30 条
[1]  
Bruch J, 2000, CANCER RES, V60, P4526
[2]   Frequent activating mutations of FGFR3 in human bladder and cervix carcinomas [J].
Cappellen, D ;
De Oliveira, C ;
Ricol, D ;
de Medina, SGD ;
Bourdin, J ;
Sastre-Garau, X ;
Chopin, D ;
Thiery, JP ;
Radvanyi, F .
NATURE GENETICS, 1999, 23 (01) :18-20
[3]   Fusion of splicing factor genes PSF and NonO (p54(nrb)) to the TFE3 gene in papillary renal cell carcinoma [J].
Clark, J ;
Lu, YJ ;
Sidhar, SK ;
Parker, C ;
Gill, S ;
Smedley, D ;
Hamoudi, R ;
Linehan, WM ;
Shipley, J ;
Cooper, CS .
ONCOGENE, 1997, 15 (18) :2233-2239
[4]   Identification of amplified and expressed genes in breast cancer by comparative hybridization onto microarrays of randomly selected cDNA clones [J].
Clark, J ;
Edwards, S ;
John, M ;
Flohr, P ;
Gordon, T ;
Maillard, K ;
Giddings, I ;
Brown, C ;
Bagherzadeh, A ;
Campbell, C ;
Shipley, J ;
Wooster, R ;
Cooper, CS .
GENES CHROMOSOMES & CANCER, 2002, 34 (01) :104-114
[5]  
Cornford PA, 2000, CANCER RES, V60, P7099
[6]   Peculiar structure and location of 9p21 homozygous deletion breakpoints in human cancer cells [J].
Florl, AR ;
Schulz, WA .
GENES CHROMOSOMES & CANCER, 2003, 37 (02) :141-148
[7]   Identification of E-box factor TFE3 as a functional partner for the E2F3 transcription factor [J].
Giangrande, PH ;
Hallstrom, TC ;
Tunyaplin, C ;
Calame, K ;
Nevins, JR .
MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (11) :3707-3720
[8]  
Hovey RM, 1998, CANCER RES, V58, P3555
[9]   Gene expression phenotypic models that predict the activity of oncogenic pathways [J].
Huang, E ;
Ishida, S ;
Pittman, J ;
Dressman, H ;
Bild, A ;
Kloos, M ;
D'Amico, M ;
Pestell, RG ;
West, M ;
Nevins, JR .
NATURE GENETICS, 2003, 34 (02) :226-230
[10]  
Humbert PO, 2000, GENE DEV, V14, P690