Fibroblast growth factor receptor 3 (FGFR3) -: Analyses of the S249C mutation and protein expression in primary cervical carcinomas

被引:12
作者
Dai, HY
Holm, R
Kristensen, GB
Abeler, VM
Borresen-Dale, AL
Helland, Å [1 ]
机构
[1] Norwegian Radium Hosp, Inst Canc Res, Dept Genet, N-0310 Oslo, Norway
[2] Norwegian Radium Hosp, Inst Canc Res, Dept Pathol, N-0310 Oslo, Norway
[3] Norwegian Radium Hosp, Inst Canc Res, Dept Gynaecol Oncol, N-0310 Oslo, Norway
来源
ANALYTICAL CELLULAR PATHOLOGY | 2001年 / 23卷 / 02期
关键词
FGFR3; S249C mutation; IHC; cervical carcinomas; FGFR3 protein levels;
D O I
10.1155/2001/521873
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Fibroblast growth factor receptor 3 (FGFR3) seems to play an inhibitory role in bone development, as activating mutations in the gene underlie disorders such as achondroplasia and thanatophoric dysplasia. Findings from multiple myeloma (MM) indicate that FGFR3 also can act as an oncogene, and mutation of codon 249 in the fibroblast growth factor receptor 3 (FGFR3) gene was recently detected in 3/12 primary cervical carcinomas. We have analysed 91 cervical carcinomas for this specific S249C mutation using amplification created restriction site methodology (ACRS), and detected no mutations. Immunohistochemistry was performed on 73 of the tumours. Reduced protein staining was seen in 43 (58.8%) samples. Six of the tumours (8.2%) revealed increased protein staining compared with normal cervical tissue. These patients had a better prognosis than those with reduced or normal levels, although not statistically significant. This report weakens the hypothesis of FGFR3 as an oncogene of importance in cervical carcinomas.
引用
收藏
页码:45 / 49
页数:5
相关论文
共 21 条
[1]   THE FGF FAMILY OF GROWTH-FACTORS AND ONCOGENES [J].
BASILICO, C ;
MOSCATELLI, D .
ADVANCES IN CANCER RESEARCH, 1992, 59 :115-165
[2]   PREVALENCE OF HUMAN PAPILLOMAVIRUS IN CERVICAL-CANCER - A WORLDWIDE PERSPECTIVE [J].
BOSCH, FX ;
MANOS, MM ;
MUNOZ, N ;
SHERMAN, M ;
JANSEN, AM ;
PETO, J ;
SCHIFFMAN, MH ;
MORENO, V ;
KURMAN, R ;
SHAH, KV ;
ALIHONOU, E ;
BAYO, S ;
MOKHTAR, HC ;
CHICAREON, S ;
DAUDT, A ;
DELOSRIOS, E ;
GHADIRIAN, P ;
KITINYA, JN ;
KOULIBALY, M ;
NGELANGEL, C ;
TINTORE, LMP ;
RIOSDALENZ, JL ;
SARJADI ;
SCHNEIDER, A ;
TAFUR, L ;
TEYSSIE, AR ;
ROLON, PA ;
TORROELLA, M ;
TAPIA, AV ;
WABINGA, HR ;
ZATONSKI, W ;
SYLLA, B ;
VIZCAINO, P ;
MAGNIN, D ;
KALDOR, J ;
GREER, C ;
WHEELER, C .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1995, 87 (11) :796-802
[3]   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
[4]   The t(4;14) translocation in myeloma dysregulates both FGFR3 and a novel gene, MMSET, resulting in IgH/MMSET hybrid transcripts [J].
Chesi, M ;
Nardini, E ;
Lim, RSC ;
Smith, KD ;
Kuehl, WM ;
Bergsagel, PL .
BLOOD, 1998, 92 (09) :3025-3034
[5]   Frequent translocation t(4;14)(p16.3;q32.3) in multiple myeloma is associated with increased expression and activating mutations of fibroblast growth factor receptor 3 [J].
Chesi, M ;
Nardini, E ;
Brents, LA ;
Schrock, E ;
Ried, T ;
Kuehl, WM ;
Bergsagel, PL .
NATURE GENETICS, 1997, 16 (03) :260-264
[6]   Fibroblast growth factor receptor 3 is a negative regulator of bone growth [J].
Deng, CX ;
WynshawBoris, A ;
Zhou, F ;
Kuo, A ;
Leder, P .
CELL, 1996, 84 (06) :911-921
[7]   APPLICATION OF NATURAL AND AMPLIFICATION CREATED RESTRICTION SITES FOR THE DIAGNOSIS OF PKU MUTATIONS [J].
EIKEN, HG ;
ODLAND, E ;
BOMAN, H ;
SKJELKVALE, L ;
ENGEBRETSEN, LF ;
APOLD, J .
NUCLEIC ACIDS RESEARCH, 1991, 19 (07) :1427-1430
[8]  
Goldfarb Mitchell, 1996, Cytokine and Growth Factor Reviews, V7, P311, DOI 10.1016/S1359-6101(96)00039-1
[9]   ISOLATION OF AN ADDITIONAL MEMBER OF THE FIBROBLAST GROWTH-FACTOR RECEPTOR FAMILY, FGFR-3 [J].
KEEGAN, K ;
JOHNSON, DE ;
WILLIAMS, LT ;
HAYMAN, MJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (04) :1095-1099
[10]   A Lys644Glu substitution in fibroblast growth factor receptor 3 (FGFR3) causes dwarfism in mice by activation of STATs and ink4 cell cycle inhibitors [J].
Li, CL ;
Chen, L ;
Iwata, T ;
Kitagawa, M ;
Fu, XY ;
Deng, CX .
HUMAN MOLECULAR GENETICS, 1999, 8 (01) :35-44