Role of BRCA gene dysfunction in breast and ovarian cancer predisposition

被引:60
作者
Scully, R
机构
[1] Dana Farber Canc Inst, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Boston, MA 02115 USA
关键词
breast cancer; DNA repair; homologous recombination; ovarian cancer; tumor suppressor genes;
D O I
10.1186/bcr76
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tumor suppressor genes that perform apparently generic cellular functions nonetheless cause tissue-specific syndromes in the human population when they are mutated in the germline. The two major hereditary breast/ovarian cancer predisposition genes, BRCA1 and BRCA2, appear to participate in a common pathway that is involved in the control of homologous recombination and in the maintenance of genomic integrity. How might such functions translate into the specific suppression of cancers of the breast and ovarian epithelia? Recent advances in the study of BRCA1 and BRCA2, discussed herein, have provided new opportunities to address this question.
引用
收藏
页码:324 / 330
页数:7
相关论文
共 88 条
[1]  
Breast Canc Linkage Consortium, 1999, JNCI-J NATL CANCER I, V91, P1310
[2]   Transcriptional activation by BRCA1 [J].
Chapman, MS ;
Verma, IM .
NATURE, 1996, 382 (6593) :678-679
[3]   Stable interaction between the products of the BRCA1 and BRCA2 tumor suppressor genes in mitotic and meiotic cells [J].
Chen, JJ ;
Silver, DP ;
Walpita, D ;
Cantor, SB ;
Gazdar, AF ;
Tomlinson, G ;
Couch, FJ ;
Weber, BL ;
Ashley, T ;
Livingston, DM ;
Scully, R .
MOLECULAR CELL, 1998, 2 (03) :317-328
[4]  
Chen JJ, 1999, CANCER RES, V59, p1752S
[5]   Mammary epithelial stem cells: Our current understanding [J].
Chepko, G ;
Smith, GH .
JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA, 1999, 4 (01) :35-52
[6]  
COLLINS N, 1995, ONCOGENE, V10, P1673
[7]   Tumorigenesis and a DNA repair defect in mice with a truncating Brca2 mutation [J].
Connor, F ;
Bertwistle, D ;
Mee, PJ ;
Ross, GM ;
Swift, S ;
Grigorieva, E ;
Tybulewicz, VLJ ;
Ashworth, A .
NATURE GENETICS, 1997, 17 (04) :423-430
[8]   The importance of repairing stalled replication forks [J].
Cox, MM ;
Goodman, MF ;
Kreuzer, KN ;
Sherratt, DJ ;
Sandler, SJ ;
Marians, KJ .
NATURE, 2000, 404 (6773) :37-41
[9]  
Cressman VL, 1999, MOL CELL BIOL, V19, P7061
[10]  
Cressman VL, 1999, CELL GROWTH DIFFER, V10, P1