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
[71]   Arrest of the cell cycle by the tumour-suppressor BRCA1 requires the CDK-inhibitor p21(WAF1/CiP1) [J].
Somasundaram, K ;
Zhang, HB ;
Zeng, YX ;
Houvras, Y ;
Peng, Y ;
Zhang, HX ;
Wu, GS ;
Licht, JD ;
Weber, BL ;
ElDeiry, WS .
NATURE, 1997, 389 (6647) :187-190
[72]   Brca2 is required for embryonic cellular proliferation in the mouse [J].
Suzuki, A ;
delaPompa, JL ;
Hakem, R ;
Elia, A ;
Yoshida, R ;
Mo, R ;
Nishina, H ;
Chuang, T ;
Wakeham, A ;
Itie, A ;
Koo, W ;
Billia, P ;
Ho, A ;
Fukumoto, M ;
Hui, CC ;
Mak, TW .
GENES & DEVELOPMENT, 1997, 11 (10) :1242-1252
[73]  
TOKUNAGA M, 1979, J NATL CANCER I, V62, P1347
[74]   INCIDENCE OF FEMALE BREAST-CANCER AMONG ATOMIC-BOMB SURVIVORS, HIROSHIMA AND NAGASAKI, 1950-1980 [J].
TOKUNAGA, M ;
LAND, CE ;
YAMAMOTO, T ;
ASANO, M ;
TOKUOKA, S ;
EZAKI, H ;
NISHIMORI, I .
RADIATION RESEARCH, 1987, 112 (02) :243-272
[75]   INCIDENCE OF FEMALE BREAST-CANCER AMONG ATOMIC-BOMB SURVIVORS, 1950-1985 [J].
TOKUNAGA, M ;
LAND, CE ;
TOKUOKA, S ;
NISHIMORI, I ;
SODA, M ;
AKIBA, S .
RADIATION RESEARCH, 1994, 138 (02) :209-223
[76]  
Tsai YC, 1996, CANCER RES, V56, P402
[77]   Targeted disruption of the Rad51 gene leads to lethality in embryonic mice [J].
Tsuzuki, T ;
Fujii, Y ;
Sakumi, K ;
Tominaga, Y ;
Nakao, K ;
Sekiguchi, M ;
Matsushiro, A ;
Yoshimura, Y ;
Morita, T .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (13) :6236-6240
[78]   Absence of Brca2 causes genome instability by chromosome breakage and loss associated with centrosome amplification [J].
Tutt, A ;
Gabriel, A ;
Bertwistle, D ;
Connor, F ;
Paterson, H ;
Peacock, J ;
Ross, G ;
Ashworth, A .
CURRENT BIOLOGY, 1999, 9 (19) :1107-1110
[79]   Differential subcellular localization, expression and biological toxicity of BRCA1 and the splice variant BRCA1-Delta 11b [J].
Wilson, CA ;
Payton, MN ;
Elliott, GS ;
Buaas, FW ;
Cajulis, EE ;
Grosshans, D ;
Ramos, L ;
Reese, DM ;
Slamon, DJ ;
Calzone, FJ .
ONCOGENE, 1997, 14 (01) :1-16
[80]   Second cancers following pediatric Hodgkin's disease [J].
Wolden, SL ;
Lamborn, KR ;
Cleary, SF ;
Tate, DJ ;
Donaldson, SS .
JOURNAL OF CLINICAL ONCOLOGY, 1998, 16 (02) :536-544