BRCA1 promoter methylation associated with poor survival in Chinese patients with sporadic breast cancer

被引:23
作者
Chen, Yanglin [2 ]
Zhou, Jing [2 ]
Xu, Ye [1 ]
Li, Zhaosheng [1 ]
Wen, Xianzi [2 ]
Yao, Lihua [1 ]
Xie, Yuntao [1 ]
Deng, Dajun [2 ]
机构
[1] Peking Univ, Sch Oncol, Beijing Canc Hosp & Inst,Breast Ctr, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100871, Peoples R China
[2] Peking Univ, Sch Oncol, Beijing Canc Hosp & Inst,Etiol Lab, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100871, Peoples R China
关键词
TUMOR-SUPPRESSOR GENES; HYPERMETHYLATION; REPAIR; WOMEN;
D O I
10.1111/j.1349-7006.2009.01225.x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Transcriptional inactivation of breast cancer gene 1 (BRCA1) by DNA methylation is a frequent event in sporadic breast cancers. To investigate whether BRCA1 methylation is associated with survival in Chinese patients with sporadic breast cancer, BRCA1 methylation was determined using methylation specific PCR in 536 sporadic breast cancers. Survival curves for patients with methylated and unmethylated BRCA1 were compared using the log-rank tests. Twenty-six percent (139/536) of patients exhibited BRCA1 methylation in their tumors. The degree of BRCA1 methylation was correlated with clinical stages of breast cancer, but was not significant. Patients with BRCA1 methylated tumors had a significantly worse 5-year disease-free survival (DFS) and 5-year disease-specific survival (DSS) than did patients with unmethylated tumors (DFS: 73.2% vs 82.6%, P = 0.045; DSS 80.5% vs 87%, P = 0.038, two-sided). In conclusions, BRCA1 methylation is a frequent event in breast cancer and is associated with poor clinical outcome in Chinese women with breast cancer. (Cancer Sci 2009; 100: 1663-1667).
引用
收藏
页码:1663 / 1667
页数:5
相关论文
共 25 条
[1]   Aberrant CpG-island methylation has non-random and tumour-type-specific patterns [J].
Costello, JF ;
Frühwald, MC ;
Smiraglia, DJ ;
Rush, LJ ;
Robertson, GP ;
Gao, X ;
Wright, FA ;
Feramisco, JD ;
Peltomäki, P ;
Lang, JC ;
Schuller, DE ;
Yu, L ;
Bloomfield, CD ;
Caligiuri, MA ;
Yates, A ;
Nishikawa, R ;
Huang, HJS ;
Petrelli, NJ ;
Zhang, XL ;
O'Dorisio, MS ;
Held, WA ;
Cavenee, WK ;
Plass, C .
NATURE GENETICS, 2000, 24 (02) :132-138
[2]  
Cuiju W, 2004, J PATHOL, V202, P215
[3]  
Eads Cindy A, 2002, Methods Mol Biol, V200, P71
[4]   Promoter hypermethylation and BRCA1 inactivation in sporadic breast and ovarian tumors [J].
Esteller, M ;
Silva, JM ;
Dominguez, G ;
Bonilla, F ;
Matias-Guiu, X ;
Lerma, E ;
Bussaglia, E ;
Prat, J ;
Harkes, IC ;
Repasky, EA ;
Gabrielson, E ;
Schutte, M ;
Baylin, SB ;
Herman, JG .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2000, 92 (07) :564-569
[5]   CpG island hypermethylation and tumor suppressor genes: a booming present, a brighter future [J].
Esteller, M .
ONCOGENE, 2002, 21 (35) :5427-5440
[6]  
Esteller M, 2001, CANCER RES, V61, P3225
[7]  
Gordon S, 2001, AM J PATHOL, V158, P1121
[8]   Mechanisms of disease: Gene silencing in cancer in association with promoter hypermethylation [J].
Herman, JG ;
Baylin, SB .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (21) :2042-2054
[9]   Methylation-specific PCR: A novel PCR assay for methylation status of CpG islands [J].
Herman, JG ;
Graff, JR ;
Myohanen, S ;
Nelkin, BD ;
Baylin, SB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (18) :9821-9826
[10]  
HUTTER RVP, 1990, CANCER-AM CANCER SOC, V66, P1363, DOI 10.1002/1097-0142(19900915)66:14+<1363::AID-CNCR2820661411>3.0.CO