Mutational analysis of the p73 gene in human breast cancers

被引:0
|
作者
Shishikura, T
Ichimiya, S
Ozaki, T
Nimura, Y
Kageyama, H
Nakamura, Y
Sakiyama, S
Miyauchi, M
Yamamoto, N
Suzuki, M
Nakajima, N
Nakagawara, A
机构
[1] Chiba Canc Ctr, Res Inst, Div Biochem, Chuoh Ku, Chiba 2608717, Japan
[2] Chiba Canc Ctr, Div Breast Surg, Chiba 2608717, Japan
[3] Chiba Univ, Sch Med, Dept Surg 1, Chiba 280, Japan
关键词
D O I
10.1002/(SICI)1097-0215(19990621)84:3<321::AID-IJC21>3.0.CO;2-S
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
In primary breast cancer, mutations of the p53 tumor suppressor gene lead to loss of growth-suppressive properties and poor outcome. Recently, a p53-related gene, termed p73, has been cloned and its gene product possesses a function similar to p53. p73 has been mapped at chromosome 1p36.3, a region frequently deleted in breast cancer, neuroblastoma and other malignancies. To elucidate the functional significance of p73 in the oncogenesis of breast cancer, we have studied genetic alterations of p73 in tissue specimens obtained from 87 patients with primary breast cancer. Thirteen percent of informative cases showed loss of heterozygosity (LOH) at the p73 gene. However, there was no correlation between the p73 LOH and clinical features such as histopathological types, metastatic behavior or expression of estrogen or progesterone receptor. The levels of p73 transcript in primary breast cancer were not significantly different from those in normal breast tissue. Moreover, PCR-SSCP analysis failed to detect any missense or frameshift mutations in the p73 gene. Our observations suggest that allelic loss, expression levels and mutations of the p73 gene may not contribute to oncogenesis of primary breast cancers. Int. J. Cancer (Pred. Oncol.) 84:321-325, 1999. (C) 1999 Wiley-Liss, Inc.
引用
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页码:321 / 325
页数:5
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