Kurose Keisuke, Gilley Kristie, Matsumoto Satoshi, Watson Peter H, Zhou Xiao-Ping, Eng Charis
Comprehensive Cancer Center, and the Division of Human Genetics, Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210, USA.
Nat Genet. 2002 Nov;32(3):355-7. doi: 10.1038/ng1013. Epub 2002 Oct 15.
We have recently shown that loss of heterozygosity of specific markers, including those at 10q23, 17p13-p15 and 16q24, can occur in the stromal and epithelial compartments of primary invasive breast carcinomas. Here, we demonstrate high frequencies of somatic mutations in TP53 (encoding tumor protein p53) and PTEN (encoding phosphate and tensin homolog) in breast neoplastic epithelium and stroma. Mutations in TP53 and PTEN are mutually exclusive in either compartment. In contrast, mutations in WFDC1 (16q24, encoding WAP four-disulfide core domain 1) occur with low frequency in the stroma.
我们最近发现，原发性浸润性乳腺癌的基质和上皮成分中可出现特定标志物的杂合性缺失，包括位于10q23、17p13 - p15和16q24的标志物。在此，我们证实在乳腺肿瘤上皮和基质中，TP53（编码肿瘤蛋白p53）和PTEN（编码磷酸酶和张力蛋白同源物）存在高频体细胞突变。TP53和PTEN的突变在任何一个成分中都是相互排斥的。相比之下，WFDC1（16q24，编码WAP四二硫键核心结构域1）的突变在基质中出现频率较低。
