Frequent somatic mutations in PTEN and TP53 are mutually exclusive in the stroma of breast carcinomas
K Kurose, K Gilley, S Matsumoto, PH Watson… - Nature …, 2002 - nature.com
K Kurose, K Gilley, S Matsumoto, PH Watson, XP Zhou, C Eng
Nature genetics, 2002•nature.comWe 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 …
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 …
Abstract
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.
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