Frequent somatic mutations in PTEN and TP53 are mutually exclusive in the stroma of breast carcinomas

Keisuke Kurose; Kristie Gilley; Satoshi Matsumoto; Peter H Watson; Xiao-Ping Zhou; Charis Eng

doi:10.1038/ng1013

Frequent somatic mutations in PTEN and TP53 are mutually exclusive in the stroma of breast carcinomas

Nat Genet. 2002 Nov;32(3):355-7. doi: 10.1038/ng1013. Epub 2002 Oct 15.

Authors

Keisuke Kurose¹, Kristie Gilley, Satoshi Matsumoto, Peter H Watson, Xiao-Ping Zhou, Charis Eng

Affiliation

¹ Comprehensive Cancer Center, and the Division of Human Genetics, Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210, USA.

PMID: 12379854
DOI: 10.1038/ng1013

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.

Publication types

Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

MeSH terms

Base Sequence
Breast Neoplasms / genetics*
Breast Neoplasms / pathology
Epithelium / pathology
Exons
Gene Silencing
Genes, p53*
Humans
Loss of Heterozygosity
Molecular Sequence Data
Mutation*
Neoplasm Invasiveness
PTEN Phosphohydrolase
Phosphoric Monoester Hydrolases / genetics*
Protein Structure, Tertiary
Proteins / genetics
Tumor Suppressor Proteins / genetics*

Substances

Proteins
Tumor Suppressor Proteins
WFDC1 protein, human
Phosphoric Monoester Hydrolases
PTEN Phosphohydrolase
PTEN protein, human