Frequent somatic mutations in PTEN and TP53 are mutually exclusive in the stroma of breast carcinomas
- 15 October 2002
- journal article
- Published by Springer Nature in Nature Genetics
- Vol. 32 (3) , 355-357
- https://doi.org/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.Keywords
This publication has 6 references indexed in Scilit:
- Loss of heterozygosity analysis: Practically and conceptually flawed?Genes, Chromosomes and Cancer, 2002
- Genetic model of multi-step breast carcinogenesis involving the epithelium and stroma: clues to tumour-microenvironment interactionsHuman Molecular Genetics, 2001
- Regulation of PTEN Transcription by p53Published by Elsevier ,2001
- The WFDC1 gene encoding ps20 localizes to 16q24, a region of LOH in multiple cancersMammalian Genome, 2000
- Altered PTEN Expression as a Diagnostic Marker for the Earliest Endometrial PrecancersJNCI Journal of the National Cancer Institute, 2000
- Immunohistochemical Evidence of Loss of PTEN Expression in Primary Ductal Adenocarcinomas of the BreastThe American Journal of Pathology, 1999