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PMID: 11737885 Published · ppublish English Journal Article Review

PTEN deficiency: a role in mammary carcinogenesis.

Breast cancer research : BCR ·Vol. 3 ·No. 6 ·2001-00-00 ·Pages 356-60

Petrocelli T, Slingerland JM

Abstract

The PTEN gene is often mutated in primary human tumors and cell lines, but the low rate of somatic PTEN mutation in human breast cancer has led to debate over the role of this tumor suppressor in this disease. The involvement of PTEN in human mammary oncogenesis has been implicated from studies showing that germline PTEN mutation in Cowden disease predisposes to breast cancer, the frequent loss of heterozygosity at the PTEN locus, and reduced PTEN protein levels in sporadic breast cancers. To assay the potential contribution of PTEN loss in breast tumor promotion, Li et al. [1] crossed Pten heterozygous mice with mouse mammary tumor virus-Wnt-1 transgenic (Wnt-1 TG, Pten+/-) mice. Mammary ductal carcinoma developed earlier in Wnt-1 TG, Pten+/- mice than in mice bearing either genetic change alone, and showed frequent loss of the remaining wild-type PTEN allele. These data indicate a role for PTEN in breast tumorigenesis in an in vivo model.

MeSH Terms
Animals Breast Neoplasms/genetics Female Humans Mammary Neoplasms, Animal/genetics Mice PTEN Phosphohydrolase Phosphoric Monoester Hydrolases/deficiency,genetics Tumor Suppressor Proteins/deficiency,genetics
Chemicals
Tumor Suppressor Proteins Phosphoric Monoester Hydrolases PTEN Phosphohydrolase PTEN protein, human
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Petrocelli T
Sunnybrook and Women's College Health Sciences Centre, Toronto, Ontario, Canada. [email protected]
Slingerland J M
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Article Info
Journal
Breast cancer research : BCR
Abbr.
Breast Cancer Res
ISSN
1465-5411
DOI
10.1186/bcr322
Email
[email protected]
Published
2001-00-00
Epub
2001-00-01
Pages
356-60
Language
English
Region
England
NLM ID
100927353
PMCID
PMC138700
Subset
IM
External Links
PubMed source DOI: 10.1186/bcr322 PMC Full Text View journal details
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