Transcription profiling of PTEN-deficiency in luminal MMTV-ErbB-2 mouse model to investigate its effect on mammary tumorigenesis and metastasis

ABSTRACT: Overexpression and/or amplification of the ErbB-2 oncogene, as well as inactivation of the tumor suppressor PTEN, are two important genetic events in human breast carcinogenesis. To address the biological impact of conditional inactivation of PTEN on ErbB-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the MMTV promoter to directly couple expression of activated ErbB-2 and Cre recombinase to the same mammary epithelial cell (MMTV-NIC). Disruption of PTEN in the mammary epithelium of the MMTV-NIC model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology. PTEN-deficient/NIC tumorigenesis was associated with an increase in angiogenesis. Moreover, inactivation of PTEN

ORGANISM(S): Mus musculus

SUBMITTER: Robert Lesurf 

PROVIDER: E-GEOD-13916 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress