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Gene expression profiles from mammary tissue of control mice, small K5ΔNβcat hyperplasia, large K5ΔNβcat hyperplasia and K5ΔNβcat tumor

ABSTRACT: Basal-like breast cancer is a heterogeneous disease characterised by the expression of basal cell markers, no oestrogen or progesterone receptor expression and a lack of HER2 overexpression. Recent studies have linked activation of the Wnt/beta-catenin pathway to basal-like breast cancer. Transgenic mice expressing N-terminally truncated stabilised beta-catenin in the mammary basal/myoepithelial cell layer (K5deltaNbetacat strain) develop mammary hyperplasias that progress to invasive carcinomas. Histological and microarray analyses of these lesions have revealed their high similarity to a subset of basal-like human breast tumours with squamous differentiation. As in human basal-like carcinomas, the Myc pathway was found to be activated in the mammary lesions of K5deltaNbetacat mice. Mammosphere and transplantation assays showed that a basal cell population with stem/progenitor characteristics was amplified in K5deltaNbetacat mouse preneoplastic glands. Myc deletion from the mammary basal layer of K5deltaNbetacat mice abolished both basal cell regenerative capacity and tumorigenesis. These results show that Myc is essential for beta-catenin-induced stem cell amplification and tumorigenesis and that basal stem/progenitor cells may be at the origin of a subset of basal-like breast tumours.

ORGANISM(S): Mus musculus

PROVIDER: GSE43825 | GEO | 2013/12/31

SECONDARY ACCESSION(S): PRJNA187503

REPOSITORIES: GEO

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Gene expression profiles from mammary tissue of control mice, small K5M-NM-^TNM-NM-2cat hyperplasia, large K5M-NM-^TNM-NM-2cat hyperplasia and K5M-NM-^TNM-NM-2cat tumor

Project description:Basal-like breast cancer is a heterogeneous disease characterised by the expression of basal cell markers, no oestrogen or progesterone receptor expression and a lack of HER2 overexpression. Recent studies have linked activation of the Wnt/beta-catenin pathway to basal-like breast cancer. Transgenic mice expressing N-terminally truncated stabilised beta-catenin in the mammary basal/myoepithelial cell layer (K5deltaNbetacat strain) develop mammary hyperplasias that progress to invasive carcinomas. Histological and microarray analyses of these lesions have revealed their high similarity to a subset of basal-like human breast tumours with squamous differentiation. As in human basal-like carcinomas, the Myc pathway was found to be activated in the mammary lesions of K5deltaNbetacat mice. Mammosphere and transplantation assays showed that a basal cell population with stem/progenitor characteristics was amplified in K5deltaNbetacat mouse preneoplastic glands. Myc deletion from the mammary basal layer of K5deltaNbetacat mice abolished both basal cell regenerative capacity and tumorigenesis. These results show that Myc is essential for beta-catenin-induced stem cell amplification and tumorigenesis and that basal stem/progenitor cells may be at the origin of a subset of basal-like breast tumours. mammary tissue from K5M-NM-^TNM-NM-2cat mice were dissected at successive stages of development (small hyperplasia (n=5), large hyperplasia (n=5), tumor (n=11) and control (n=4)) for RNA extraction and hybridization on Affymetrix microarrays

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Lysyl oxidase-like 2 (LOXL2) a new regulator of cell polarity required for metastatic dissemination of basal-like breast carcinomas

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β-catenin signaling is a critical event in ErbB2-mediated mammary tumor progression.

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