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Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer (miRNA expression data).

ABSTRACT: miRNA profiling of normal and tumorigenic mouse mammary tissue. Mouse genotypes consist of wildtype, MMTV-Met, MMTV-Met;Trp53fl/+;Cre, and Trp53fl/+;Cre.

ORGANISM(S): Mus musculus

PROVIDER: GSE41723 | GEO | 2013/03/04

SECONDARY ACCESSION(S): PRJNA178026

REPOSITORIES: GEO

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Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer (aCGH data).

Project description:Transcriptional profiling of normal and tumorigenic mouse mammary tissue. Mouse genotypes consist of wildtype, MMTV-Met, MMTV-Met;Trp53fl/+;Cre, and Trp53fl/+;Cre. Two-color common reference design. Samples consist of 4 normal tissues, 8 MMTV-Met tumors, 10 MMTV-Met;Trp53fl/+;Cre tumors, and 8 Trp53;Cre tumors.

2013-03-04 | E-GEOD-41632 | biostudies-arrayexpress

Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer (miRNA expression data).

Project description:miRNA profiling of normal and tumorigenic mouse mammary tissue. Mouse genotypes consist of wildtype, MMTV-Met, MMTV-Met;Trp53fl/+;Cre, and Trp53fl/+;Cre. One-color design. Samples consist of 2 normal tissues, 7 MMTV-Met tumors, 8 MMTV-Met;Trp53fl/+;Cre tumors, and 8 Trp53;Cre tumors.

2013-03-04 | E-GEOD-41723 | biostudies-arrayexpress

Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer (mRNA expression data).

Project description:Transcriptional profiling of normal and tumorigenic mouse mammary tissue. Mouse genotypes consist of wildtype, MMTV-Met, MMTV-Met;Trp53fl/+;Cre, and Trp53fl/+;Cre. Two-color common reference design. Samples consist of 11 normal tissues, 8 MMTV-Met tumors, 14 MMTV-Met;Trp53fl/+;Cre tumors, and 8 Trp53;Cre tumors.

2013-03-04 | E-GEOD-41601 | biostudies-arrayexpress

Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer (aCGH data).

Project description:Transcriptional profiling of normal and tumorigenic mouse mammary tissue. Mouse genotypes consist of wildtype, MMTV-Met, MMTV-Met;Trp53fl/+;Cre, and Trp53fl/+;Cre.

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Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer (mRNA expression data).

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Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer.

Project description:Triple-negative breast cancer (TNBC) accounts for ?20% of cases and contributes to basal and claudin-low molecular subclasses of the disease. TNBCs have poor prognosis, display frequent mutations in tumor suppressor gene p53 (TP53), and lack targeted therapies. The MET receptor tyrosine kinase is elevated in TNBC and transgenic Met models (Met(mt)) develop basal-like tumors. To investigate collaborating events in the genesis of TNBC, we generated Met(mt) mice with conditional loss of murine p53 (Trp53) in mammary epithelia. Somatic Trp53 loss, in combination with Met(mt), significantly increased tumor penetrance over Met(mt) or Trp53 loss alone. Unlike Met(mt) tumors, which are histologically diverse and enriched in a basal-like molecular signature, the majority of Met(mt) tumors with Trp53 loss displayed a spindloid pathology with a distinct molecular signature that resembles the human claudin-low subtype of TNBC, including diminished claudins, an epithelial-to-mesenchymal transition signature, and decreased expression of the microRNA-200 family. Moreover, although mammary specific loss of Trp53 promotes tumors with diverse pathologies, those with spindloid pathology and claudin-low signature display genomic Met amplification. In both models, MET activity is required for maintenance of the claudin-low morphological phenotype, in which MET inhibitors restore cell-cell junctions, rescue claudin 1 expression, and abrogate growth and dissemination of cells in vivo. Among human breast cancers, elevated levels of MET and stabilized TP53, indicative of mutation, correlate with highly proliferative TNBCs of poor outcome. This work shows synergy between MET and TP53 loss for claudin-low breast cancer, identifies a restricted claudin-low gene signature, and provides a rationale for anti-MET therapies in TNBC.

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2012-05-29 | E-GEOD-35855 | biostudies-arrayexpress

Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-03-04 | E-GEOD-41748 | biostudies-arrayexpress

Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

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