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

ABSTRACT: Transcriptional 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: GSE41632 | GEO | 2013/03/04

SECONDARY ACCESSION(S): PRJNA177952

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 (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.

2013-03-04 | GSE41723 | GEO

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.

2013-03-04 | GSE41601 | GEO

Co-dependency for MET and FGFR1 in basal triple negative breast cancers

Project description:Triple-negative breast cancer (TNBC) is a heterogeneous disease that lacks both effective patient stratification strategies and therapeutic targets. In the present study, we assay tumour-initiating cells (TICs) properties, using established Met-dependent transgenic mouse models of TNBC, breast cancer cell lines and, patient-derived xenografts, to directly investigate the role of Met in tumour initiation and identify FGFR1 signaling as a key convergent pathway with Met for the maintenance of TICs. To understand the events that occur in TICs upon inhibition of Met and FGFR1, we performed gene expression profiling by RNA-Sequencing of RNA prepared from tumoursphere from 3 independent MMTV-Metmt;Trp53fl/+;Cre derived spindloid tumour cell lines (A1005, A1129, A1471) following treatment with Met or FGFR inhibitor alone (Crizotinib or PD173074, respectively), or in combination for 24h.

2020-11-28 | GSE162272 | GEO

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.

| S-EPMC3619286 | biostudies-literature

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

Lunatic fringe deficiency cooperates with the Met/Caveolin amplicon to induce basal-like breast cancer

Project description:Mammary specific deletion of Lfng induces basal-like and claudin-low tumors with accumulation of Notch intracellular domain fragments, increased expression of proliferation-associated Notch targets, amplification of the Met/Caveolin locus, and elevated Met and Igf-1R signaling. Tumor DNAs from Lfngflox/flox; MMTV-Cre conditional mutant mice are being compared to control DNAs from the same animals in order to identify common alterations associated with tumor progression

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.

2013-03-04 | GSE41748 | GEO