Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA327586 | ENA |
REPOSITORIES: ENA
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Project description:Breast cancer is one of the most common cancers in women. Of the different subtypes of breast cancer, the triple negative breast cancer subtype of breast cancer is the most aggressive. A proteomic screen of nucleolar content across breast cancer subtypes found that triple negative breast cancer cell lines have a distinct nucleolar proteome signature in comparison to non-TNBC breast cancer cell lines.
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Project description:Analysis of 97 formalin-fixed, paraffin-embedded (FFPE) primary breast tumors using Illumina DASL microarray technology on a Custom Breast Cancer Panel and the Illumina Human Cancer Panel. Molecular markers between the pathology defined subtypes of breast cancer were assessed to hypothesize potential therapeutic targets specific to the subtypes Molecular Characterization of 97 primary breast tumor formalin-fixed, paraffin-embedded (FFPE) specimens including 24 triple negative (TN: ER-, PR-, HER2-), 9 HER2-positive (HER2+: ER-, PR-, HER2+), and 64 hormone receptor-positive (HR+: ER+ and/or PR+). 91 of the 97 specimens were characterized on the Illumina Human Cancer DASL Panel and 86 of 97 specimens were characterized on a custom Breast Cancer DASL Panel, 80 of these specimens were common to both the Human Cancer DASL Panel and the custom Breast Cancer DASL Panel.
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Project description:The dire need for more effective treatments for clinically aggressive breast cancers has motivated intensive investigations into their cellular and molecular etiology. Breast cancers that are “triple-negative” for the clinical markers, ESR1, PGR, and HER2, typically belong to the Basal-like molecular subtype. Defective Rb, p53, and Brca1 pathways are each associated with triple-negative and Basal-like subtypes. Our mouse genetic studies demonstrate that concomitant inactivation of all three pathways in mammary epithelium has an additive effect on tumor latency, and predisposes highly penetrant, metastatic, adenocarcinomas. These tumors are poorly differentiated with histologic features that are common among human Brca1-mutated tumors, including heterogeneous morphology, metaplasia, and necrosis. Transcriptomic analyses demonstrated that the tumors shared attributes of both Basal-like and Claudin-low signatures, two molecular subtypes encompassed by the broader triple-negative category defined by clinical markers. Ex vivo tumorsphere formation, which was suppressed by Notch and Wnt pathway inhibition, and tumor antigen profiles and are consistent with enrichment of stem-like and luminal progenitor cells among these tumors. These studies establish a novel mouse model of malignant breast cancer based on events in the human disease and underscore the non-reciprocal requirements of three canonical tumor suppressor pathways in breast cancer evolution. Morphogenetic pathways may provide additional avenues for targeted therapeutic intervention. Gene expression analysis of mouse mammary tumors with perturbation of Rb family pathways, p53, and/or Brca1 are compared to other mouse model tumors (n=152)
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