Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Activation of Host Wound Responses in Breast Cancer Microenvironment

ABSTRACT: Cancer progression is mediated by processes that are also important in wound repair. As a result, cancers have been conceptualized as overhealing wounds or "wounds that do not heal," and gene expression signatures reflective of wound repair have shown value as predictors of breast cancer survival. Despite the widespread acknowledgment of commonalities between host responses to wounds and host responses to cancer, the gene expression responses of normal tissue adjacent to cancers have not been well characterized. Using RNA extracted from histologically normal breast tissue from 105 patients, 121 arrays were performed, including 72 arrays representing 58 reduction mammoplasty patients and 49 arrays representing 47 cancer patients, we measured whole genome expression profiles and identified a gene expression signature that is induced in response to breast cancer.

ORGANISM(S): Homo sapiens

SUBMITTER: Melissa Troester

PROVIDER: E-GEOD-16113 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Activation of host wound responses in breast cancer microenvironment.

Troester Melissa A MA Lee Myung Hee MH Carter Matthew M Fan Cheng C Cowan David W DW Perez Erick Roman ER Pirone Jason R JR Perou Charles M CM Jerry D Joseph DJ Schneider Sallie Smith SS

Clinical cancer research : an official journal of the American Association for Cancer Research 20091103 22

<h4>Purpose</h4>Cancer progression is mediated by processes that are also important in wound repair. As a result, cancers have been conceptualized as overhealing wounds or "wounds that do not heal," and gene expression signatures reflective of wound repair have shown value as predictors of breast cancer survival. Despite the widespread acknowledgment of commonalities between host responses to wounds and host responses to cancer, the gene expression responses of normal tissue adjacent to cancers ...[more]

PMID: 19887484

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Project description:Metaplastic breast cancers (MBC) are aggressive, chemoresistant tumors characterized by lineage plasticity. To advance understanding of their pathogenesis and relatedness to other breast cancer subtypes, 28 MBCs were compared with common breast cancers using comparative genomic hybridization, transcriptional profiling, and reverse-phase protein arrays and by sequencing for common breast cancer mutations. MBCs showed unique DNA copy number aberrations compared with common breast cancers. PIK3CA mutations were detected in 9 of 19 MBCs (47.4%) versus 80 of 232 hormone receptor-positive cancers (34.5%; P = 0.32), 17 of 75 HER-2-positive samples (22.7%; P = 0.04), 20 of 240 basal-like cancers (8.3%; P < 0.0001), and 0 of 14 claudin-low tumors (P = 0.004). Of 7 phosphatidylinositol 3-kinase/AKT pathway phosphorylation sites, 6 were more highly phosphorylated in MBCs than in other breast tumor subtypes. The majority of MBCs displayed mRNA profiles different from those of the most common, including basal-like cancers. By transcriptional profiling, MBCs and the recently identified claudin-low breast cancer subset constitute related receptor-negative subgroups characterized by low expression of GATA3-regulated genes and of genes responsible for cell-cell adhesion with enrichment for markers linked to stem cell function and epithelial-to-mesenchymal transition (EMT). In contrast to other breast cancers, claudin-low tumors and most MBCs showed a significant similarity to a "tumorigenic" signature defined using CD44(+)/CD24(-) breast tumor-initiating stem cell-like cells. MBCs and claudin-low tumors are thus enriched in EMT and stem cell-like features, and may arise from an earlier, more chemoresistant breast epithelial precursor than basal-like or luminal cancers. PIK3CA mutations, EMT, and stem cell-like characteristics likely contribute to the poor outcomes of MBC and suggest novel therapeutic targets. Comparison of reference samples against treatment

Dataset Information

Activation of Host Wound Responses in Breast Cancer Microenvironment

Publications

Activation of host wound responses in breast cancer microenvironment.

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