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Series GSE10885 Query DataSets for GSE10885
Status Public on Apr 01, 2009
Title An integromic analysis reveals that metaplastic carcinomas are distinct from basal-like tumors.
Organism Homo sapiens
Experiment type Expression profiling by array
Summary 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.
 
Overall design Comparison of reference samples against treatment
 
Contributor(s) Hennessy BT, Perou CM, Mills GB
Citation(s) 19435916
Submission date Mar 18, 2008
Last update date Nov 17, 2017
Contact name Charles M. Perou
E-mail(s) cperou@med.unc.edu
Organization name University of North Carolina at Chapel Hill
Department Professor of Genetics, and Pathology & Laboratory Medicine; Lineberger Comprehensive Cancer Center
Street address 12-044 Lineberger Comprehensive Cancer Center CB# 7295
City Chapel Hill
State/province NC
ZIP/Postal code 27599-7264
Country USA
 
Platforms (4)
GPL885 Agilent-011521 Human 1A Microarray G4110A (Feature Number version)
GPL887 Agilent-012097 Human 1A Microarray (V2) G4110B (Feature Number version)
GPL1390 Agilent Human 1A Oligo UNC custom Microarrays
Samples (244)
GSM34423 PB138-Int
GSM34424 BR00-0504
GSM34425 BR00-0284
Relations
BioProject PRJNA107281

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE10885_RAW.tar 6.1 Mb (http)(custom) TAR
Processed data included within Sample table

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