Research
Identification of conserved gene expression features between murine mammary carcinoma models and human breast tumors
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* Corresponding author: Charles M Perou cperou@med.unc.edu
- † Equal contributors
1 Lineberger Comprehensive Cancer Center
2 Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
3 Department of Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA
4 Department of Biology and Program in Bioinformatics and Computational Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
5 The Jackson Laboratory, Bar Harbor, ME 04609, USA
6 Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
7 Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA
8 Department of Pathology, University of Chicago, Chicago, IL 60637, USA
9 Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
10 Baylor College of Medicine, Houston, TX 77030, USA
11 Transgenic Oncogenesis Group, Laboratory of Cancer Biology and Genetics
12 Chemoprevention Agent Development Research Group, National Cancer Institute, Bethesda, MD 20892, USA
13 Department of Pathology, Thomas Jefferson University, Philadelphia, PA 19107, USA
14 Section of Hematology/Oncology, Department of Medicine, Committees on Genetics and Cancer Biology, University of Chicago, Chicago, IL 60637, USA
15 Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Genome Biology 2007, 8:R76 doi:10.1186/gb-2007-8-5-r76
Published: 10 May 2007Additional files
Additional data file 1:
Mouse tumor and normal sample associated data including source, transgene and promoter information.
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Additional data file 2:
Samples are colored according to mouse model from which they were derived, and the genes were selected using a variation filter of three-fold or more on three or more samples.
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Additional data file 3:
Complete mouse models cluster diagram using the 866 gene murine intrinsic gene list.
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Additional data file 4:
(a) CC matrices generated using the 866 gene mouse intrinsic list, by cluster numbers K = 2 through K = 15. (b) Empirical cumulative distribution (CDF) plot corresponding to the consensus matrices in the range K = 2 to 15. (c) CC directly compared to the hierarchical clustering-based results. The dendrogram from Figure 1 (using the intrinsic gene set) is shown and immediately below is a colored matrix showing sample assignments based upon the various number of K clusters from the CC. By comparison, the analysis performed on the mouse dataset using all genes (bottom matrix) is presented.
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Additional data file 5:
This unsupervised cluster analysis is based upon the orthologous gene overlap between the human and mouse microarrays, and then we selected for the subset of genes that varied three-fold or more on three or more arrays.
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Additional data file 6:
This analysis was used to determine a human samples subtype (basal-like, luminal, HER2+/ER-, and so on), which was then used the various SAM and GSEA analyses. Samples are colored according to their subtype: red = basal-like, blue = luminal, pink = HER2+/ER-, yellow = claudin-low and green = normal breast-like.
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Additional data file 7:
Histological characterization of six different human 'claudin-low' tumors using hematoxylin and eosin sections.
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Additional data file 8:
GSEA of murine pathway models versus five human subtypes.
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Additional data file 9:
GSEA of ten murine classes versus clinical ER status and HER2 status in ER negative patients.
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Additional data file 10:
GSEA of murine pathway models versus clinical ER status and HER2 status in ER negative patients.
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