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A more recent version of this article appeared on June 1, 2004 Originally published as MBoC in Press, 10.1091/mbc.E03-11-0786 on May 7, 2004
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Submitted on November 4, 2003
Revised on January 28, 2004
Accepted on March 3, 2004
1 Department of Surgery, Stanford University School of Medicine, Stanford, CA; Department of Urology, Stanford University School of Medicine, Stanford, CA
2 Department of Genetics, Norwegian Radium Hospital, University of Oslo, Oslo, Norway
3 Department of Surgery, Stanford University School of Medicine, Stanford, CA
4 Department of Pathology, Stanford University School of Medicine, Stanford, CA
5 Department of Pathology, Norwegian Radium Hospital, University of Oslo, Oslo, Norway
6 Department of Statistics, Stanford University School of Medicine, Stanford, CA
7 Department of Surgery, Akershus University Hospital, 1474 Nordbyhagen, Norway
8 Department of Surgery, Ulleval University Hospital, Oslo, Norway
9 Department of Genetics, Stanford University School of Medicine, Stanford, CA; Institute for Integrative Genomics, Princeton University, Princeton, NJ
10 Department of Surgery, Stanford University School of Medicine, MSLS Building, Room P214, 1201 Welch Road M/C 5494, Stanford CA 94305
* Corresponding author. E-mail address: ssj{at}stanford.edu.
Invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC) are the two major histological types of breast cancer worldwide. While IDC incidence has remained stable, ILC is the most rapidly increasing breast cancer phenotype in the U.S. and Western Europe. It is not clear whether IDC and ILC represent molecularly distinct entities and what genes might be involved in the development of these two phenotypes. We conducted comprehensive gene expression profiling studies to address these questions. Total RNA from 21 ILCs, 38 IDCs, 2 lymph node metastases, and 3 normal tissues were amplified and hybridized to 
42,000 clone cDNA microarrays. Data was analyzed using hierarchical clustering algorithms and statistical analyses that identify differentially expressed genes (SAM) and minimal subsets of genes (PAM) that succinctly distinguish ILCs and IDCs. 11/21 (52%) of the ILCs ("typical" ILCs) clustered together and displayed different gene expression profiles from IDCs, while the other ILCs ("ductal-like" ILCs) were distributed between different IDC subtypes. Many of the differentially expressed genes between ILCs and IDCs code for proteins involved in cell adhesion/motility, lipid/fatty acid transport and metabolism, immune/defense response, and electron transport. Many genes that distinguish typical and ductal-like ILCs are involved in regulation of cell growth and immune response. Our data strongly suggest that over half the ILCs differ from IDCs not only in histological and clinical features, but also in global transcription programs. The remaining ILCs closely resemble IDCs in their transcription patterns. Further studies are needed to explore the differences between ILC molecular subtypes and determine whether they require different therapeutic strategies.
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