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Vol. 15, Issue 6, 2523-2536, June 2004
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* Department of Surgery, Stanford University School of Medicine, Stanford, California 94305;
|| Department of Pathology, Stanford University School of Medicine, Stanford, California 94305;
# Department of Health Research and Policy and Statistics, Stanford University School of Medicine, Stanford, California 94305;
Department of Genetics, Stanford University School of Medicine, Stanford, California 94305;
Department of Genetics, Norwegian Radium Hospital, University of Oslo, N-0310 Oslo, Norway;
¶ Department of Pathology, Norwegian Radium Hospital, University of Oslo, N-0310 Oslo, Norway;
@ Department of Surgery, Akershus University Hospital, 1474 Nordbyhagen, Norway; and
** Department of Surgery, Ullevål University Hospital, N-0407 Oslo, Norway
Submitted November 4, 2003;
Revised January 28, 2004;
Accepted March 3, 2004
Monitoring Editor: Carl-Henrik Heldin
Invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC) are the two major histological types of breast cancer worldwide. Whereas IDC incidence has remained stable, ILC is the most rapidly increasing breast cancer phenotype in the United States 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, two lymph node metastases, and three normal tissues were amplified and hybridized to 
42,000 clone cDNA microarrays. Data were analyzed using hierarchical clustering algorithms and statistical analyses that identify differentially expressed genes (significance analysis of microarrays) and minimal subsets of genes (prediction analysis for microarrays) that succinctly distinguish ILCs and IDCs. Eleven of 21 (52%) of the ILCs ("typical" ILCs) clustered together and displayed different gene expression profiles from IDCs, whereas 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 to determine whether they require different therapeutic strategies.
These authors contributed equally to this work.
Present address: Department of Urology, Stanford University School of Medicine, Stanford, CA 94305
Present address: Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544.
Corresponding author. E-mail: ssj{at}stanford.edu.
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