TY - JOUR
T1 - Different gene expressions are associated with the different molecular subtypes of inflammatory breast cancer
AU - Iwamoto, Takayuki
AU - Bianchini, Giampaolo
AU - Qi, Yuan
AU - Cristofanilli, Massimo
AU - Lucci, Anthony
AU - Woodward, Wendy A.
AU - Reuben, James M.
AU - Matsuoka, Junji
AU - Gong, Yun
AU - Krishnamurthy, Savitri
AU - Valero, Vicente
AU - Hortobagyi, Gabriel N.
AU - Robertson, Fredika
AU - Symmans, W. Fraser
AU - Pusztai, Lajos
AU - Ueno, Naoto T.
N1 - Funding Information:
Acknowledgments This work was supported by the followings: the Breast Cancer Research Foundation (LP and WFS), MD Anderson Cancer Center Faculty Incentive Funds (WFS), the Commonwealth Cancer Foundation (LP and WFS) and MD Anderson’s Cancer Center Support Grant (CA016672) (NTU), the National Institute of Health R01CA138239-01 (WAW), The State of Texas Grant for Rare and Aggressive Cancers(MC and WAW), the American Airlines Komen Foundation Promise Grant KGO81287(WAW), and Morgan Welch Inflammatory Breast Cancer Research Program (MCNTU).
PY - 2011/2
Y1 - 2011/2
N2 - The goal of this study was to determine whether gene expression differences exist between inflammatory breast cancers (IBC) and T stage-matched non-IBC patients stratified by hormone receptor and HER2 status. We used Affymetrix GeneChips to analyze 82 tumor samples (25 T4d patients, and 57 T4a-c patients) of newly diagnosed breast cancers. Genes that were differentially expressed between the IBC and non-IBC specimens were identified using the t test, and differential expression of gene sets was assessed using gene set analysis. Three distinct clinical subtypes of IBC and non-IBC were compared: ER-positive/HER2-normal, HER2-amplified, and ER-negative/HER2-normal. When we compared expression data from all IBC with all non-IBC, we found no significant differences after adjusting for multiple testing. When IBC and non-IBC tumors were compared by clinical subtype, however, significant differences emerged. Complement and immune system-related pathways were overexpressed in ER-positive/HER2-normal IBC. Protein translation and mTOR signaling were overexpressed in HER2-amplified IBC. Apoptosis-, neural-, and lipid metabolism-related pathways were overexpressed in ER-negative/HER2-normal IBC compared with non-IBC of the same receptor phenotype. In this T stage-matched case-control study, the survival curves of patients with IBC and non-IBC were similar for all three clinical subtypes. IBC tumors can be divided into molecular and clinical subtypes similar to those of non-IBC. Clinical subtypes of IBC show molecular differences compared with similar subtypes of non-IBC.
AB - The goal of this study was to determine whether gene expression differences exist between inflammatory breast cancers (IBC) and T stage-matched non-IBC patients stratified by hormone receptor and HER2 status. We used Affymetrix GeneChips to analyze 82 tumor samples (25 T4d patients, and 57 T4a-c patients) of newly diagnosed breast cancers. Genes that were differentially expressed between the IBC and non-IBC specimens were identified using the t test, and differential expression of gene sets was assessed using gene set analysis. Three distinct clinical subtypes of IBC and non-IBC were compared: ER-positive/HER2-normal, HER2-amplified, and ER-negative/HER2-normal. When we compared expression data from all IBC with all non-IBC, we found no significant differences after adjusting for multiple testing. When IBC and non-IBC tumors were compared by clinical subtype, however, significant differences emerged. Complement and immune system-related pathways were overexpressed in ER-positive/HER2-normal IBC. Protein translation and mTOR signaling were overexpressed in HER2-amplified IBC. Apoptosis-, neural-, and lipid metabolism-related pathways were overexpressed in ER-negative/HER2-normal IBC compared with non-IBC of the same receptor phenotype. In this T stage-matched case-control study, the survival curves of patients with IBC and non-IBC were similar for all three clinical subtypes. IBC tumors can be divided into molecular and clinical subtypes similar to those of non-IBC. Clinical subtypes of IBC show molecular differences compared with similar subtypes of non-IBC.
KW - Gene set analysis
KW - Inflammatory breast cancer
KW - Receptor subtypes
KW - cDNA microarray
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U2 - 10.1007/s10549-010-1280-6
DO - 10.1007/s10549-010-1280-6
M3 - Article
C2 - 21153052
AN - SCOPUS:79151482682
SN - 0167-6806
VL - 125
SP - 785
EP - 795
JO - Breast Cancer Research and Treatment
JF - Breast Cancer Research and Treatment
IS - 3
ER -