Abstract
Abstract Background. Parity is an established protective factor for ER-positive but not ER-negative breast cancer and it may increase the risk of triple-negative (negative for ER, PR, and HER2) tumors. Characterizing parity-related gene expression patterns in normal breast and breast tumor tissues may improve our understanding of the biological mechanisms underlying the subtype-specific associations between parity and breast cancer risk. Method. Gene expression changes associated with parity were identified in microarray data (4x44 K Agilent) from breast tissue of 74 non-diseased reduction mammoplasty (RM) patients. This parity signature, together with published parity signatures, were compared by GSEA method with gene expression (4x44 K Agilent and Illumina arrays) from both normal (N=150) and tumor (N=208) tissues of breast cancer patients from the Polish Breast Cancer Study (PBCS), overall and by tumor ER status. Results. We identified 908 genes significantly up-regulated by parity status (parous vs. nulliparous, FDR = 0.047), including genes in inflammatory pathways. Parity-related signatures identified by us and by previously published studies were significantly enriched in normal and tumor tissue of parous PBCS patients, specifically in ER-positive tumors (FWER<0.1). Conclusions. Our analysis identified a novel parity-related gene signature in normal breast tissue from healthy women, which is also detected in normal and tumor tissues in breast cancer patients with ER-positive tumors. The lack of parity-associated signatures in ER-negative tumors may reflect the disruption of parity-associated pathways (pro-inflammatory) in ER-negative tumors. Citation Format: Melissa Rotunno, Xuezheng Sun, Jonine Figueroa, Mark Sherman, Montserrat Garcia-Closas, Paul Meltzer, Tyisha Williams, Sallie Smith Schneider, Joseph Jerry, Rose Yang, Melissa Troester. Parity-related molecular signatures and breast cancer heterogeneity. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3651. doi:10.1158/1538-7445.AM2013-3651
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