Abstract 3977: Gene-expression signature specifically associated with triple-negative breast cancer pertaining to asian ethnicity

Triple-negative breast cancer is a subtype of breast cancer with strong aggressiveness of tumor behavior and distinct patterns of metastasis. This unique phenotype of breast cancer is given by its clinically negative expression of estrogen receptor (ER), progesterone receptors (PR), and HER2 protein. Triple-negative breast cancer patients often suffer from ineffective hormone therapies, high recurrence rate, and a predilection for visceral metastasis. An accurate gene-expression signature specifically associated with triple-negative breast cancer will facilitate the identification of the existence of this disease and provide insights of its etiology. DNA microarray analysis was used to evaluate gene-expression profiles of 181 Asian breast cancer patients. There were 48 breast cancer patients who were triple-negative, and 133 of them were non-triple-negative. Several clinical information were matched in each group, including lymphovascular invasion, age, stage, grade, tumor size, tubule formation, nuclear pleomorphism, and mitotic count. After all 181 microarray data were normalized with quantile normalization, significantly expressed genes differentiated from the triple-negative group and non-triple-negative group were extracted using SAM (Significant Analysis of Microarray) and T-test. A panel of 50 genes was selected as the gene-expression signature for triple-negative breast cancer for Asian ethnicity, based on their unique patterns of gene-expression data using hierarchical clustering. Pathway analysis of the signature genes for triple-negative breast cancer was then performed in the lab. Genetic interactions of significantly expressed genes among different pathways found in this study will be shown and elaborated on the poster. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3977.