Abstract
Genome-wide association studies have revealed a multitude of breast cancer-associated SNPs. The majority of these SNPs are located in noncoding regions of the genome. Yet how they contribute to breast cancer development is unknown. Recently, a groundbreaking study by the Lupien group has shown that risk-associated SNPs of breast cancer are enriched for FOXA1 binding sites, which influences the function of this transcription factor.
Highlights
Breast cancer is a heterogeneous disease and the most frequent tumors are positive for the expression of estrogen receptor (ER) [1] or the epidermal growth factor receptor 2 (HER2) [2]
Genomic analyses have revealed that the binding of FOXA1 shows a tissue-specific occupancy and that it is associated with the binding of ER or androgen receptor [5,6,7,8]
Having shown that breast cancer risk-associated single nucleotide polymorphism (SNP) are enriched with FOXA1 binding sites, the authors tested how these SNPs modulate the binding of the transcription factor to chromatin
Summary
Breast cancer is a heterogeneous disease and the most frequent tumors are positive for the expression of estrogen receptor (ER) [1] or the epidermal growth factor receptor 2 (HER2) [2]. Background Breast cancer is a heterogeneous disease and the most frequent tumors are positive for the expression of estrogen receptor (ER) [1] or the epidermal growth factor receptor 2 (HER2) [2]. Genomic studies have uncovered a multitude of SNPs associated with the risk of breast cancer.
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