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Abstract:
A key factor involved in breast cancer development and progression is the estrogen receptor alpha (ER). Genome-wide computational studies on ER have identified over 70,000 putative Estrogen Response Elements (EREs) in the human genome. However, a genome-wide functional study using ChIP-Chip, has indicated that less than 1/10 of all putative ER binding sites are recognized by the receptor following estrogen stimulation in breast cancer cells. Through genome-wide positional analyses, we demonstrate that ER recruitment is dependent on a specific epigenetic signature characterized by mono and dimethylation of lysine 4 on histone 3 (H3K4me1/me2). Furthermore the pioneer factor FoxA1 translates this epigenetic signature into changes in chromatin structure in a cell type-specific manner for transcription factors, such as ER. Hence, this allows for the establishment of lineage-specific transcriptional enhancers and programs.
| Limitations: |
 APPROVED FOR PUBLIC RELEASE |
| Description: |
Annual summary rept. 1 Apr 2008-31 Mar 2009 |
| Pages: |
47 |
| Report Date: |
Apr 2009 |
| Contract Number: |
W81XWH-08-1-0214 W81XWH0810214 |
| Report Number: |
A722415 |
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