Journal
EPIGENETICS
Volume 3, Issue 2, Pages 59-63Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/epi.3.2.5899
Keywords
breast cancer; DNA methylation; epigenetics; Wnt signaling; beta-catenin; cancer stem cell
Funding
- NATIONAL CANCER INSTITUTE [ZIABC010794] Funding Source: NIH RePORTER
- Intramural NIH HHS [Z01 BC010253, Z01 BC010794] Funding Source: Medline
- NCI NIH HHS [N01CO12400, N01-CO-12400] Funding Source: Medline
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Breast cancer is one of the most common malignancies in women. Despite advances in treatment of endocrine-dependent tumors, the complete molecular basis of transformation is still unknown. What is clear is that a variety of genetic lesions and epigenetic modifications are present in the neoplasm. Disregulation of several signaling pathways is known to be associated with breast cancer development, among them is the wingless and integration site growth factor (Wnt) pathway. While genetic mutations of certain components of this pathway, such as APC, are significant contributing factors for colorectal cancers, they are typically not the predominate mechanism associated with breast cancer. Instead, it appears that DNA hypermethylation leads to aberrant regulation of the Wnt pathway in breast cancer, and as such, this review focuses on the epigenetic regulation of Wnt pathway components in breast cancer.
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