Epigenetic “bivalently marked” process of cancer stem cell-driven tumorigenesis
✍ Scribed by Curt Balch; Kenneth P. Nephew; Tim H.-M. Huang; Sharmila A. Bapat
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 135 KB
- Volume
- 29
- Category
- Article
- ISSN
- 0265-9247
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Silencing of tumor suppressor genes (TSGs), by DNA methylation, is well known in adult cancers. However, based on the “stem cell” theory of tumorigenesis, the early epigenetic events arising in malignant precursors remain unknown. A recent report1 demonstrates that, while pluripotent embryonic stem cells lack DNA methylation and possess a “bivalent” pattern of activating and repressive histone marks in numerous TSGs, analogous multipotent malignant cells derived from germ cell tumors (embryonic carcinoma cells) gain additional silencing modifications to those same genes. These results suggest a possible mechanism by which aberrant differentiation, mediated by histone and DNA methylation, instigates tumor progression. BioEssays 29:842–845, 2007. © 2007 Wiley Periodicals, Inc.