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Epigenetic “bivalently marked” process of cancer stem cell‐driven tumorigenesis
Author(s) -
Balch Curt,
Nephew Kenneth P.,
Huang Tim H.M.,
Bapat Sharmila A.
Publication year - 2007
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.20619
Subject(s) - epigenetics , biology , carcinogenesis , dna methylation , embryonic stem cell , cancer epigenetics , histone , cancer research , polycomb group proteins , stem cell , gene silencing , genetics , microbiology and biotechnology , gene , histone methyltransferase , gene expression , repressor
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.