Epigenetic "bivalently marked" process of cancer stem cell-driven tumorigenesis

Curt Balch, Kenneth P. Nephew, Tim H.M. Huang, Sharmila A. Bapat

Research output: Contribution to journalArticlepeer-review

36 Scopus citations


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 report(1) 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.

Original languageEnglish (US)
Pages (from-to)842-845
Number of pages4
Issue number9
StatePublished - Sep 2007
Externally publishedYes

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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