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

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

doi:10.1002/bies.20619

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 journal › Article › peer-review

35 Scopus citations

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 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 language	English (US)
Pages (from-to)	842-845
Number of pages	4
Journal	BioEssays
Volume	29
Issue number	9
DOIs	https://doi.org/10.1002/bies.20619
State	Published - Sep 2007
Externally published	Yes

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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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 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.",

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AU - Nephew, Kenneth P.

AU - Huang, Tim H.M.

AU - Bapat, Sharmila A.

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AB - 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.

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

Abstract

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