Abstract
Recently, it was suggested that tissue variation in cancer risk originates from differences in the number of stem-cell divisions underlying each tissue, leading to different mutation loads. We show that this variation is also correlated with the degree of aberrant CpG island DNA methylation in normal cells. Methylation accumulates during aging in a subset of molecules, suggesting that the epigenetic landscape within a founder-cell population may contribute to tumor formation.
Keywords:
aging; methylation; polycomb.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aging / genetics*
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Aging / metabolism
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Cell Differentiation
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Cell Division
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Cell Transformation, Neoplastic / genetics*
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Cell Transformation, Neoplastic / metabolism
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Cell Transformation, Neoplastic / pathology
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CpG Islands
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DNA Methylation
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Epigenesis, Genetic*
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Female
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Genetic Predisposition to Disease
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Humans
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Male
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Models, Genetic
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Models, Statistical*
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Morphogenesis / genetics
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Mutation
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Neoplasms / classification
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Neoplasms / genetics*
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Neoplasms / metabolism
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Neoplasms / pathology
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Organ Specificity
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Risk
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Stem Cells / cytology
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Stem Cells / metabolism*