Contribution of epigenetic mechanisms to variation in cancer risk among tissues

Michael Klutstein; Joshua Moss; Tommy Kaplan; Howard Cedar

doi:10.1073/pnas.1616556114

Contribution of epigenetic mechanisms to variation in cancer risk among tissues

Michael Klutstein, Joshua Moss, Tommy Kaplan, Howard Cedar

The Hebrew University of Jerusalem

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Pages (from-to)	2230-2234
Number of pages	5
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	114
Issue number	9
DOIs	https://doi.org/10.1073/pnas.1616556114
State	Published - 28 Feb 2017

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10.1073/pnas.1616556114

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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.",

author = "Michael Klutstein and Joshua Moss and Tommy Kaplan and Howard Cedar",

note = "Funding Information: This research was supported by grants from the European Research Council, the Israel Cancer Research Fund, Rosetrees Foundation, Lew Sanders, and the Smart Family Foundation.",

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AU - Moss, Joshua

AU - Kaplan, Tommy

AU - Cedar, Howard

N1 - Funding Information: This research was supported by grants from the European Research Council, the Israel Cancer Research Fund, Rosetrees Foundation, Lew Sanders, and the Smart Family Foundation.

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Y1 - 2017/2/28

N2 - 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.

AB - 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.

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M3 - مقالة

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Contribution of epigenetic mechanisms to variation in cancer risk among tissues

Abstract

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