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 | |
| State | Published - 28 Feb 2017 |
Bibliographical 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.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
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