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- W1635554821 endingPage "134" @default.
- W1635554821 startingPage "103" @default.
- W1635554821 abstract "The fitness of a cancer cell is shaped by its interactions with cells and other factors in its microenvironment. Clonal evolution selects for increased proliferation and survival, and can lead to invasion and metastasis. Some cancer cells acquire DNA repair defects, thus favoring the mutation rate. Alternatively, mechanisms of epigenetic control – for example, DNA methylation and histone modifications – represent another possibility to acquire stable pathological abilities. The DNA methlyome of cancer cells can exhibit two striking differences from normal cells: a reduction of global DNA methylation levels, and an aberrant hypermethylation of some sequences, particularly CpG islands that are normally unmethylated. Recent investigations have revealed that deficiency of certain epigenetic regulators (DNMTs and TETs) can be associated with carcinogenesis. Tumor stem cells express additional repressive marks (H3K9me2/3) which, coupled with DNA hypermethylation, contribute to the abnormal differentiation. The final strong piece of evidence underpinning the causative role of aberrant DNA hypermethylation in silencing tumor suppressor genes in cancer is that they can be reactivated when methylation is removed from their promoters." @default.
- W1635554821 created "2016-06-24" @default.
- W1635554821 creator A5013040378 @default.
- W1635554821 date "2016-01-01" @default.
- W1635554821 modified "2023-10-16" @default.
- W1635554821 title "DNA Methylation and Cancer" @default.
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