Abstract : The risk of having cancer increases with age probably because progenitor cells from mature organisms accumulate enough molecular lesions to evade the homeostatic control of their tissular contexts. Molecular lesions can be genetic (mutations, deletions, or translocations) and/or epigenetic. Epigenetic signaling, including DNA methylation and histone modification, is essential for normal development and becomes altered during Aging and by cancer. Several epigenetic alterations, such as global hypomethylation and CpG island hypermethylation, are progressively accumulated during Aging and directly contribute to cell transformation. Intriguingly, others, such as those involved in the control of telomere length and several epigenetic enzymes belonging to the family of nicotinamide adenine dinucleotide (NAD)(+) dependent deacetylases known as sirtuins, exhibit a well‐defined progression during Aging that is dramatically reverted in transformed cells. We discuss the biological significance of both groups of epigenetic modifications in terms of their relative contribution to ontogenic development, senescence, and cell proliferation.
Colorectal cancer (CRC) is a heterogeneous disease in which unique subtypes are characterized by distinct genetic and epigenetic alterations. Here we performed comprehensive gen...
There is a growing realization that some aging-associated phenotypes/diseases have an epigenetic basis. Here, we report the first genome-scale study of epigenomic dynamics durin...
Inactivation of the genes involved in DNA mismatch repair is associated with microsatellite instability (MSI) in colorectal cancer. We report that hypermethylation of the 5′ CpG...
The DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) removes alkyl adducts from the O6 position of guanine. MGMT expression is decreased in some tumor tissues, a...
To elucidate the relationship between intragenic DNA methylation and chromatin marks, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBE...
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