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The central role of DNA damage and epigenetic defects in DNA repair genes in carcinogenesis. DNA damage is considered to be the primary cause of cancer. [17] More than 60,000 new naturally-occurring instances of DNA damage arise, on average, per human cell, per day, due to endogenous cellular processes (see article DNA damage (naturally occurring)).
The arrest of ooctyes at the four genome copy stage appears to provide the informational redundancy needed to repair damage in the DNA of the germline. [26] The repair process used likely involves homologous recombinational repair. [26] [27] [28] Prophase arrested oocytes have a high capability for efficient repair of DNA damages. [27]
Oocyte abnormalities can be caused by a variety of genetic factors affecting different stages in meiosis. [1] Moreover, ageing is associated with oocyte abnormalities since higher maternal age is associated with oocytes with a reduced gene expression of spindle assembly checkpoints which are important in maintaining stability in the genome.
Cancer is caused by genetic changes leading to uncontrolled cell growth and tumor formation. The basic cause of sporadic (non-familial) cancers is DNA damage and genomic instability. [1] [2] A minority of cancers are due to inherited genetic mutations. [3] Most cancers are related to environmental, lifestyle, or behavioral exposures. [4]
In mammalian females the period of arrest may last for years. During this period of arrest, oocytes are subject to spontaneous DNA damage including double-strand breaks. However, the oocytes can efficiently repair DNA double-strand breaks, allowing the restoration of genetic integrity and the protection of offspring health. [8]
Bile acids cause DNA damage, including oxidative DNA damage, double-strand DNA breaks, aneuploidy and chromosome breakage. [55] High-normal levels of the bile acid deoxycholic acid cause apoptosis in human colon cells, [ 56 ] but may also lead to colon cancer if repair and apoptotic defenses are insufficient.
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