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Cohesion loss due to a decrease in REC8-cohesin complex, which would normally maintain the integrity of paired chromosomes (bivalents). [5] DNA damage (especially involving radiation or chemotherapy) which results in oocyte elimination if picked up by the body. [15]
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]
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)).
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]
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.
The response of oocytes to DNA double-strand break damage involves a pathway hierarchy in which ATR kinase signals to CHEK2 which then activates p53 and p63 proteins. [ 15 ] In the fruit fly Drosophila , irradiation of germ line cells generates double-strand breaks that result in cell cycle arrest and apoptosis .