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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)).
DNA damage appears to be the primary underlying cause of cancer, [78] and deficiencies in DNA repair appears to underlie many forms of cancer. [79] If DNA repair is deficient, DNA damage tends to accumulate. Such excess DNA damage may increase mutational errors during DNA replication due to error-prone translesion synthesis.
Inflammation-induced ROS that cause DNA damage can trigger apoptosis, [52] [53] but may also cause cancer if repair and apoptotic processes are insufficiently protective. [45] Bile acids, stored in the gall bladder, are released into the small intestine in response to fat in the diet. Higher levels of fat cause greater release. [54]
Depending on the extent of injury, the cellular response may be adaptive and where possible, homeostasis is restored. [1] Cell death occurs when the severity of the injury exceeds the cell's ability to repair itself. [2] Cell death is relative to both the length of exposure to a harmful stimulus and the severity of the damage caused. [1]
The absence of p21 or 14-3-3 cannot sufficiently inhibit the CyclinB-Cdc2 complex, thus exhibiting the regulatory control of p53 and p21 in the G2 checkpoint in response to DNA damage. [12] p53 mutations can result in a significant checkpoint deficit, which has important implications in the treatment of cancer.
DNA damage response mechanisms trigger cell-cycle arrest, and attempt to repair DNA lesions or promote cell death/senescence if repair is not possible. Replication stress is observed in preneoplastic cells due to increased proliferation signals from oncogenic mutations.
There are many causes of primary malignant transformation, or tumorigenesis. Most human cancers in the United States are caused by external factors, and these factors are largely avoidable. [1] [2] [3] These factors were summarized by Doll and Peto in 1981, [1] and were still considered to be valid in 2015. [2] These factors are listed in the ...
It can initiate apoptosis (i.e., programmed cell death) if DNA damage proves to be irreparable. It is essential for the senescence response to short telomeres. p53 pathway: In a normal cell, p53 is inactivated by its negative regulator, mdm2. Upon DNA damage or other stresses, various pathways will lead to the dissociation of the p53 and mdm2 ...