As people age, they show signs of aging, such as chloasma on the skin and greyish hair. These are just phenotypes, and the root cause is genomic change. Errors introduced during DNA damage and replication accumulate, making the genome different in each cell. As cells divide, the changes continue to be passed on, with more and more effects. If the change - known as a mutation - shuts off the system that controls cell proliferation and survival, it could lead to cancer.
Cancer has familial components, and cancer-susceptible genes, such as BRCA1 and TP53, are involved in coordinating the cell's response to DNA damage. A defect in the BRCA1 gene increases a woman's risk of developing breast and ovarian cancer. In addition, the DNA repair mechanism collapsed, damaged cells can accumulate mutations, the occurrence of cancer is inevitable. In addition to genetics, environmental and lifestyle factors can also influence cancer risk.
Lung cancer patients who compared smokers with non-smokers had different mutation patterns, because chemicals in cigarette smoke attack DNA. One of the most common mutations in cancer or normal cells is the methylated DNA reaction. DNA methylation is a small chemical modification that helps control the opening and closing of genes. This small change is crucial for normal development, but methylation also makes DNA more vulnerable to damage.
Although the occurrence of cancer is directly related to the accumulation of DNA damage, our immune system also plays an important role.
Lifestyle differences, such as stress, diet and so on will also produce certain risks.
The results suggest that some people accumulate more DNA damage than others, and measuring these differences may help reduce risk.