Life expectancy and cancer: Long life will not cancer?

In nature there is a close relationship between age and the likelihood of cancer. For mice with an average life expectancy of 2 years, the age of cancer is most likely to be 1 year after age. This period of time is after 10 years for dogs, and about a few decades for humans. Understanding how the body is healthy against cancer cells will help to better understand cancer.The question is whether there is a link between aging and cancer?

The research group Kenyon, University of California, USA used mutations to increase life expectancy and cancer-causing mutations in the C. elegans worm model to answer this question. The results showed that the long-term mutation of worms reduces the formation of cancer and this result is published in the leading science journal Science (Science Volume 313 No. 5789, page 971- 975 August 18, 2006 http://www.sciencemag.org/cgi/content/abstract/313/5789/971).

C.elegans worm (Photo: yourgenome)

To examine the relationship between aging and cancer, the team first studied two independent processes that affect life expectancy and cancer separately. Then the interaction of these two processes is monitored in the same organism. The mutation of the daf-2 gene that encodes the insulin receptor increases the lifespan of the worm twice. In contrast, mutations in the cancer suppressor gene gld-1 make the germ cells continue to multiply, increase cell turnover and develop tumors that kill the organism. When combining these two mutations in the same organism, the process of increasing the life of the daf-2 gene mutation is not affected, but the carcinogenic effect of the gld-1 gene mutation is completely gone.

The question is how the lack of insulin signals boosts resistance to cancer growth. Insulin is a hormone secreted by the pancreas and plays a role in controlling blood glucose (blood sugar). In organisms with 2 mutations simultaneously daf-2 and gld-1, the cell lines have a reduction in the division process and enhance the process of cell death according to predetermined programs (apoptosis - the process of cytotoxicity) Compared to organisms that have 1 mutation gld-1. Surprisingly, mutations in the daf-2 gene only work on germ cells in tumors that do not affect other normal natural germ cells.

In addition, the team studied the effect of these mutations on the deficiency of p53 protein. p53 or p53 tumor suppressor (p53) is an important protein that plays a role in cell cycle regulation. It has the ability to destroy tumors and regulate abnormal cell growth as well as the ability to control apoptosis. The p53 is synthesized from the TP53 gene and is also called TP53. Normally, this protein is maintained at a low level due to its rapid conversion ability but when there are abnormalities in DNA as well as cancer cells, it is concentrated and activated. More than 50% of cancer patients are found to have mutations or complete loss of the TP53 gene, which causes structural changes or loss of p53 protein.

When the p53 protein deficiency is introduced into the two mutated worms, daf-2 and gld-1 reduce life expectancy and reduce tumor growth but do not reduce apoptosis. This, in contrast to the biological role of p53, is a mutation or lack of p53 which reduces apoptosis, increasing tumor growth without affecting life expectancy.

Is the anti-cancer effect due to the special effect of insulin signal metabolism or another process in the process of increasing the life expectancy? Further studies show that mutations in genes that reduce the absorption of food or inhibit cellular respiration also increase life expectancy in worms. However, unlike in mutated worms daf-2, mutations in food absorption and cellular respiration do not completely reduce the carcinogenic effects of mutation gld-1. In the two mutants, daf-2 and gld-1 mutations in the gene reduce the absorption of food and inhibit cellular respiration, making the organism live longer. These mutations also reduce the incidence of cancer but do not affect apoptosis. The rate of cancer reduction in this mutation may be due to possible effects on energy metabolism. A decrease in nutrient supply and energy can make these cancer cells malnutrition leading to cell stress and eventually cell cycle cessation.

The results show that different pathways of the aging process can control cancer development . Genetically modified worms to increase longevity have avoided cancer because of increased protection mechanisms including increased apoptosis and reduced growth of cells in the tumor. The results also suggest that many mutations can affect aging and cancer, as opposed to the carcinogenic effects of p53 mutations. If this test result is repeated in the mouse model, this will be a breakthrough detection. Cell changes that prolong life are the cause of cancer cell growth.

Thai Khac Minh