Cancer in the elderly is not an inevitability
The risk of developing cancer increases with age. Traditionally, this pattern is explained by the age-related accumulation of cancer-causing mutations. However, researchers at the University of Colorado, working under the leadership of Dr. James DeGregori, formulated a slightly different hypothesis, according to which normal cells are optimized for functioning in an ecosystem of healthy tissue, changes in which provide conditions for the emergence of another, more adapted population. Inflammation, often (but not necessarily) associated with aging, is a common mechanism of imbalance in tissues, allowing cells with cancer-causing mutations to displace healthy rivals, which leads to a change of the dominant healthy population to a population of pathologically altered cells.
According to the authors, in earlier studies they used a computer to simulate the process of cancer development triggered by "natural selection", and in the latest work they received confirmation of their hypothesis in experiments on mice.
The object of the study was to study the ecosystem of precursors of B-lymphocytes, whose pathological changes lead to the development of leukemia. And the goal is to clarify the role of bone marrow inflammation, which is one of the manifestations of age–related changes in the tissue in which populations of B-lymphocyte precursors are localized.
The authors found that inflammation really disrupts the growth and functioning of B-lymphocyte progenitor cells. However, this leads not only to a slowdown in the renewal of the B-lymphocyte population in the elderly, but also to the fact that the cells carrying "bad" mutations gain an advantage for survival in conditions of inflammation of the surrounding tissue.
They came to such conclusions as a result of working with different lines of mice, including those resistant to the development of inflammation. In particular, it was shown that in the absence of the effects of inflammation, the progenitor cells of B-lymphocytes did not lose their viability. At the same time, suppression of already existing inflammation prevented the "capture" of the bone marrow niche by cells expressing the NRAS oncogene.
Experiments on animals of different ages have also shown that older mice are more predisposed to the development of leukemia, but only against the background of age-related inflammatory status. When age-related inflammation was blocked, the risk of developing leukemia in such animals was comparable to the risk typical for young mice.
Traditionally, it is believed that aging people inevitably enter the risk group for the development of cancer, that is, the more time a person has lived, the more likely it is that the accumulation of mutations will lead to the development of the disease. However, the new results suggest that an increase in cancer risk is not so inevitable, and the development of cancer in older people is not just a matter of time, but partly depends on inflammation-associated changes in tissues.
In addition, the authors' study showed that the elimination of inflammation in the tissue can prevent the formation of cancer. There are many anti-inflammatory drugs, including a whole class of nonsteroidal anti-inflammatory drugs, whose ability to reduce the incidence of cancer in humans has been demonstrated recently. At the same time, inflammation is a critical program for our body, necessary, for example, to fight infections. Therefore, it is necessary to further clarify how inflammatory processes in the elderly body should be modulated in order to obtain maximum effect with minimal negative impact on the state of health in general.
Article by Curtis J. Henry et al. Aging-associated inflammation promotes selection for adaptive oncogenic events in B cell progenitors published in Journal of Clinical Investigation/
Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru
13.11.2015