Ambivalent Impact of Senescent Cells on the Proliferation of Neoplastic Cells

The study shows that carcinogenesis in old age occurs through a direct pathway, i.e. through the action of mediators excessively produced by senescent cells on subsequent stages of oncogenesis, and/or through an indirect pathway. The second possibility occurs through the aforementioned mediators involved in the process of aging-related inflammation (inflammaging). In this reaction, immune system cells are also recruited by pro-inflammatory substances secreted by senescent cells. Aging-related inflammation has many features of “internal inflammation” without an infectious factor and can induce cancer, and conversely, cancer induces internal inflammation as a response to its action. A key role in this process is attributed to the tumor microenvironment (TME) on its progression and vice versa. Mutations in the cell’s environmental genes (landscape genes) contribute to the creation of conditions for uncontrolled proliferation of these cells. The paper also presents senescent cells in the process of evolution, emphasizing the fact that evolution has not eliminated cancer, as they are probably the only structures that guarantee cellular “immortality”. Cancer, therefore, is likely a structure corresponding to infinite (“immortal”) fractures.