Abstract
Recent advances in clinical oncology is based on exploiting the capacity of the immune system to combat cancer: immuno-oncology. Thus, immunotherapy of cancer is now used to treat a variety of malignant diseases. A striking feature is that even patients with late-stage disease may experience curative responses. However, most patients still succumb to disease, and do not benefit from treatment. Exercise has gained attention in clinical oncology and has been used for many years to improve quality of life, as well as to counteract chemotherapy-related complications. However, more recently, exercise has garnered interest, largely due to data from animal studies suggesting a striking therapeutic effect in preclinical cancer models; an effect largely mediated by the immune system. In humans, physical activity is associated with a lower risk for a variety of malignancies, and some data suggest a positive clinical effect for cancer patients. Exercise leads to mobilization of cells of the immune system, resulting in redistribution to different body compartments, and in preclinical models, exercise has been shown to lead to immunological changes in the tumor microenvironment. This suggests that exercise and immunotherapy could have a synergistic effect if combined.
Highlights
The treatment of disseminated cancer has been revolutionized by the introduction of immunotherapy
Blocking of this interaction is based on the use of monoclonal antibodies specific for either PD1 or PDL1, and blocking the inhibitory signaling in cells of the immune system [1]
The mutational burden has been shown to correlate with response to therapy; treatment is provided if tested positive for microsatellite instability, which is indicative of high mutational load [10]
Summary
The treatment of disseminated cancer has been revolutionized by the introduction of immunotherapy. The mutational burden has been shown to correlate with response to therapy; treatment is provided if tested positive for microsatellite instability, which is indicative of high mutational load [10] In this case, it is purported that the mutational burden renders cancer cells more immunogenic due to the expression of a higher fraction of none-self neoantigens derived from gene mutations [11]. Several studies have shown a correlation between response to PD1/PDL1 blockade and the infiltration of T cells This makes a lot of sense, given the supposed mechanism of action; that tumor-specific T cells in the TME are functionally suppressed via the engagement of PD1 expressed by the T cell, with PDL1 expressed by cancer cells. Exercise has been shown to mobilize cells of the immune system, both in man and mouse, and could play a role to increase immune cell infiltration to tumors and modulate the tumor microenvironment
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