There is growing evidence that links chronic stress to ovarian cancer (OC) progression. Cancer diagnosis, chemotherapy, and other traumatic life events can lead to altered psychological states, such as chronic stress. Chronic stress induces sustained activation of the sympathetic nervous system (SNS), releasing stress hormones that modulate physiological responses across different systems, including the immune system. Specifically, chronic SNS activation alters the distribution of T-cells, thus influencing clinical outcomes. The aim of this work was to determine the effects of restraint stress on a syngeneic mouse model of OC and characterize its effects on T-cell responses. We hypothesized that restraint stress would lead to accelerated growth of existing tumors and deregulation T-cell subpopulations, promoting an immunosuppressed tumor microenvironment. To determine the effect of daily restraint stress on tumor progression, we used 8 to 12-week-old female C57/BL6 mice. After three days of daily restraint stress, mice were injected with IG10 or ID8 (1 × 10^6 cells/ 100μL) murine ovarian cancer cells. Mice were sacrificed 8–12 weeks after inoculation. Once sacrificed, tumors were removed and weighted. Our results indicate that daily restraint stress increased OC growth in both IG10/ID8 groups. Moreover, IG10 tumor-bearing mice showed increased ascites production. These results suggest an association between psychological factors and disease progression. Future experiments will assess the effects of chronic stress on T-cell maturation, effector functions, exhaustion, and activation in these samples. Results obtained from this project will support future in vivo experiments regarding the effect of restraint stress and immunotherapy efficacy.
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