ArticleFrontiers in immunology2025
Chronic stress drives ovarian cancer progression via myeloid-derived suppressor cells infiltration and Notch signaling pathway activation.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Chronic stress and myeloid immunosuppression in cancer: A neuroimmune link to behavioral dysfunction.Brain, behavior, & immunity - health · 2026Review
- Mechanisms of Paclitaxel Resistance: Recent Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- Cell type-specific pharmacological modulation of the neuro-immune axis: the role of ADRB2 signaling in reshaping the tumor ecosystem.Frontiers in pharmacology · 2026Review
- Targeting glucocorticoid receptor signaling in platinum-resistant ovarian cancer: translational rationale and clinical advances following the ROSELLA trial.Oncology reviews · 2026Review
- Beyond survival: psychoneuroimmunology-driven cancer psychological rehabilitation-a paradigm shift from symptom management to biobehavioral remodeling.Frontiers in oncology · 2026Review
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Authors and funding
18 authors.
Funding
Abstract
Background: Ovarian cancer (OC) is a leading cause of cancer-related death among women, with elevated levels of stress hormones linked to OC progression and immune evasion in the tumor microenvironment (TME). Chronic psychosocial stress has been associated with the expansion of immunosuppressive myeloid-derived suppressor cells (MDSCs), which promote tumor growth and negatively impact patient outcomes. This study tested how chronic daily restraint stress affected ovarian cancer progression, Notch signaling, and MDSCs in the OC TME. We hypothesized that chronic stress increases MDSCs infiltration in the TME, enhances Notch signaling in OC cells, and promotes cancer progression. Methods: Female C57BL/6 mice were injected with ID8 Results: Chronic daily restraint stress increased MDSCs infiltration and enriched polymorphonuclear (PMN)-MDSCs in the TME and bone marrow in both models. Conclusion: These data indicate that chronic stress leads to MDSCs infiltration and suppressive activity, which contributes to an immunosuppressive TME and OC progression.
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