Steroid-induced modulation of the tumor immune microenvironment: Implications for cancer progression and immunotherapy outcomes.
3/5 보강
TL;DR
Clinical data indicate that the timing, dose, and duration of steroid exposure are decisive, with early or high-dose administration frequently associated with poorer immunotherapy outcomes, and clarifying GC-driven immune modulation is critical to balance toxicity control while preserving anti-tumor efficacy in precision immunotherapy.
OpenAlex 토픽 ·
Immune cells in cancer
Cancer Immunotherapy and Biomarkers
Immunotherapy and Immune Responses
Clinical data indicate that the timing, dose, and duration of steroid exposure are decisive, with early or high-dose administration frequently associated with poorer immunotherapy outcomes, and clarif
APA
Kanimozhi Kaliyamoorthi (2026). Steroid-induced modulation of the tumor immune microenvironment: Implications for cancer progression and immunotherapy outcomes.. The Journal of steroid biochemistry and molecular biology, 259, 106978. https://doi.org/10.1016/j.jsbmb.2026.106978
MLA
Kanimozhi Kaliyamoorthi. "Steroid-induced modulation of the tumor immune microenvironment: Implications for cancer progression and immunotherapy outcomes.." The Journal of steroid biochemistry and molecular biology, vol. 259, 2026, pp. 106978.
PMID
41775287 ↗
Abstract 한글 요약
Glucocorticoids (GCs) remain indispensable in oncology due to their strong anti-inflammatory, anti-oedema, and immunosuppressive effects, which are crucial for controlling cancer symptoms and treatment-related toxicities. However, the expanding use of immunotherapies, particularly immune checkpoint blockade and CAR-T cell approaches, has highlighted the paradoxical influence of steroids on anti-tumor immunity. GCs profoundly reshape the tumor immune microenvironment (TIME) by suppressing cytotoxic T-cell activity, enhancing regulatory T cells, polarizing macrophages toward tumor-promoting states, inhibiting NK and dendritic cell function, and expanding myeloid-derived suppressor cells. Together, these alterations weaken immune surveillance and may promote tumor progression, metastasis, and therapeutic resistance. Both systemic and tumor-derived GC signaling further interact with niches that sustain cancer stemness. Clinical data indicate that the timing, dose, and duration of steroid exposure are decisive, with early or high-dose administration frequently associated with poorer immunotherapy outcomes. Therefore, clarifying GC-driven immune modulation is critical to balance toxicity control while preserving anti-tumor efficacy in precision immunotherapy.
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