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Review
. 2024 Dec 31;15(1):849.
doi: 10.1007/s12672-024-01675-w.

Sex hormones and immune regulation in ovarian cancer

Affiliations
Review

Sex hormones and immune regulation in ovarian cancer

Rui Zhao et al. Discov Oncol. .

Abstract

Ovarian cancer continues to be a major cause of morbidity and mortality in women, with immune regulation playing a critical role in its progression and treatment response. This review explores the interplay between sex hormones, particularly estrogen and progesterone, and immune regulation in ovarian cancer. We delve into the mechanisms by which these hormones influence immune cell function, modulate immune checkpoints, and alter the tumor microenvironment. Key pathways involving estrogen and progesterone receptors are examined, highlighting their impact on tumor growth and immune evasion. The review also discusses the therapeutic implications of these interactions, including the potential for combining hormone-based therapies with immune checkpoint inhibitors. Personalized medicine approaches, leveraging biomarkers for predicting treatment response, are considered essential for optimizing patient outcomes. Finally, we address current research gaps and future directions, emphasizing the need for advanced research technologies and novel therapeutic strategies to improve the treatment of ovarian cancer through a better understanding of hormone-immune interactions.

Keywords: Estrogen; Immune regulation; Ovarian cancer; Progesterone; Sex hormones.

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Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Primary ways estrogen affects the behavior of ovarian cancer cells
Fig. 2
Fig. 2
The effects of endocrine therapies on the estrogen receptor pathway. Endocrine therapies play a pivotal role in the treatment of hormone-sensitive ovarian cancer by targeting the estrogen receptor (ER) pathway. These therapies include aromatase inhibitors, selective estrogen receptor modulators (SERMs), and selective estrogen receptor degraders (SERDs), each of which employs a distinct mechanism to inhibit ER signaling

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