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Ovarian cancer is the fifth leading cause of cancer-related death among women, which is one of the most common gynecological cancers worldwide. Although several cytoreductive surgeries and chemotherapies have been attempted to address ovarian cancer, the disease still shows poor prognosis and survival rates due to prevalent metastasis. Peritoneal metastasis is recognized as the primary route of metastatic progression in ovarian cancer. It causes severe symptoms in patients, but it is generally difficult to detect at an early stage. Current anti-cancer therapy is insufficient to completely treat metastatic ovarian cancer due to its high rates of recurrence and resistance. Therefore, developing strategies for treating metastatic ovarian cancer requires a deeper understanding of the tumor microenvironment (TME) and the identification of effective therapeutic targets through precision oncology. Given that various signaling pathways, including TGF-β, NF-κB, and PI3K/AKT/mTOR pathways, influence cancer progression, their activity and significance can vary depending on the cancer type. In ovarian cancer, these pathways are particularly important, as they not only drive tumor progression but also impact the TME, which contributes to the metastatic potential. The TME plays a critical role in driving metastatic features in ovarian cancer through altered immunologic interactions. Recent therapeutic advances have focused on targeting these distinct features to improve treatment outcomes. Deciphering the complex interaction between signaling pathways and immune populations contributing to metastatic ovarian cancer provides an opportunity to enhance anti-cancer efficacy. Hereby, this review highlights the mechanisms of signaling pathways in metastatic ovarian cancer and immunological interactions to understand improved immunotherapy against ovarian cancer.
Choe et al. (Tue,) studied this question.