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Aggressive pro-angiogenic signaling drives rapid, dysfunctional vessel formation, causing poor perfusion, tissue hypoxia, and vascular leakiness that elevates interstitial fluid pressure. These conditions restrict therapeutic delivery and worsen efficacy. The TME also contains multiple immunosuppressive cell populations that secrete inhibitory cytokines, contributing to limited responses to immune checkpoint inhibitor therapy. 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Ogilvie , Cielle Lockington, Duncan Petrik, Jan Soeren Eichhorn and Jim Petrik *  \nCitation: Garlisi, B.; Lauks, S.; Aitken, C.; Ogilvie, L.M.; Lockington, C.; Petrik, D.; Eichhorn, J.S.; Petrik, J. The Complex Tumor Microenvironment in Ovarian Cancer: Therapeutic Challenges and Opportunities. Curr. Oncol. 2024, 31, 3826–3844. [https://](https://)[ ](https://)[doi.org/10.3390/curroncol31070283](doi.org/10.3390/curroncol31070283)  \nReceived: 15 May 2024  \nRevised: 27 June 2024  \nAccepted: 28 June 2024  \nPublished: 1 July 2024  \nCopyright: © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \nDepartment of Biomedical Sciences, University of Guelph, Guelph, ON N1G 2W1, Canada;  \n[bgarlisi@uoguelph.ca](bgarlisi@uoguelph.ca) (B.G.); [slauks@uoguelph.ca](slauks@uoguelph.ca) (S.L.); caitke01@uoguelph.ca (C.A.);  \n[ogilviel@uoguelph.ca](ogilviel@uoguelph.ca) (L.M.O.); [clocking@uoguelph.ca](clocking@uoguelph.ca) (C.L.); [petrikd@uoguelph.ca](petrikd@uoguelph.ca) (D.P.); [jeichhor@uoguelph.ca](jeichhor@uoguelph.ca) (J.S.E.)  \n* [Correspondence: jpetrik@uoguelph.ca](Correspondence: jpetrik@uoguelph.ca)  \nAbstract: The tumor microenvironment (TME) in ovarian cancer (OC) has much greater complexity than previously understood. In response to aggressive pro-angiogenic stimulus, blood vessels form rapidly and are dysfunctional, resulting in poor perfusion, tissue hypoxia, and leakiness, which leads to increased interstitial fluid pressure (IFP). Decreased perfusion and high IFP significantly inhibit the uptake of therapies into the tumor. Within the TME, there are numerous inhibitor cells, such as myeloid-derived suppressor cells (MDSCs), tumor association macrophages (TAMs), regulatory T cells (Tregs), and cancer-associated fibroblasts (CAFs) that secrete high numbers of immunosuppressive cytokines. This immunosuppressive environment is thought to contribute to the lack of success of immunotherapies such as immune checkpoint inhibitor (ICI) treatment. This review discusses the components of the TME in OC, how these characteristics impede therapeutic efficacy, and some strategies to alleviate this inhibition.  \nKeywords: tumor microenvironment; ovarian cancer; immunosuppression; interstitial fluid pressure; vascular normalization; tumor angiogenesis  \n1. Introduction  \n1.1. OC Biology and Subtypes  \nOC is the most lethal gynecologic malignancy and the fifth leading cause of cancerrelated death in women. Due to its vague, non-specific symptoms and the lack of effective screening strategies, OC is often not diagnosed until advanced stages of disease, where treatments have reduced efficacy, and the 5-year survival rate is poor. Therapeutic strategies for advancedOC have remained unchanged for decades and typically involve cytoreductive surgery followed by platinum-and taxane-based chemotherapy. The inhospitable and immunosuppressive ovarian TME presents several potent barriers to chemotherapeutic success, frequently resulting in therapy resistance and disease relapse. Thus, there is a need for innovative approaches to improve the management and prognosis of this devastating disease. This review focuses on a description of the OC microenvironment, its impact on therapeutic success, and potential avenues to address these issues.  \n1.2. Classification and Histopathology  \nOC is classified by histological subtype, according to which ~90% of OCs are of epithelial origin (Figure 1) . Non-epithelial subtypes include germ cell and sex cord stromal cancers, which comprise less than 10% of all OCs and are","cbCaiv2pLesqkcsp","https://ap.wps.com/l/cbCaiv2pLesqkcsp","pdf",1761550,"English","# Introduction\n## OC Biology and Subtypes\n## Classification and Histopathology\n## Diagnosis and Standard of Care","[{\"question\":\"Why does the ovarian cancer tumor microenvironment reduce therapeutic effectiveness?\",\"answer\":\"Rapid, dysfunctional angiogenesis leads to poor perfusion, hypoxia, and increased interstitial fluid pressure, which significantly inhibit therapy uptake into tumors.\"},{\"question\":\"Which immunosuppressive cell types are highlighted in the review?\",\"answer\":\"The review describes inhibitor cells including myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), regulatory T cells (Tregs), and cancer-associated fibroblasts (CAFs) that secrete immunosuppressive cytokines.\"},{\"question\":\"How is ovarian cancer typically diagnosed and what limits early detection?\",\"answer\":\"Diagnosis is complicated by vague, non-specific symptoms and the lack of biomarkers with sufficient sensitivity and specificity. Standard approaches include transvaginal sonography and CA125 blood testing, while definitive diagnosis requires tissue biopsy.\"}]","The Complex Tumor Microenvironment in Ovarian Cancer - Therapeutic Challenges and Opportunities | PDF",1790021402,48]