Tumor Microenvironment of Gynecological Tumors

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 10 January 2026 | Viewed by 455

Special Issue Editors


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Guest Editor
School of Life Sciences, University of Sussex, Falmer, Brighton BN1 9RH, UK
Interests: angiogenesis; tumor microenvironment; endothelial cells; ovarian cancer; immunomodulation
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Pathology, Gomel State Medical University, 246000 Gomel, Belarus
Interests: endometrial cancer; tumor immunology; uterine cancer; immunohistochemistry

Special Issue Information

Dear Colleagues,

The tumor microenvironment (TME) of gynecological cancers, including ovarian, uterine, endometrial, and cervical cancers, plays a crucial role in tumor progression, immune evasion, and therapeutic resistance. This dynamic ecosystem consists of cancer cells, immune cells, cancer-associated fibroblasts (CAFs), endothelial cells, and extracellular matrix components that interact to modulate tumor behavior.

Immunomodulation within the TME enables tumor cells to evade immune surveillance by suppressing cytotoxic T cells and recruiting immunosuppressive regulatory T cells and myeloid-derived suppressor cells. Cancer-associated fibroblasts contribute to tumor progression by secreting growth factors and remodeling the extracellular matrix, promoting invasion and metastasis. Endothelial cells drive angiogenesis, ensuring a continuous supply of oxygen and nutrients to support tumor growth while also forming an abnormal vasculature that impairs drug delivery.

Metastatic niches in gynecological cancers, such as the omental and peritoneal environments in ovarian cancer or the lymphatic spread in cervical cancer, provide a supportive microenvironment for disseminated tumor cells. These niches are preconditioned by tumor-derived exosomes, cytokines, and extracellular matrix remodeling, creating a permissive site for colonization and growth. The interplay between metastatic niches and the TME further enhances tumor plasticity and resistance to therapy.

Critical signaling pathways within the gynecological TME regulate tumor progression and therapeutic responses. The transforming growth factor-beta (TGF-β) pathway promotes immune suppression and CAF activation, while the PI3K/AKT/mTOR pathway drives tumor cell survival and angiogenesis. The Wnt/β-catenin signaling axis is implicated in immune evasion by altering T-cell infiltration, and the hypoxia-inducible factor-1 alpha (HIF-1α) pathway facilitates adaptation to hypoxic conditions, promoting tumor aggressiveness. Understanding these pathways enables the discovery of potential therapeutic targets to disrupt the pro-tumorigenic functions of the gynecological TME.

Prof. Dr. Zahid Pranjol
Dr. Dmitry Aleksandrovich Zinovkin
Guest Editors

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Keywords

  • tumor microenvironment
  • gynecological cancers
  • immunomodulation
  • cancer-associated fibroblasts
  • angiogenesis
  • cancer-like stem cells
  • extracellular matrix
  • immune evasion
  • cell signaling
  • therapeutics

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Published Papers (1 paper)

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Research

20 pages, 2130 KB  
Article
Interaction Between Mesenchymal Stromal Cells and Tumor Cells Present in Cervical Cancer Influences Macrophage Polarization
by Eduardo Bautista-Sebastián, Víctor Adrián Cortés-Morales, Guadalupe Rosario Fajardo-Orduña, Alberto Monroy-García, Marta Elena Castro-Manrreza, Alberto Daniel Saucedo-Campos, Marcos Gutiérrez-de la Barrera, Héctor Mayani and Juan José Montesinos
Cancers 2025, 17(19), 3099; https://doi.org/10.3390/cancers17193099 - 23 Sep 2025
Viewed by 93
Abstract
Background/Objectives: Macrophages with the M2 phenotype are an immune population with great relevance for tumor development. We have previously demonstrated that mesenchymal stromal cells (MSCs) from cervical cancer (CeCa-MSCs) enhance the immunomodulatory activity of CeCa cells on T lymphocytes; however, the effect of [...] Read more.
Background/Objectives: Macrophages with the M2 phenotype are an immune population with great relevance for tumor development. We have previously demonstrated that mesenchymal stromal cells (MSCs) from cervical cancer (CeCa-MSCs) enhance the immunomodulatory activity of CeCa cells on T lymphocytes; however, the effect of these cells on the ability of tumor cells to polarize macrophages had not been evaluated to date. Methods: To address this, we set out to analyze the effect of normal cervix (NCx) and CeCa-MSCs interacting with CeCa tumor cells (TCs) to polarize macrophages in a coculture system. Results: Our results show that macrophages from TC/NCx-MSC cocultures decreased CD163 expression. In turn, we observed that macrophages from TC/CeCa-MSC cocultures, in contrast to those in the presence of TCs/NCx-MSCs, increased the intracellular production of IDO, IL-4, and IL-10; decreased T lymphocyte proliferation; and increased the presence of soluble IL-10. Interestingly, coculture in the presence of TCs/NCx-MSCs decreased the capacity of macrophages to generate regulatory T lymphocyte populations, as well as their phagocytic capacity, and increased IL-6 secretion, unlike the coculture of macrophages in the presence of TCs/CeCa-MSCs. Our results show that TCs/CeCa-MSCs in cocultures, unlike TCs/NCx-MSCs, have a greater capacity to polarize macrophages to an M2 phenotype and that such macrophages have a greater immunosuppressive potential. Conclusions: This in vitro study suggests that intracellular communication between MSCs and tumor cells in CeCa may promote tumor growth through the polarization of macrophages with increased immunosuppressive activity. Full article
(This article belongs to the Special Issue Tumor Microenvironment of Gynecological Tumors)
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