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A narrative review on tumor microenvironment in malignant tumors

Zuleyha Doganyigit

Zuleyha Doganyigit

Yozgat Bozok University, Faculty of Medicine, Department of Histology and Embryology, Erdogan Akdag CampusYozgat, Turkey
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Doganyigit, Zuleyha
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Ece Eroglu

Ece Eroglu

Yozgat Bozok University, Faculty of Medicine, Erdogan Akdag CampusYozgat, Turkey
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Aslı Okan

Aslı Okan

Yozgat Bozok University, Faculty of Medicine, Department of Histology and Embryology, Erdogan Akdag CampusYozgat, Turkey
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Seher Yilmaz

Seher Yilmaz

Yozgat Bozok University, Faculty of Medicine, Department of Anatomy, Erdogan Akdag CampusYozgat, Turkey
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Yilmaz, Seher
  
17 kwi 2025
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Kategoria artykułu: Review
Data publikacji: 17 kwi 2025
Zakres stron: 50 - 60
Otrzymano: 15 lip 2024
Przyjęty: 19 lut 2025
DOI: https://doi.org/10.2478/ahem-2025-0005
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© 2025 Zuleyha Doganyigit et al., published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Figure 1.

Cell Populations in the Tumor Microenvironment (created by BioRender.com). The tumor microenvironment comprises cancer cells, extracellular matrix, and stromal tissue. In addition, there are macrophage cells, dendritic cells, natural killer cells, and T and B lymphocyte cells around cancer cells in the tumor microenvironment. When you move towards the center of the tumor microenvironment, the oxygen level decreases, and by-products such as anti-inflammatory cytokines and chemokines accumulate in the environment. A. CD8+T cells diversify into cytotoxic T cells and enter the tumor microenvironment [9]. These cells then exhibit cytotoxicity against tumor cells and provide immune control of the tumor microenvironment. B. Subpopulations of tumor-associated macrophages, anti-tumor M1-like and pre-tumor M2-like, tumor-associated macrophages coexist within the tumor. Contrasting effects of M1/M2 subpopulations on tumors modulate anti-tumor immune control. Moreover, Treg cells in the tumor microenvironment can be differentiated induced by conventional T cells with a potent immunosuppressive function, promoting the formation and development of tumors [10]. As cancer cells proliferate, they pass mutations that cause them to metastasize to other sites. In this context, DNA damage of cancer cells in the tumor microenvironment creates genomic instability (Treg, regulatory T cells). Genomic instability is characterized by events such as DNA damage, chromosomal aberrations, and mutations in cancer cells, which increase tumor heterogeneity and alter how the immune system interacts with the tumor. This figure was created by Biorender (https://biorender.com/)
Cell Populations in the Tumor Microenvironment (created by BioRender.com). The tumor microenvironment comprises cancer cells, extracellular matrix, and stromal tissue. In addition, there are macrophage cells, dendritic cells, natural killer cells, and T and B lymphocyte cells around cancer cells in the tumor microenvironment. When you move towards the center of the tumor microenvironment, the oxygen level decreases, and by-products such as anti-inflammatory cytokines and chemokines accumulate in the environment. A. CD8+T cells diversify into cytotoxic T cells and enter the tumor microenvironment [9]. These cells then exhibit cytotoxicity against tumor cells and provide immune control of the tumor microenvironment. B. Subpopulations of tumor-associated macrophages, anti-tumor M1-like and pre-tumor M2-like, tumor-associated macrophages coexist within the tumor. Contrasting effects of M1/M2 subpopulations on tumors modulate anti-tumor immune control. Moreover, Treg cells in the tumor microenvironment can be differentiated induced by conventional T cells with a potent immunosuppressive function, promoting the formation and development of tumors [10]. As cancer cells proliferate, they pass mutations that cause them to metastasize to other sites. In this context, DNA damage of cancer cells in the tumor microenvironment creates genomic instability (Treg, regulatory T cells). Genomic instability is characterized by events such as DNA damage, chromosomal aberrations, and mutations in cancer cells, which increase tumor heterogeneity and alter how the immune system interacts with the tumor. This figure was created by Biorender (https://biorender.com/)

Figure 2.

Interaction of ECM with Tumor Cells. Tumor cells suppress the response of T cells, leading to immunosuppression. These cells remodel the ECM by activating fibroblasts, which are the major cells of the TME. Macrophage polarization, cancer cells, and fibroblast cells contribute to ECM remodeling about matrix stiffness. Matrix stiffness is mainly related to excess collagen in the TME. (ECM, Extracellular matrix, TME, Tumor microenvironment). This figure was created by Biorender (https://biorender.com/)
Interaction of ECM with Tumor Cells. Tumor cells suppress the response of T cells, leading to immunosuppression. These cells remodel the ECM by activating fibroblasts, which are the major cells of the TME. Macrophage polarization, cancer cells, and fibroblast cells contribute to ECM remodeling about matrix stiffness. Matrix stiffness is mainly related to excess collagen in the TME. (ECM, Extracellular matrix, TME, Tumor microenvironment). This figure was created by Biorender (https://biorender.com/)
Język:
Angielski
Częstotliwość wydawania:
1 razy w roku
Dziedziny czasopisma:
Nauki biologiczne, Biologia molekularna, Mikrobiologia i wirusologia, Medycyna, Podstawowe nauki medyczne, Immunologia
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