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- W4312467594 startingPage "137" @default.
- W4312467594 abstract "It has been broadly accepted that the tumor microenvironment (TME) has a significant impact on the aggressive behavior of malignant solid tumors. One of the cell types connected with the tumor microenvironment is tumor macrophages, which perform an essential job in promoting cancer cells, especially in breast malignancy. Tumor-associated macrophages (TAM) contribute to breast cancer development and progression by boosting angiogenesis and inducing cancer stemness, tumor cell metastasis, controlling energy metabolism, and suppressing the immune system. It has been revealed that the abundant population of TAMs is characterized by breast cancer, and experimental studies have revealed a variety of mechanisms in which tumor-associated macrophages interrelate with and greatly influence the adjoining tumor cells. Tumor cells invade the constraining extracellular matrix (ECM) and acquire access to the tissue presenting angiogenic substances like VEGF, which help in the establishment of the network of capillaries around tumor cells for their nourishment and also serve as transport pathway into the extracellular matrix (ECM). In addition, TAMs secrete various proinflammatory substances that dampen the antitumor response and let tumor cells escape. Correspondingly, hypoxia conditions established inside TME promote phagocytes to secrete VEGF and decrease the immune response of T cells and intensify tumor cells evasion, and ultimately spread. TAMs tend to show a remarkable degree of cellular plasticity. TAMs can enhance tumor regression by repolarizing tumor-linked macrophages into M1 macrophages." @default.
- W4312467594 created "2023-01-04" @default.
- W4312467594 creator A5007941009 @default.
- W4312467594 creator A5021030114 @default.
- W4312467594 creator A5079529210 @default.
- W4312467594 date "2022-01-01" @default.
- W4312467594 modified "2023-10-16" @default.
- W4312467594 title "Role of tumor-associated macrophages in the breast tumor microenvironment" @default.
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