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The concept of the tumor microenvironment (TME) dates back to 1863 when Rudolf Virchow established a connection between inflammation and cancer. However, it was not until 1889 that Stephen Paget's seed and soil theory introduced the important role of TME in cancer metastasis, highlighting the intricate relationship between tumors and their surrounding microenvironment.
A cancer-associated fibroblast (CAF) (also known as tumour-associated fibroblast; carcinogenic-associated fibroblast; activated fibroblast) is a cell type within the tumor microenvironment that promotes tumorigenic features by initiating the remodelling of the extracellular matrix or by secreting cytokines.
The composition of monocyte-derived macrophages and tissue-resident macrophages in the tumor microenvironment depends on the tumor type, stage, size, and location, thus it has been proposed that TAM identity and heterogeneity is the outcome of interactions between tumor-derived, tissue-specific, and developmental signals. [2]
The tumor microenvironment, composed of stromal cells, immune cells and singaling molecules, supports invasion by creating good and favorable conditions for tumor cell migration. [20] For example, cancer- associated fibroblasts (CAFS) produce substances that remodel the ECM and promote cancer progression.
Tumor-associated immune cells in the tumor microenvironment (TME) of breast cancer models. Cancer immunology (immuno-oncology) is an interdisciplinary branch of biology and a sub-discipline of immunology that is concerned with understanding the role of the immune system in the progression and development of cancer; the most well known application is cancer immunotherapy, which utilises the ...
Tumor stroma and extracellular matrix in hypoxia. Tumor hypoxia is the situation where tumor cells have been deprived of oxygen.As a tumor grows, it rapidly outgrows its blood supply, leaving portions of the tumor with regions where the oxygen concentration is significantly lower than in healthy tissues.
The tumor-associated endothelium has been found to be able to function as an immune barrier to T-cells, inhibiting the effectiveness of immune therapies. [29] These tumor-associated endothelial cells have been found to over-express the endothelin B receptor, which suppresses T-cell adhesion and targeting to tumors upon activation by ET-1. [30]
1) TIL therapy needs to overcome the heterogeneity of solid tumors, which adds difficulty to the identification of a target for all tumor cells. [2] 2) Achieving full function of T cells and tumor microenvironment (TME) with different immunosuppressive mechanisms is another primary concern. [2]