Tumor microenvironment: Difference between revisions

Latest revision as of 11:28, 23 March 2025

Overview of the tumor microenvironment

Tumor Microenvironment[edit]

The tumor microenvironment (TME) is the environment surrounding a tumor within the body, consisting of various cell types, signaling molecules, and the extracellular matrix (ECM). The TME plays a crucial role in tumorigenesis, influencing tumor growth, progression, and response to therapy.

Components of the tumor microenvironment

Components[edit]

The TME is composed of a variety of cellular and non-cellular components:

Cancer cells: The primary component of the tumor, these cells proliferate uncontrollably and can invade surrounding tissues.
Stromal cells: These include fibroblasts, endothelial cells, and pericytes, which contribute to the structural framework of the tumor.
Immune cells: The TME contains various immune cells such as macrophages, T cells, and natural killer cells, which can either attack the tumor or be co-opted to support tumor growth.
Extracellular matrix (ECM): A complex network of proteins and polysaccharides that provides structural support and influences cell behavior.

Tumor Stroma[edit]

The tumor stroma is the supportive tissue around the tumor, consisting of the ECM and stromal cells. It plays a significant role in tumor progression by providing structural support and modulating the behavior of cancer cells.

Hypoxia[edit]

Hypoxia, or low oxygen levels, is a common feature of the TME. It results from the rapid growth of tumors outpacing their blood supply. Hypoxia can lead to the activation of hypoxia-inducible factors (HIFs), which regulate the expression of genes involved in angiogenesis, metabolism, and cell survival.

Immune Evasion[edit]

Tumors can evade the immune system through various mechanisms, including the expression of immune checkpoint molecules that inhibit T cell activation. The TME can also recruit regulatory T cells and myeloid-derived suppressor cells to suppress immune responses.

Angiogenesis[edit]

Angiogenesis, the formation of new blood vessels, is critical for tumor growth and metastasis. The TME promotes angiogenesis through the secretion of growth factors such as vascular endothelial growth factor (VEGF).

Metastasis[edit]

The TME facilitates metastasis by providing pathways for cancer cells to invade surrounding tissues and enter the bloodstream or lymphatic system. The ECM and stromal cells can be remodeled to support this process.

Related Pages[edit]

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+{{Short description|Overview of the tumor microenvironment}}
 == Tumor Microenvironment ==
+The '''tumor microenvironment''' (TME) is the environment surrounding a [[tumor]] within the body, consisting of various cell types, signaling molecules, and the [[extracellular matrix]] (ECM). The TME plays a crucial role in [[tumorigenesis]], influencing tumor growth, progression, and response to therapy.
-The '''tumor microenvironment''' (TME) is the environment surrounding a [[tumor]], including the surrounding [[blood vessels]], [[immune cells]], [[fibroblasts]], [[signaling molecules]], and the [[extracellular matrix]] (ECM). The TME plays a crucial role in tumor development, progression, and response to therapy.
+[[File:Components-of-the-tumor-microenvironment.png|Components of the tumor microenvironment|thumb|right]]
-== Components ==
-The tumor microenvironment is composed of several key components:
-=== Cancer Cells ===
-[[Cancer cells]] are the primary component of the tumor microenvironment. They interact with other components of the TME to promote tumor growth and metastasis.
+=== Components ===
+The TME is composed of a variety of cellular and non-cellular components:
-=== Stromal Cells ===
+* '''Cancer cells''': The primary component of the tumor, these cells proliferate uncontrollably and can invade surrounding tissues.
+* '''Stromal cells''': These include [[fibroblasts]], [[endothelial cells]], and [[pericytes]], which contribute to the structural framework of the tumor.
+* '''Immune cells''': The TME contains various immune cells such as [[macrophages]], [[T cells]], and [[natural killer cells]], which can either attack the tumor or be co-opted to support tumor growth.
+* '''Extracellular matrix (ECM)''': A complex network of proteins and polysaccharides that provides structural support and influences cell behavior.
-[[Stromal cells]] include [[fibroblasts]], [[endothelial cells]], and [[pericytes]]. These cells contribute to the formation of the tumor stroma, which provides structural support and influences tumor behavior.
+[[File:Stromal_cell_in_tumor_microenvironment.jpg|Stromal cell in tumor microenvironment|thumb|left]]
-=== Immune Cells ===
+=== Tumor Stroma ===
+The tumor stroma is the supportive tissue around the tumor, consisting of the ECM and stromal cells. It plays a significant role in tumor progression by providing structural support and modulating the behavior of cancer cells.
-The TME contains various [[immune cells]], such as [[T cells]], [[B cells]], [[macrophages]], and [[natural killer cells]]. These cells can have both tumor-promoting and tumor-suppressing roles, depending on their state and the signals they receive from the tumor and its environment.
+[[File:Tumour_stroma_and_extracellular_matrix_in_hypoxia.svg|Tumor stroma and extracellular matrix in hypoxia|thumb|right]]
-=== Extracellular Matrix ===
+=== Hypoxia ===
+Hypoxia, or low oxygen levels, is a common feature of the TME. It results from the rapid growth of tumors outpacing their blood supply. Hypoxia can lead to the activation of [[hypoxia-inducible factors]] (HIFs), which regulate the expression of genes involved in angiogenesis, metabolism, and cell survival.
-The [[extracellular matrix]] (ECM) is a network of proteins and polysaccharides that provides structural support to the cells. It also plays a role in cell signaling and can influence cancer cell behavior.
+[[File:HIF_regulates_interactions_of_cancer_cells_with_ECM_and_ECM_biosynthesis.svg|HIF regulates interactions of cancer cells with ECM|thumb|left]]
-=== Signaling Molecules ===
+=== Immune Evasion ===
+Tumors can evade the immune system through various mechanisms, including the expression of immune checkpoint molecules that inhibit T cell activation. The TME can also recruit regulatory T cells and myeloid-derived suppressor cells to suppress immune responses.
-The TME is rich in [[signaling molecules]] such as [[cytokines]], [[chemokines]], and [[growth factors]]. These molecules mediate communication between cancer cells and the surrounding stromal and immune cells.
+[[File:Immune_checkpoints_of_immunosuppressive_actions_associated_with_breast_cancer.svg|Immune checkpoints in breast cancer|thumb|right]]
-== Role in Cancer Progression ==
+=== Angiogenesis ===
+Angiogenesis, the formation of new blood vessels, is critical for tumor growth and metastasis. The TME promotes angiogenesis through the secretion of growth factors such as [[vascular endothelial growth factor]] (VEGF).
-The tumor microenvironment is not just a passive bystander but actively participates in cancer progression. It can influence tumor growth, angiogenesis, immune evasion, and metastasis. The interactions between cancer cells and the TME can lead to the development of drug resistance, making the TME a target for therapeutic interventions.
+=== Metastasis ===
+The TME facilitates [[metastasis]] by providing pathways for cancer cells to invade surrounding tissues and enter the bloodstream or lymphatic system. The ECM and stromal cells can be remodeled to support this process.
-== Therapeutic Implications ==
+[[File:Tumor-associated_immune_cells_in_the_tumor_microenvironment_(TME)_of_breast_cancer_models.svg|Tumor-associated immune cells in the tumor microenvironment (TME) of breast cancer models|thumb|left]]
-Targeting the tumor microenvironment offers potential therapeutic strategies. Approaches include modifying the immune response, targeting stromal components, and altering the ECM to inhibit tumor progression and improve the efficacy of existing treatments.
 == Related Pages ==
 * [[Cancer]]
 * [[Metastasis]]
 * [[Angiogenesis]]
-* [[Immunotherapy]]
+* [[Hypoxia-inducible factor]]
+* [[Immune checkpoint]]
-== References ==
-{{Reflist}}
-== Gallery ==
-<gallery>
-File:Components-of-the-tumor-microenvironment.png|Components of the tumor microenvironment
-File:Tumour_stroma_and_extracellular_matrix_in_hypoxia.svg|Tumor stroma and extracellular matrix in hypoxia
-File:Stromal_cell_in_tumor_microenvironment.jpg|Stromal cell in tumor microenvironment
-File:HIF_regulates_interactions_of_cancer_cells_with_ECM_and_ECM_biosynthesis.svg|HIF regulates interactions of cancer cells with ECM
-File:Tumor_microenvironment.jpg|Tumor microenvironment
-File:Tumor-associated_immune_cells_in_the_tumor_microenvironment_(TME)_of_breast_cancer_models.svg|Tumor-associated immune cells in TME of breast cancer
-File:Immune_checkpoints_of_immunosuppressive_actions_associated_with_breast_cancer.svg|Immune checkpoints in breast cancer
-</gallery>
+[[Category:Oncology]]
 [[Category:Cancer]]
-[[Category:Oncology]]
+[[Category:Cell biology]]
-==Tumor_microenvironment==
-<gallery>
-File:Components-of-the-tumor-microenvironment.png|Components of the tumor microenvironment
-File:Stromal_cell_in_tumor_microenvironment.jpg|Stromal cell in tumor microenvironment
-File:Tumor-associated_immune_cells_in_the_tumor_microenvironment_(TME)_of_breast_cancer_models.svg|Tumor-associated immune cells in the tumor microenvironment (TME) of breast cancer models
-File:Immune_checkpoints_of_immunosuppressive_actions_associated_with_breast_cancer.svg|Immune checkpoints of immunosuppressive actions associated with breast cancer
-</gallery>