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Invasion & Metastasis - Coggle Diagram
Invasion & Metastasis
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Cross-talk & feedback
Mesenchymal stem cells in the tumor stroma can secrete CCL5 (chemokine ligand 5) in response to signals released by cancer cells - CCL5 then acts on the cancer cells - stimulates invasive behaviour
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Implication: The invasion-metastasis cascade may be acquired without additional mutations beyond those that were needed for primary tumor formation
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Cell adhesion molecules
Multiple classes of CAMs expressed on cancer cells including: cadherins, integrins', immunoglobulin superfamily cell adhesion molecules
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Invading cancer cells experience changing tissue environments and matrix components - adapt by altering CAM expression (e.g. there are >22 types of alternately expressed integrins)
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Cathepsin proteases
Proteases such as cathepsin-B degrade collagens in connective tissue -> Allow penetration of the basal lamina and the stroma, to support exit from organs and entry to the circulatory system: intravasation.
Normally housed in membrane-bound vesicles (lysosomes) inside the cell (function to degrade cellular proteins)
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Heterotypic contribution from non-cancer cells: macrophages at the tumor periphery support local invasion by supplying matrix-degrading enzymes such as metalloproteinases & cathepsin proteases
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Site specificity
Seed & soil hypothesis
Concluded that some types of tumour cell (‘seed’) have an affinity for specific organ environments (‘soil’).
But: contralateral metastases are rare! Contralateral metastases - e.g. cancer cells spreading from one breast to another
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Experimental evidence: Intravenous injection of B16 melanoma cels into mice - directly into circulation
Tumor foci formed in lungs but also where fragments or lung or ovarian tissue implanted into the muscle
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Shows that certain tissue microenvironments ("soil") are intrinsically hospitable to certain cancer cells
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