Metastasis of cancer is the spreading of tumour cells to other organs. This often adds to the deadliness of the disease, and therefore is an important feature to study. Scientists from MIT have shown that a component of the blood aids spreading of cancer cells throughout the body. Blood platelets function in blood clotting, but also seem to produce chemical signals that turn tumour cells into travellers, which are consequently able to find a home in a different organ. The findings are relevant, because if we are able to develop drugs that inhibit this process, we could greatly reduce the deadliness of some cancers.
In the lab, MIT scientists showed that when cancer cells come in contact with platelets, they transform themselves into a more primitive cell, that no longer attaches to others. This process is called epithelial to mesenchymal transition (EMT), and is commonly found in the body. As a consequence the malicious cells are free to roam the body, and can enter the bloodstream. Eventually they enter a different organ than where they came from. They will start growing again, to form a secondary tumour.
Further analysis of platelet-induced activation of tumour cells showed that a chemical called TGFß is key in the transition process. However, this molecule was, on its own, unable to induce metastasis. More research is needed to unravel the full signalling pathway that underlies tumour metastasis.
The MIT study reveals a clear anti-cancer target, that can be used for the development of new cancer drugs. If we manage to somehow inhibit platelet signalling in cancer patients, we may be able to stop metastasis, and confine the tumour to its primary location. A possible downside is that side-effects may include problems with blood clotting.
EMT is an important process that plays a role throughout life. It starts during development, when EMT is key to development of certain structures, such as the neural tube that later forms a large part of our central nervous system. It is also associated with organ damage. Epithelium, the cells that form the outer layer of an organ, is a specialized cell type, but when it gets transformed into mesenchyme, it loses its functionality. Endothelium, the inner layer of cells that are important in blood vessels, can undergo a similar process, dubbed EndoMT. Both are suspected to be an important process in fibrosis, when functional tissue is replaced by dysfunctional scar tissue.
In the lab, MIT scientists showed that when cancer cells come in contact with platelets, they transform themselves into a more primitive cell, that no longer attaches to others. This process is called epithelial to mesenchymal transition (EMT), and is commonly found in the body. As a consequence the malicious cells are free to roam the body, and can enter the bloodstream. Eventually they enter a different organ than where they came from. They will start growing again, to form a secondary tumour.
Further analysis of platelet-induced activation of tumour cells showed that a chemical called TGFß is key in the transition process. However, this molecule was, on its own, unable to induce metastasis. More research is needed to unravel the full signalling pathway that underlies tumour metastasis.
The MIT study reveals a clear anti-cancer target, that can be used for the development of new cancer drugs. If we manage to somehow inhibit platelet signalling in cancer patients, we may be able to stop metastasis, and confine the tumour to its primary location. A possible downside is that side-effects may include problems with blood clotting.
EMT is an important process that plays a role throughout life. It starts during development, when EMT is key to development of certain structures, such as the neural tube that later forms a large part of our central nervous system. It is also associated with organ damage. Epithelium, the cells that form the outer layer of an organ, is a specialized cell type, but when it gets transformed into mesenchyme, it loses its functionality. Endothelium, the inner layer of cells that are important in blood vessels, can undergo a similar process, dubbed EndoMT. Both are suspected to be an important process in fibrosis, when functional tissue is replaced by dysfunctional scar tissue.
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