Closer to an Understanding of Mesothelioma Metastasis
Researchers at MIT (the Massachusetts Institute of Technology) are coming closer to tracing the cause of mesothelioma metastasis (spreading) after identifying the mechanism that causes cancer cells to detach from the original tumor site and travel to other parts of the body. Most of the time cancer cells are stationary, but in some cases they break free and circulate. Researchers are hopeful that a deeper understanding of why and how this happens could lead to new approaches to treating cancers like mesothelioma.
According to the MIT researchers, roughly 90 percent of cancer deaths are caused by metastasis. One type of cancer that is especially aggressive and fast-spreading is pleural mesothelioma. Experts at the National Cancer Institute state that the purpose for treatment of metastasized cancers is to alleviate symptoms and prevent further growth of the disease, hopefully extending the patient’s life expectancy.
The MIT study was published in Nature Communications on October 9. Researchers reported that the anchors that hold cancer cells in place, proteins known as integrins, are located on the surface of the cells. As cells become more metastatic the anchors release, freeing cells to move and adhere to other tissues, forming another tumor.
The leader of the research team, the John and Dorothy Wilson Professor of Health Sciences and Technology and Electrical Engineering and Computer Science, Sangeeta Bhatia, states, “If we can prevent (cancer cells) from growing at these new sites, we may be able to interfere with metastatic disease.
The study authors found that proteins that contain or bind to sugars, fibronictin and galectin-3, are especially common cells for metastatic tumors to adhere to. The team is hopeful that this finding will lead to the development of improved cancer drugs that focus on “ a specific protein-protein or protein-sugar interaction, rather than a particular gene mutation.” They are now working on creating drugs that will inhibit interactions between tumor cells and galectin-3.