published: Feb. 21, 2011, recorded: June 2006, views: 343
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No diagnosis of cancer is welcome, but some scenarios are more dreaded than others. Richard Hynes discusses what happens “when cells in the primary tumor lose their sense of address and wander off to places they’re not supposed to go.” His talk lays out the process of invasion, by which the cancer spreads into tissues adjacent to the tumor, and that of metastasis, where the cancer disseminates to distant sites.
Hynes describes the transitions a cancer undergoes as it spreads. He explains how tissue in our bodies is made of sheets of epithelial cells that are carefully arranged on a “basement membrane” by a series of adhesion receptors. These receptors, if functioning properly, don’t usually allow the cells to go anywhere. When a cell becomes tumorigenic, it loses some adhesion, and then if it becomes more damaged “wanders off into the underlying tissue.” This is called invasion. Hynes and other researchers are looking at the molecules responsible for cells’ adhesive qualities, and at the mutations in genes that trigger a loss of adhesion. Some of these processes are part of normal development, but occasionally, a “switch gets thrown in cells that should have stayed epithelial” and they become migratory instead.
Once on the move, cancer cells “need plumbing to grow,” says Hynes. Tumors recruit blood vessels to feed them and remove waste, and they can also exploit the body’s white blood cells and platelets to promote their own growth. Hynes describes “cross talk between tumor cells and cells in bone,” where the “two cells get together in evil combination to damage the bone and enhance the growth of metastases.” Scientists have discovered “a lot of different mechanisms by which metastatic cells learn new tricks and suborn the mechanism of the host to get them where they’re going.” Hynes finds such insidious workings an “appealing thing, since these alterations offer opportunities for therapies.” Researchers can tinker with circuits between cells, restore growth suppression and interfere with blood vessel recruitment. It’s “a complex problem,” says Hynes, but there are “lots of ways to get at this.”
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