CAMBRIDGE, Mass. (June 21, 2004) Scientists know a great deal about how tumors originate and develop, but relatively little about how cancer manages to metastasize and invade distant tissues and organs. Now, a team of researchers led by Whitehead Member Robert Weinberg has discovered that tumors spread by reactivating and commandeering a "sleeper" protein that should have been shut off permanently in early embryo development.
"As a result, cancer cells acquire in one fell swoop many of the abilities they need to execute the complex stages of metastasis," says Weinberg, who also is a professor of biology at MIT.
Metastasis is a highly inefficient, multi-step process that requires cancer cells to jump through many hoops. The cells first must invade a nearby tissue, then make their way into the blood or lymphatic vessels. Next they must migrate through the bloodstream to a distant site, exit the bloodstream, and establish new colonies. The entire operation involves so many steps that it raises an obvious question: How do cancer cells cobble these behaviors together and acquire the ability to do all this? According to the new study, they don't. Rather, they hijack an existing cellular process and use it to disperse throughout the body.
Reporting in the June 25 issue of the journal Cell, the research team headed by Weinberg describes how a breast carcinoma in mice misappropriates a protein called Twist. Twist is a gene regulator, meaning that it tells genes when to turn on and when to turn off. But Twist is mainly active in early embryonic development, where it enables cells to move from one part of an embryo to another and allocate these cells into different tissues. As an embryo develops, Twist's functions no longer are necessary, and it soon becomes dormant in most tissues throughout the rest of an organism's life.
Through a process that still is somewhat unclear to researchers, tumor cells reacPage: 1 2 3 Related biology news :1
Contact: David Cameron
Whitehead Institute for Biomedical Research
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