Word: celling
(lookup in dictionary)
(lookup stats)
Dates: during 1990-1999
Sort By: most recent first
(reverse)
Metastasis is an event of awesome complexity, one that requires multiple genes to cooperate as closely as musicians in an orchestra. Some of these genes code for chemical solvents that enable the advancing cell to dissolve surrounding tissue. Others order up the production of adhesion molecules that, like treads under a tank, move the cell forward. Why would genes do that? The answer, notes Patricia Steeg of the National Cancer Institute, is that while the genes important to metastasis are abnormally turned on, they are not necessarily abnormal themselves. A cancer cell, in many ways, is not that different from...
What makes MTS1 so significant is its clear role in the cell-division cycle. A cell divides not at will but in response to specific signals, such as growth factors produced by white blood cells rushing to repair a wound. These signals are picked up by receptors on the membrane of the cell and passed along -- like batons in a high-speed relay -- through the interior, all the way to a master "on" switch positioned deep in the nucleus. Not surprisingly, many oncogenes, including one called ras, the first human cancer gene ever identified, are involved in this type...
Theoretically, any gene that goes awry in a cancer cell offers a way to attack the problem. But those that directly influence a cell's decision to divide are spurring particular interest. The protein made by the MTS1 gene seems exceptionally promising, for it has characteristics suggesting it may be easily fashioned into a drug, which then might be able to stop tumor cells in their tracks. "In terms of therapeutic potential," declares Kamb, "MTS1 may be the most important tumor-suppressor gene yet discovered...
...discovery announced last week that cancer cells rely on the enzyme telomerase to stay alive opens up a different attack strategy. The leader of that research team, Calvin Harley, has taken a leave from McMaster University to work at Geron Corp. in Menlo Park, California. The company is trying to craft a drug that will block the action of telomerase. "The cancer cell," explains Harley, "is already very old. If we can inhibit telomerase, we might cause the tumor to die after a few doublings." Even better, the fact that cancer cells produce telomerase and that normal cells (save...
Indeed, what seems most significant about all the new therapies, what joins them together, is not their power, for this has yet to be proved. Rather, it is the seismic shift in strategy they collectively represent. Increasingly, researchers speak not of slaughtering the cancer cell but of tricking it into dying naturally, perhaps of old age, as other cells do. They also talk of reining in the cancer cell, even rehabilitating it, a task that demands the development of less toxic drugs that can be tolerated over a lifetime. The model for cancer therapy of the future already exists. "After...