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...intrinsically evil villain but an ordinary machine that has broken down in very specific, and potentially reparable, ways. They have studied the life history of a cancer cell and found errant genes at almost every step of the way, from the initial formation of a tumor to the advanced stages of metastasis, the lethal spread of the disease through the body...

Author: /time Magazine | Title: Stopping Cancer in Its Tracks | 4/25/1994 | See Source »

Even so, cancer is hardly inevitable. For example, 50% of Americans will develop at least one precancerous polyp in their colon at some point, but only a fraction of such polyps will develop into aggressive tumors. Why? Usually it takes so long for colon cancer to unfold that most people end up dying of ! other causes. Indeed, contrary to popular perception, getting cancer is not at all easy. To begin with, a cell must accumulate mutations not in just one or two genes but in several. In the case of colon cancer, Dr. Bert Vogelstein and his colleagues at Baltimore...

Author: /time Magazine | Title: Stopping Cancer in Its Tracks | 4/25/1994 | See Source »

...some ingredients of cigarette smoke. Many carcinogens, it turns out, are not blunderbusses but leave highly individualized fingerprints in the DNA they touch. At the National Cancer Institute, Dr. Curtis Harris, a molecular epidemiologist, has been examining cells from liver- and lung-cancer patients, searching for mutations in a tumor-suppressor gene known as p53 (p stands for the protein the gene makes and 53 for the protein's molecular weight). Smokers who develop lung cancer, Harris has found, show tiny alterations in the p53 gene that differ from those in nonsmokers. They also vary from the changes found...

Author: /time Magazine | Title: Stopping Cancer in Its Tracks | 4/25/1994 | See Source »

...tumor-suppressor gene p53 is often described as "the guardian of the genome" because it keeps watch over DNA during cell division. When damage occurs, p53 commands other genes to bring cell division to a halt. If repairs are made, then p53 allows the cell cycle to continue. But in some cases, if the damage is too serious to be patched, p53 activates other genes that cause the cell to self-destruct. Mutations in p53, which have been detected in more than 50% of all human cancers, are thus extremely dangerous. In laboratory cultures, some cancer cells that possess mutant...

Author: /time Magazine | Title: Stopping Cancer in Its Tracks | 4/25/1994 | See Source »

Perhaps the most critical stage in the life of a tumor comes after it expands to about a million cells. At this point, it is "much smaller than a BB," says Dr. Judah Folkman of Harvard Medical School. This tiny mass -- known as a carcinoma in situ, literally cancer in place -- is malignant, but not yet dangerous. Why? Because the cells at the center of the tumor are too far from the bloodstream to obtain essential nutrients, they are less vigorous. Like a society with zero population growth, a carcinoma in situ adds about as many new cells...

Author: /time Magazine | Title: Stopping Cancer in Its Tracks | 4/25/1994 | See Source »

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