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Cancer is ultimately a disease of malfunctioning genes. Perhaps 10 percent of all cancers occur in people who have inherited genes that make them vulnerable. In some cases, those genes are so influential the risk of cancer is very high. However, most of us are born with good genes that succeed in flawlessly organizing our growth and development. After all, our genes have been optimized by more than 600 million years of evolution; they ought to work well. During the course of our lifetimes, though, genes are damaged in various cells throughout the body. It is these mutated genes that drive most cancers.
Every cell contains growth-promoting genes called "proto-oncogenes" and growth-stopping genes called "tumor suppressor" genes. Mutations that activate a proto-oncogene can cause the gene to release an unceasing stream of growth-stimulating molecular signals that cause the cell to multiply. Conversely, mutations that inactivate tumor-suppressor genes cause their growth-stopping messages to be silenced. In most human-cancer cells, there are multiple mutations—some that activate oncogenes and some that silence tumor-suppressor genes. In other words, cancer cells have stuck accelerator pedals and faulty brakes. During our lifetime, the cells in our bodies will divide 1016 times—that's 10,000 trillion times—creating 10,000 trillion opportunities for our "start" and "stop" signals to malfunction, and for a tumor to start.
Another important gene, called telomerase, is turned off in healthy cells, causing the cells to die after they have doubled about 50 times. Telomerase is turned on, however, in many cancer cells, which allows them to multiply indefinitely. There are other genes that cause a cell to "commit suicide" when the cell senses that it has been damaged; if such a cell suicide gene becomes disabled, a cancer cell will be allowed to multiply.
Genes also affect a cancerous cell's ability to metastasize—to detach itself from the primary tumor, crawl through the walls of nearby small blood or lymph vessels and spread through the circulation to other parts of the body. Research published in the past year has identified sets of genes that normally are active only when cells in an embryo need to migrate from one part of the embryo to another. In cancer cells that metastasize, these long-silent genes have somehow been activated. The genes make it easy for a cell to detach itself from the tissue around it and they improve the cell's ability to move toward and through the walls of blood and lymph vessels. Recently, a small molecule called microRNA-10b was discovered to powerfully affect the ability of breast-cancer cells to metastasize. This is exciting because, at least theoretically, such small molecules are attractive targets for treatments.
But what causes the various genetic changes that lead to cancer? Mutation-inducing chemicals—mutagens—in our environment can do so. Exhibit A, of course, is tobacco smoke. However, other environmental chemicals that many people suspect of causing cancer—food preservatives, contaminants in our drinking water, pollutants pouring out of smokestacks—rarely do so. In fact, in the developed nations, only 1 to 2 percent of cancers are attributable to such environmental pollutants.
Instead, most cancer-inducing mutations occur when cells damage their own genes accidentally. Each of our cells continuously produces mutation-inducing chemicals as byproducts of its normal metabolism. When our cells generate energy by converting oxygen into water, modified oxygen molecules called "oxygen radicals" are produced. These radicals strike wildly at all the molecules in our cells, including the DNA of our genes. Although our cells have the ability to repair this damage, the protection is not perfect, and so mutations and mutant genes accumulate as we grow older.
Mutations, while necessary, are not sufficient. Something else—something from outside the cancer cell—needs to fan the flames. A cell with several mutations may be primed to become cancerous, or may even be in the sluggish early stages of cancer, but that cell usually needs to be stimulated by additional growth-promoting signals to become a full-blown tumor. In fact, development of the great majority of human cancers is likely to be driven by these non-mutagenic "cancer promoting" molecular signals.
We don't know precisely how the Western diet increases our risk of cancer. The foods we eat contain chemicals that can mutate genes and that therefore could cause cancer. For example, red meat cooked at high temperatures generates potent mutagens called heterocyclic amines. Foods contain many different chemicals, and those chemicals are transformed in our body into many other chemicals, making it very difficult to pinpoint just what it is about the Western diet that raises our risk of cancer. But there is no doubt that it does.
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