What is Cancer, Really?
Selfish Cells
Cancer cells don’t work for the team. In fact, they hurt it. They divide too much, splitting wildly into new cells faster than the normal cells around them. And they don’t stop dividing, regardless of the damage they cause. They simply ignore the biological cues that tell your cells when to stop.
Eventually, this unchecked cell growth can lead to a tumor – a semiautonomous mass of tissue that serves no productive purpose and that may, through its growth, damage surrounding cells. Worse still, unlike normal cells, a cancer cell can detach from its neighbors and travel to other parts of your body, causing even more damage someplace else.
The worse the cancer gets, the more the cancer cells tend to take an undifferentiated, “immature” form. Your body contains 220 different types of cells, each with a specific job to do and a form that follows that function. Cancer cells, however, are both incapable of doing a useful job and increasingly aggressive.
In the Genes
Cancer cells get this way because they’re broken. Your cells work by following specific instructions. These instructions are found in each cell’s nucleus, laid out in sequences of DNA called genes. Each of your genes – and there are tens of thousands of them – contains a code that tells a cell how to do a specific job.
At least two of these gene types, proto-oncogenes and tumor suppressor genes, can cause serious trouble if they get messed up, or mutate. Proto-oncogenes regulate when, how, and how much your cells divide. Tumor suppressor genes help keep this process in line and can put the brakes on cellular reproduction if necessary. They’re also the genes that tell your cells how to fix damaged genes.
With an unlucky mutation or two, proto-oncogenes can turn into oncogenes (basically, genes that cause cancer). The affected cell becomes hyperactive, and divides free of the usual constraints. Fortunately, your tumor suppressor genes can still slam on the brakes, repair the DNA, or call for the ultimate sacrifice: apoptosis, or “cell suicide.” When a cell’s DNA sustains so much damage that it is beyond repair, a healthy cell still thinking of the team can destroy itself to prevent greater problems.
But if genetic errors prevent your tumor suppressor genes from doing their job, too, troublemaking oncogenes are more likely to cause cancer. And that’s why cancer tends to strike older people. It takes more than one genetic mutation to make a cancer cell, and those mutations can take a long time to occur. (Unfortunately, some people are born with some mutations already.)
When Good Genes Go Bad
There are almost as many ways in which genes can go bad as there are genes involved in cancer. Molecular mutations can change your DNA sequence, scrambling the code and turning healthy genes into oncogenes. Or, errors in cell division can cause entire genes to move to a new location, get repeated, or be deleted altogether.
Sometimes, these mutations are hereditary. Other times, they happen over your own lifetime. They could be random genetic accidents, or caused by environmental exposure to carcinogens, like cigarette smoke and the UV radiation in sunlight. Even certain viral infections can lead to cancer.
In fact, part of what makes cancer so tough to cure is that it isn’t a single disease with a single cause. The word “cancer” actually covers more than 100 distinct diseases, all characterized by out-of-control cell growth. Because the diseases are different, treatments that are effective for one aren’t necessarily effective for others. The weapon we need to kill cancer once and for all may be an entire arsenal.
