According to the American Cancer Society statistics on cancer death in the U.S. from 1999-2007, one in every three women, and one in every two men will develop cancer in their lifetime. Statistically, if a man in the US manages to avoid all other preventable causes of death, he will die of prostate cancer.
You may think of cancer, as I once did, as a disease that either you have or you don’t. Like a parasitic bacterium unknowingly picked up from a door knob, I thought, one day you are cancer free, and the next, though you might not know it yet, it’s there. And just as one salmonella bacterium will look and act the same as most every other salmonella bacterium, it makes sense that one man’s cancer should look just like another man’s disease. It turns out that cancer (at least as we currently understand it) is not like that at all.
Cancer is not a single disease, but a term used to describe a collection of over 100 related diseases. What these share in common is rogue cells. As described by the National Cancer Institute, “The body is made up of many types of cells. These cells grow and divide in a controlled way to produce more cells as they are needed to keep the body healthy. When cells become old or damaged, they die and are replaced with new cells.” And so it goes, over and over, until something goes wrong. A cell’s DNA is changed so that it no longer follows the rules, and it starts growing too quickly, or dividing much faster than it should, or not dying when it should, or sometimes, wandering off to grow someplace where it doesn’t belong.
Normally, this doesn’t happen in one shot. Due to the body’s incredible system of safeguards, small DNA mutations can be kept in check. For example, if a cell’s DNA is changed such that the genes that regulate growth are damaged and it grows too fast, other genes produce signals to slow growth, kill the cell, or repair the damage. Therefore, it requires a succession of events to give rise to cancer. Not only must cells’ genes that regulate growth and division be changed, but the genes that normally protect and repair the cells, or kill the unhealthy ones, must be damaged as well. Colon cancer, for example, is a prototype for cancer progression. As many as six to eight specific mutations are necessary to give rise to a fully invasive growth. This is why the terms "precancerous" and "benign" tumor are used. A benign tumor is not cancerous, and cells from these tumors are rarely a threat to life, but such precancerous tissue can indicate that the path to cancer has begun. There is not a clear line of demarcation between benign and cancerous cells or tissue. If these cells are not removed, additional genetic mutations could give rise to malignant, or cancerous, tissue. Cancer, then, is a multi-step process.
So then, how do these mutations occur? Anything that can change or damage cell DNA can produce cancer. Inherited genetic mutations are probably the most commonly known, though these are a minority compared to those that are caused by environmental factors. Other causes include damaging radiation, viruses, cellular trauma, tumor promoting chemicals, and some metals. Even if these don’t get you, statistics will. Every time a cell divides, there is a chance that it will make a mistake. This is the reason that age is the single greatest risk factor for cancer. For every additional year of our lives, the chance that these mistakes will occur increases exponentially.
To further complicate the issue, not all the cells in a cancerous tumor necessarily have the same mutations. Say for example that the genes that code for cell damage prevention are mutated in a lung cell. This cell then goes on to produce more cells with the same mutation. Then, one of these cells develops another mutation such that a controlling checkpoint no longer works, and unhealthy cells do not die. Again, these mutations are repeated over and over as the cell replicates itself. Finally, a virus comes along and inserts some DNA into one of these cells that tells it to divide many more times than normal, while another cell is damaged by a chemical such that it grows too fast. These cells are then uniformly identified as “lung cancer”, but their DNA and behavior are not the same. Similarly, cancerous cells that originate in the lungs possess different biochemistry and genes than those that originate, for instance, in the liver.
All of these factors combine to produce a disease that is very difficult to eliminate. Chemotherapy drugs that kill one type of cancer cell may not be effective on another. Additionally, the same drugs that initially treat one diagnosed form of cancer may actually promote another later on. It is not uncommon that a chemotherapy agent is also a known carcinogen.
But it is not all bad news. There are things we can do to protect ourselves, such as limiting exposure to carcinogens, eating foods that combat harmful chemicals, and aiding our doctors in early detection. Also, supported by billions of dollars in funds, cancer researchers are making huge breakthroughs in understanding and treatment. Chemotherapy cocktails have had success where single therapies had little effect. Researchers are hoping that soon personal and localized treatments will work more effectively and improve patient quality of life. Early reports indicate that these efforts are working. The American Cancer Society's 2010 Cancer Facts and Figures notes that, "Compared to the peak rate of 215.1 per 100,000 in 1991, the cancer death rate decreased 17% to 178.4 in 2007. Rates for other major chronic diseases decreased substantially during this period." That's progress.