One of my college biology professors once told his students that when a person lives long enough, he or she will eventually get cancer. He wasn’t wrong—older age is a major risk for developing cancer as more than 60 percent of cancer cases occur in people 65 years or older.

At first glance, aging and cancer seem like polar opposites. Aging is associated with senescence and death. Cancer is associated with uncontrolled growth. But there is a wealth of scientific evidence that leads scientists to believe aging and cancer have more in common that one might think.

What makes the elderly population more susceptible to cancer? What is the link between aging and cancer? To address these questions, we need to delve into one of hallmarks of cancer and aging: genome instability.

Genome instability is defined as an increased tendency of mutations to occur in your genome (defined as a complete set of your DNA). A cell does not suddenly have higher mutation frequency: genome instability is often a consequence of another mutation(s). A series of mutations must occur before the cell experiences full-blown genome instability.

Mutations arise from erroneous DNA replication

Mutations are consequences of errors made in DNA replication, a process that copies the DNA in order to prepare a cell for cell division. Before a cell divides, the DNA must be copied so the parent cell and the daughter cell have the equal amounts of identical DNA.

DNA is perhaps the most important material in a cell—it is a blueprint for the cell’s survival, maintenance, and reproduction. One can imagine how important it is for the copying process to be extremely accurate. An incorrect message can be harmful not only for the parent cell, but also for all of its descendants.

DNA replication is indeed extremely accurate, averaging only one mistake for every 109 to 1010 copying events. On top of that, cells can detect and correct errors by proofreading the new product to make sure everything is correct. And as a cherry on top, the process is extremely efficient. In eukaryotic cells, there are 50 copying events per second on average. We are looking at a highly efficient machine that is more accurate than any man-made product.

But nothing is perfect—our cells would never get mutations if DNA replication were flawless. Spontaneous errors are made and can persist in the final DNA product as mutations when the errors somehow escape the cell’s surveillance system.

Mutagens increase mutations and chances of genome instability

You might think, “So mutations can spontaneously arise, but one mistake for every 109 to 1010 events does not seem like much!” While that is true, our cells are constantly exposed to mutagens that damage the DNA and increase the chances of permanent error occurring.

Some of the mutagens are “endogenous,” meaning that they are byproducts of natural processes in the cell. There are two major classes of endogenous mutagens. First, spontaneous chemical reactions can cause errors. Second, byproducts of metabolism, such as reactive chemical molecules with oxygen, can damage the DNA. Unfortunately, there is not much we can do to avoid these.

Others are “exogenous”—these are the environmental mutagens that we can sometimes avoid. These include mutagens that are often heard about in the media, like UV light from the sun. The exogenous mutagens can increase DNA damage either by directly causing damages to the DNA or by increasing the amounts of endogenous mutagens.

Once a cell has more DNA damage because of mutagens, it becomes more susceptible to mutations in the DNA—including genes that are important for fixing DNA damages. Without a mechanism to properly fix the damages, the cell’s DNA becomes even more susceptible to mutations. In other words, the cell’s genome is now unstable.

Genome instability is a hallmark in both cancer and aging

Normal cells grow and die, much like people and other organisms. A cancer cell, on the other hand, is immortal because it can grow and divide indefinitely. In a cancer cell, the mechanism that stops the cell from uncontrolled growth is often mutated. So a cell with genome instability can transform into a cancer cell if genes important for stopping the uncontrolled growth get mutations and become non-functional. This is one of the reasons why genome instability is a hallmark of cancer.

In spite of the high accuracy, the endogenous and exogenous mutagens pose a great threat to the DNA. These mutagens are all around us. We are constantly exposed, and damages will accumulate over time. Naturally, an older organism will have dealt with more mutagens and is more likely to have DNA damages and errors than a younger organism. The fact that an older organism has more mutations than a younger organism is true not just for people, but for other organisms too, like budding yeast (used in baking and making beer).

Cells’ genomes can become really unstable when they age because mutations accumulate over time. In an older cell, genes that are important for fixing DNA damages and control the cell’s growth are more likely to have mutations than in a younger cell. The accumulation of mutations due to aging can also cause cells to lose control of their growth and become “cancerous.”

In an era of aging population

Although cancer and aging do have some common biological grounds, they are still very complex and are not completely understood. Researchers cannot over-generalize and say the lack of proper responses to DNA damages is what causes both aging and cancer. Is aging a direct consequence of the DNA damage itself or the genome instability that follows the damage? If DNA damage does cause both aging and cancer, why are the two consequences so different?

But what we do know is that aging is a risk for developing cancer. We live in an era of an aging population. People are living longer thanks to better sanitation and medical knowledge, and they are not having as many kids. The 65+-year-old population is the fastest growing segment of the U.S. population. Currently, 1 in 8 people in the States are older than 65. By 2030, 1 in 5 people of the U.S. population will be older than 65.

These changing U.S. demographics are creating new challenges for cancer care. First, the medical workforce may be too small to care for the increased number of cancer patients. Second, the cost of the cancer care is increasing rapidly, faster than other sectors of medicine. The cost of cancer care has increased from $72 million in 2004 to $125 million in 2010 and is projected to increase to $173 million by 2020. As a result, the Centers for Medicare and Medicaid Services, which is the largest insurer for people over 65, is facing financial challenges.

Healthcare providers will need to anticipate the epidemic and address it in many different ways, including research, clinical practice, and education, to fill the gap of evidence-based practice for treating the elderly population with cancer. A greater focus on the elderly population with cancer will result in improved treatments that are necessary with the projected demographic growth.

Further Reading:

Image Credit:  Ari Bakker via flickr

About The Author

Irene Park
Academic Correspondent, Medicine and Genetics

Irene Park is a third-year Human Genetics PhD student at the University of Michigan Medical School. She double-majored in Biological Sciences and Philosophy at Cornell University, allowing her to explore and learn both biology and logical writing. Currently, Irene’s PhD thesis project is focused on a phenomenon called genome instability, which is an accumulation of mutations in the cells. Genome instability is a hallmark for many human diseases, including cancer. When she is not manipulating cells in her laboratory, Irene works a news reporter at The Michigan Daily, a student-run newspaper at the U of M, mainly covering issues and events about science, technology, and health. She also is a student blogger for her graduate school, often writing about more personal topics like dealing with the Imposter Syndrome. Combining her interests in science and writing, Irene wants to communicate science to a broader audience to both educate the public about science and learn more about the diverse science topics herself.