The relationship between cancer and aging: Why it is relevant

By Irene Park

At first glance, aging and cancer are polar opposites. Many people will think of aging as growing old and dying. Cancer, on the other hand, is tumors and abnormal, uncontrolled cell growth.

But aging and cancer have more in common than we might think.  Both cancerous and aged cells show genome instability an increased tendency of mutations to occur in your genome. There are multiple factors that lead to genome instability, but we will focus on how gene mutation arise, which is a permanent error in genes.

All mutations are consequences of errors made during DNA replication, the process of copying DNA so parent cell and daughter cell can have equal amount of identical DNA. DNA is arguably the most important material in a cell because it contains instructions for the cells’ survival, maintenance, and reproduction. An incorrect message is not only harmful for the parent cell but for all of its descendant cells.

Thankfully, DNA replication is extremely accurate. It is six times more likely for you or I to win the lottery than for a cell to make even one mistake every time it divides. This is because cells are equipped with various ways, like proofreading the new product and fixing mistakes, to make sure everything is correct.

If DNA replication is so accurate, how do mutations even arise? While mutations are usually rare, our cells are constantly exposed to mutagens (something that can cause mutations) that damage the DNA and increase the chances of mutations occurring.

Some mutagens are “endogenous,” meaning that they are byproducts of natural processes in the cell. For example, one of natural processes in the cell is cell respiration, a process that generates energy from oxygen that we breathe in and carbohydrates that we eat (e.g. cereal, bread, and sugar). Cell respiration produces what are called reactive oxygen species (ROS) that damage the DNA.

Others are “exogenous.” They are the environmental mutagens we have some control over avoiding. These include many substances you know are dangerous: like arsenic, UV light, cigarettes. Exogenous mutagens cause mutations by damaging DNA directly or by producing more of endogenous mutagens.

Endogenous and exogenous mutagens pose a great threat to DNA since these mutagens are all around us. As we age, we are exposed to more mutagens, so an older person is likely to have more accumulated mutations than a younger person.

If there are mutations in genes that are important for keeping the DNA error-free (e.g. proofreading), the genes may not be able to function properly. This makes the DNA more vulnerable to mutations. More mutations accumulate, and the cell’s genome eventually becomes “unstable.”

A normal cell can transform into a cancer cell as more mutations accumulate. A cancer cell grows and divides uncontrollably and escapes programmed cell death, known as apoptosis. If genes important for stopping the uncontrolled growth have mutations and become non-functional, a normal cell can become cancerous.

The genome of the cell can also become unstable when it ages due to the accumulation of mutations over time. This accumulation of mutations can cause cells to grow uncontrollably and become cancerous if the mutations impair functions of genes that are important for monitoring cell growth and apoptosis.

Hence, older people are more likely to have mutations in the critical genes and develop cancer. In fact, aging is a major risk for developing cancer as more than 60% of cancer cases occur in people 65 years or older.

The reason why the link between aging and cancer is relevant is our aging population. The 65+ year-old population is the fastest growing segment of the US population, and currently 1 in 8 people in the States are older than 65. By 2030, 20% of the US population is predicted to be older than 65, thus putting more of the population at risk for cancer. Here is a graphic that illustrates this concept.

Image source.

The changing demographics create new challenges for cancer care. First, the medical workforce may be too small to care for the increasing number of cancer patients. Second, the cost of the cancer care is increasing more rapidly than other medical sectors. The cost has increased from $72 million in 2004 to $125 million in 2010 and is projected to increase to $173 million by 2020. Unsurprisingly, the Centers for Medicare and Medicaid Services (CMS), which is the largest insurer for people over 65, is facing financial challenges.

How do we address the anticipated problems with the projected demographics? There is a definite need for more evidence-based research on treating elderly cancer patients to improve the quality of the treatment for the specific patient group, especially because treating older cancer patients can be more difficult than treating younger patients.

We may also need to ask ourselves whether it is worthwhile prolonging our lives while compromising our quality of life. The overall mortality rate has declined since the early 1990s, leading to more cancer survivors, with almost half of the survivors older than 70 years old. But surviving cancer is not an end point. Patients can experience physical, emotional, and financial burdens. In addition, cancer survivors are at a greater risk to develop secondary cancers and other health problems. And considering that almost half of the survivors are older, the burdens can greatly affect their lifestyle post-survival.

As a society, it is important to be aware, especially of issues that affect a large number of people. Cancer is exactly that, since everyone grows old and becomes more vulnerable to cancer. While there is no one perfect solution, what we need to do come up with the best solution for our society is be aware, investigate, and discuss.

An earlier version of this article was published in HIPPO Reads.

About the author

ireneSo Hae (Irene) Park is a fourth-year Human Genetics PhD student at the University of Michigan Medical School and the Science Column Editor (keep your eye out for more info about our upcoming weekly column in The Michigan Daily). Before attending UMich, she received her BA in Biological Sciences and Philosophy at Cornell University. Now under the joint supervision of Drs. Thomas Wilson and Thomas Glover, Irene is investigating what causes genome instability—an accumulation of mutations in the cells—and how it can be avoided. Genome instability is commonly seen in many human diseases, like cancer. When she is not working during the wee hours in her laboratory or writing about the latest cool topics in science and medicine in The Michigan Daily or HIPPO Reads, Irene likes to watch movies, watch The Food Network, collect anything cute, learn how to make different types of coffee drinks, listen to music, travel, and read. Follow her on Twitter (@S_Park89).

Read all posts by Irene here.

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