Cancer is one of the deadliest human diseases and will affect almost 40 percent of men and women at some point in their lives. While each type of cancer is different, they all share one common theme: They start from a single cell and develop the ability to divide uncontrollably. Determining our risk for getting cancer is complicated because there are many factors, both inherited and environmental, that play a role.

By understanding our own genetics, it may be possible to identify people at greatest risk, allowing us to prevent or diagnose cancer early. As the rate of cancer rises around the world, wouldn’t it be useful to know if you were at greater risk based on your own genetic profile?

The human genome serves as your genetic playbook and contains about 20,000 genes composed of DNA building blocks strung together just like letters to form words. Each cell in your body activates different genes in this playbook to carry out specific functions. Throughout life, your cells are exposed to things that can cause damage to these genes, such as ultraviolet rays from the sun, environmental and household chemicals, and even natural processes associated with aging. Left uncorrected, this damage can lead to permanent changes in these genes called mutations.

Luckily, we have a variety of DNA repair and tumor prevention genes that work together to monitor the genome for damage and stop uncontrolled cell growth. Proteins produced by these genes serve as safeguards to ensure that cells with damaged DNA do not divide. Despite these protective safeguards, some DNA damage is left uncorrected, leading to mutations. While most mutations are harmless or cause a cell to die, some may occur in genes that control cell division. If a cell collects enough mutations in these critical genes, that cell may begin to divide more than normal, resulting in cancer.

Our cells may gain mutations either by inheriting them from our parents, or by collecting them throughout life.

The inherited mutations are present in every cell and only a few may affect risk for cancer. The mutations that we collect over time occur only in certain cells because of unrepaired DNA damage. The vast majority of human cancers are caused by a lifetime of collected mutations, which is why most cancers occur later in life.

While some inherited mutations can contribute to the risk of cancer if present in a cancer-related gene, additional mutations must also occur in a cell to overcome our genetic safeguards.

If a single cell collects multiple mutations that destroy these safeguards, that cell will divide more than it should. We recognize it as a cancer when it produces so many offspring that it interferes with the function of other cells and distorts the tissue around it.

Lung cancer is the deadliest type of cancer in the United States, killing almost 160,000 people each year — more than the next three deadliest cancers combined (breast, colon, and prostate), and about 20 percent of lung cancer cases occur in non-smokers. Early diagnosis is important because it gives doctors the chance to treat the disease when it is curable. For example, among lung cancers that are diagnosed through screening, 85 percent are in an early stage and can be cured with surgery. Without screening, the majority are in late stage and cannot be cured.

The research in our lab is focused on developing tests to diagnose cancer as early as possible and to identify people who may be at increased risk later in life because of a combination of factors.

My research focuses on developing a blood test that allows us to identify both the mutations that we inherit and those that we collect over our lifetime. Our idea is simple: If a person collects mutations at an unusually rapid rate, he or she likely does not repair DNA very well, and there is a higher likelihood of mutations in critical safeguard genes. This leads to an elevated risk for developing cancer.

This information is important because it allows us to look at inherited and environmental factors that contribute to cancer at the same time in a simple blood test. Identifying at-risk individuals before they develop cancer would allow doctors to create, and insurance companies to justify, a personalized screening plan to catch a potential cancer in its earliest stage when it is most treatable. This would not only save lives, but also save tremendously in healthcare spending.

Our research team works closely with researchers and pulmonary physicians at the University of Toledo, the Toledo Hospital, the University of Michigan, Vanderbilt University, Cleveland Clinic, the National Cancer Institute, and many other centers of excellence in lung cancer research. We are grateful for the support received from the National Institutes of Health and the George Isaac Cancer Research Fund.

Daniel J. Craig is a student studying for his PhD in the University of Toledo College of Medicine and Life Sciences Biomedical Science Program, formerly the Medical College of Ohio. Mr. Craig is doing his research in the laboratory of Dr. James C. Willey in the department of medicine. For more information, contact Daniel.Craig@rockets.utoledo.edu or go to utoledo.edu/ med/ grad/ biomedical.

First Published October 1, 2017, 7:20 p.m.