Cancer is both genetic and environmental, but not in equal measure. Only 5% to 10% of cancers develop from inherited genetic mutations passed down through families. The vast majority arise from a combination of environmental exposures, lifestyle factors, and random mutations that accumulate in your cells over a lifetime. About 40% of all cancer cases are linked to modifiable risk factors like tobacco use, diet, obesity, and UV exposure, meaning a significant share of cancers could theoretically be prevented.
How Inherited Genes Cause Cancer
Every cell in your body carries a copy of the DNA you inherited from your parents. When one of those inherited copies contains a harmful change, called a germline mutation, that change exists in every cell from birth. These mutations typically affect genes responsible for repairing damaged DNA or controlling cell growth. With one layer of protection already compromised, it takes fewer additional hits for a cell to become cancerous.
The most well-known examples are mutations in the BRCA1 and BRCA2 genes, which dramatically increase the risk of breast and ovarian cancer. Other inherited gene changes raise the risk of specific cancers: CDH1 and CHEK2 are linked to breast cancer, while BRIP1, RAD51C, and RAD51D increase ovarian cancer risk specifically. Mutations in the TP53 gene cause Li-Fraumeni syndrome, which raises the risk of multiple cancer types starting at a young age. Inherited mutations in mismatch repair genes can cause Lynch syndrome, increasing the likelihood of colorectal and endometrial cancers.
Still, carrying one of these mutations doesn’t guarantee you’ll develop cancer. It shifts the odds, sometimes substantially, but other factors determine whether a tumor actually forms.
How Environmental Factors Drive Most Cancers
The mutations responsible for most cancers aren’t inherited. They’re somatic mutations, changes to DNA that happen after conception in ordinary cells throughout your body. Every time a cell divides, there’s a small chance of a copying error. Environmental exposures accelerate this process by directly damaging DNA or by pushing cells to divide more frequently, which multiplies the opportunities for mistakes.
In the United States, 40% of all cancers are associated with modifiable risk factors. Tobacco alone accounts for nearly 20% of all cancer cases and 30% of cancer deaths. A combination of excess body weight, poor diet, physical inactivity, and alcohol consumption accounts for another 20% of new diagnoses. UV radiation causes 95% of skin melanomas and roughly 6% of all cancers. Poor diet on its own, particularly diets high in processed foods and low in fruits and vegetables, is responsible for about 5% of cancers.
Globally, the picture is similar. A 2022 analysis estimated that 37.1% of 18.7 million new cancer cases worldwide were linked to 30 modifiable risk factors. Infections also play a major role: 12.2% of new cancer cases globally in 2018 were attributable to infectious agents, with 90% of those caused by just four pathogens: the bacterium H. pylori (linked to stomach cancer), hepatitis B and C viruses (linked to liver cancer), and human papillomaviruses (linked to cervical and other cancers). In the U.S., the infection-related share is lower, around 3%, largely because of vaccination programs and lower rates of chronic infection.
The Space Between: Gene-Environment Interactions
The genetic-versus-environmental framing is useful but incomplete, because the two constantly interact. Your genetic makeup can determine how vulnerable you are to a given environmental exposure. A clear example involves a gene called NAT2, which helps your body process certain chemicals. Smokers are at least three times more likely than nonsmokers to develop bladder cancer. But smokers who carry a specific NAT2 variant face an even higher risk than smokers with other versions of the gene. The cancer risk comes not from the gene alone or from smoking alone, but from the combination.
This kind of interaction plays out across many cancer types. Two people can have the same toxic exposure, but their genetic differences determine how efficiently their cells repair the resulting DNA damage, how quickly they metabolize the harmful compound, and how effectively their immune system detects and destroys abnormal cells.
Epigenetic Changes: When Environment Rewrites Gene Behavior
Beyond directly damaging DNA, environmental exposures can change how your genes behave without altering the genetic code itself. These are epigenetic changes, essentially chemical tags that turn genes on or off. Unlike permanent mutations, epigenetic changes are potentially reversible, which makes them a particularly important area in cancer biology.
A wide range of carcinogens, including tobacco smoke, heavy metals, air pollution, asbestos, and endocrine-disrupting chemicals like BPA and phthalates, have been shown to cause epigenetic disruption. These exposures can silence genes that normally suppress tumor growth or activate genes that promote uncontrolled cell division. The result is genomic instability, a state where cells become increasingly prone to the kind of errors that lead to cancer.
Diet plays a role here too, partly through its interaction with gut bacteria. When bacteria in your digestive tract ferment dietary fiber, they produce short-chain fatty acids, particularly one called butyrate. Butyrate can activate tumor-suppressing genes and repress cancer-promoting ones while also supporting normal immune function. This is one mechanism by which a fiber-rich diet may reduce cancer risk at the molecular level.
Signs That Cancer Might Run in Your Family
Most cancers develop without an inherited genetic cause, but certain patterns in a family’s medical history suggest a hereditary syndrome may be at play. Red flags include cancer diagnosed at an unusually young age (such as colon cancer before 50), the same type of cancer appearing in multiple close relatives, several different cancers developing in one person, cancer in both organs of a pair (both breasts or both kidneys), or rare cancer types like male breast cancer.
Clinical guidelines recommend genetic testing for people diagnosed with triple-negative breast cancer, ovarian cancer, pancreatic cancer, colorectal cancer before age 50, metastatic prostate cancer, or male breast cancer. Testing can identify inherited mutations that may affect not only the patient’s treatment decisions but also the screening recommendations for their blood relatives.
What This Means for Prevention
The fact that roughly 40% of cancers are tied to modifiable risk factors means prevention efforts can have enormous impact at a population level. The highest-leverage changes are well established: not smoking, maintaining a healthy weight, eating a diet rich in whole foods and fiber, limiting alcohol, protecting your skin from UV radiation, staying physically active, and getting vaccinated against HPV and hepatitis B.
For the 5% to 10% of cancers driven by inherited mutations, prevention looks different. It centers on early detection through enhanced screening, and in some high-risk cases, preventive surgery or medications that reduce the likelihood of a tumor developing. Knowing your family history is the first step in determining whether genetic testing could be valuable for you.
The remaining cancers, those not clearly explained by inheritance or known environmental exposures, likely result from random somatic mutations during normal cell division, combined with gene-environment interactions we don’t yet fully understand. Cancer, in most cases, is not a single-cause disease. It’s the cumulative result of genetic susceptibility, environmental exposure, and biological chance playing out over decades.