Is Cancer Genetic or Environmental? (Or Can It Be Both)

You’ve probably heard people say that cancer is “in your genes.” But here’s the truth: genes are not our fate.

As Craig Venter, one of the world’s leading genomic researchers, once said, “our DNA can give us useful information about disease risk, but it rarely decides the outcome on its own”. 

What matters is how those genes interact with our environment, everything from the food we eat and the air we breathe to the tiny cellular neighborhoods where our tissues live.

So, when we ask, “Is cancer genetic or environmental?” The most honest answer is: it’s both. Our genes may set the stage, but the environment often decides how the story unfolds.

In this article, we will take a deep dive into the origins of cancer while trying to answer the question of whether cancer is genetic or environmental. We will also find out if nurture can override nature in our susceptibility to cancer.

Understanding the Origins of Cancer: A Multifactorial Disease

A 2024 review by the National Cancer Centre on Genetic Testing for Inherited Cancer Risks shows that only about 5–10% of cancers come from inherited genetic mutations, the kind you’re born with, like mutations in BRCA1 or TP53. The other 90–95% are linked to non-inherited factors such as lifestyle, environmental exposures, and even random errors when cells divide.

Even when someone has a genetic predisposition, it often takes an environmental trigger for cancer to develop.

For example, an article review on the incidence of childhood cancer in twins who share the same DNA showed that if one develops cancer, the other’s risk is increased. However, this study states the other twin has only about a 20–30% (depending on the type of cancer) chance of also developing it. Genes alone don’t tell the whole story.

Furthermore, in population studies, researchers have observed that cancer rates vary widely across different regions of the world. However, when people move from countries with lower cancer rates to those with higher ones, their risk increases significantly over time, often becoming similar to that of the local population.

This change cannot be explained by genetics alone because it highlights the powerful influence of environment and lifestyle on cancer risk.

What Does It Mean for Cancer to Be Genetic? Inherited vs. Acquired Mutations

Cancer is considered genetic because it arises from mutations in the DNA that disrupt normal cell growth and division.These changes usually come from two main forms: inherited and acquired mutations.

Inherited (Germline) Mutation

Each person inherits a pair of chromosomes from their parents. The chromosomes are packed with thousands of genes. When a gene already carries a mutation, we inherit them from our parents. It is passed down from the moment an egg cell is fertilised by a sperm cell, forming a single cell called a zygote, which eventually develops into a human being.

Since all human cells originate from this single cell, the mutation is present in every cell of the body and is passed down to future generations. It typically takes more than one mutation for a cell to be cancerous.

So, when one starts with a mutated gene, it makes it easier and quicker for other mutations to occur. This is why those with inherited mutations tend to have cancers earlier in life than those without them.

Examples of faulty genes passed down from parents are BRCA1, BRCA2, and TP53.

Acquired (Somatic) Mutation

These cannot be passed down or inherited by your children because it doesn’t affect your sperm and egg. These kinds of mutations can occur from exposure to environmental carcinogens, DNA replication errors during cell division, or age-related changes.

When cells divide, they make a copy of their DNA in the new cell. During this process, errors can occur; if not corrected, they can accumulate over time and cause cancer or genetic disease.

Cancer is genetic because it begins with DNA mutations. Cancer that is considered genetic doesn’t mean that it is hereditary. Most cancers occur from environmental and lifestyle factors.

Key Genes Linked to Hereditary Cancer Risk 

There are several hereditary cancer susceptibility genes.

All mutations are permanent changes in DNA. Mutations in these genes can be passed from parent to child and increases the likelihood of developing certain cancers. However, inheriting a mutation doesn’t mean cancer is inevitable. It only raises risk, with environmental and lifestyle factors also playing a huge role.

Some of these genes and the types of cancers they cause are explained in detail int he following parapgrahs.

BRCA1 and BRCA2 Genes

BRCA means BReast CAncer gene. BRCA1 and BRCA2 genes are present in everyone.

They are important genes that are tumor suppressors. They help repair DNA damage and prevent uncontrolled cell growth. A mutation to these genes creates variants that can cause cells to further mutate or grow out of control.

This type of mutation is rare, and according to a 2024 review on BRCA Gene Changes: Cancer Risk and Genetic Testing by the National Cancer Institute,only 1 out of every 400 people is estimated to have a BRCA1 and BRCA2 gene change. Your ethnicity is also suspected to play a role in your susceptibility to this change.

The following cancers may develop from a BRCA1 mutation and a BRCA2 mutation, respectively:

• Breast cancer;
• Ovarian cancer;
• Prostate cancer;
• Pancreatic cancer.

In breast cancer, the focus is on women, but the BRCA1 and BRCA2 are also expressed in men. Men with the BRCA mutations also face increased risk of breast cancer. However, the chance that a man will get breast cancer from the mutation of these genes is low.

PALB2 Gene

Errors in the PALB2 gene increase your risk of developing cancer of the breast, ovaries, and pancreas.

A 2024 article by the UK Cancer Research Institute on Inherited genes and cancer types estimated that almost 45% of women who have faults in their PALB2 gene will develop breast cancer by the age of 80.

CHEK2 Gene

The CHEK2 gene helps with the repair of DNA. A change in this gene can increase your risk of breast cancer.

According to this 2025 study on CHEK2-Related Cancer Predisposition, people with a family history of a change in this gene have a 20-44% chance of developing breast cancer in their lifetime.

TP53 Gene

The TP53 is a suppressor gene which plays several other roles in maintaining the structural integrity of the cell.

These roles include:

• Inducing cell cycle arrest;
• DNA repair;
• Senescence;
• Apoptosis.

Unfortunately, when this gene is mutated, not only does it lose its tumor suppressor role, but it may require functions that actually promote tumour development. Li-Fraumeni Syndrome is a common disease associated with a TP53 mutation.

People with this condition have an increased risk of developing breast cancer, which is the most common, and other possible ones are:

• Bone cancer;
• Acute myeloid leukaemia;
• Brain tumors;
• Soft tissue sarcoma;
• Cancer of the adrenal gland.

While inherited DNA mutations increase the risk of cancer, this doesn’t always mean that you’ll eventually have the disease. Lifestyle modification, medical screenings and prevention efforts can reduce the incidence of cancer.

How Environmental Factors Contribute to Cancer Development

A good number of cancers are caused by environmental factors.

This estimate comes from several epidemiological studies showing that cancer risks may vary according to:

• Migration patterns: People who move to a new location can adopt the lifestyle of their new host, which can predispose them to cancer.
• Geographical variation: Certain cancers are more common in specific regions, suggesting the role of environmental factors.
• Cancer clusters: Some unusual cancer concentrations may indicate shared environmental cancer risk factors.
• Changes in risk over time: Shifts in lifestyle, industrialisation, and exposure patterns affect cancer incidence.
• Correlation studies: Statistical links between environmental cancer lifestyle factors like tobacco smoke and cancer rates.

The rapid industrialisation of many parts of the world has led to increased exposure to environmental carcinogens, including air and water pollutants, industrial chemicals, and radiation.

These harmful chemicals and others can cause cancer in the following ways:

• Formation of DNA adducts: This occurs through the metabolic conversion of carcinogens in tobacco smoke to forms that can bond to DNA and cause miscoding during DNA replication.
• Oxidative stress: Through the production of reactive oxygen species, environmental factors like the sun can cause DNA damage.
• Disabling of tumour suppression genes: Viruses like the human papilloma virus can integrate themselves into the DNA of their host, which may cause genome instability with the disabling of tumour suppressor genes as a consequence.

Though many of these agents have been proven to be harmful to the DNA, you can reduce your risks by minimising exposures and following the guidelines provided by the World Health Organisation.

Common Environmental Carcinogens: From Tobacco to Radiation

Carcinogens aren’t just found in factories; they surround us in daily life.

They range from secondhand smoke and UV rays to polluted air, contaminated water, and even some cosmetics. These hidden toxin exposures can raise cancer risks.

An industrial worker may face asbestos when working, while others encounter pesticides or heavy metals at home. Though we can’t avoid every risk, awareness helps. Simple steps like quitting smoking, using sunscreen, choosing safer products, and wearing protective gear can greatly reduce vulnerability and exposure to carcinogens.

Epigenetics: Where Genetics and Environment Intersect in Cancer Risk

Epigenetic refers to changes in gene expression that do not alter the DNA sequence. These changes are brought about by chemical modifications to DNA or its associated proteins, and affect how genes are turned off or on.

Common epigenetic changes include:

• DNA methylation: addition of a methyl group to cytosines bases to DNA, often silencing genes.
• Histone modifications: Chemical changes to histone proteins, altering how tightly DNA is packed.
• Nucleosome repositioning: Shifting the position of DNA-wrapped nucleosomes to make genes more or less accessible.

Epigenetic changes occur when these chemical marks are added, removed, or altered, affecting how genes are expressed without changing the DNA code itself. This can occur due to environmental factors. For example, the gene-environment interaction occurs when arsenic and 1,3-butadiene interact, causing epigenetic changes through the demethylation of the DNA.

Pharmaceuticals such as tamoxifen, phenobarbital, and oxazepam, as well as biological agents like mycotoxins and aflatoxin B1, have been shown to induce epigenetic changes as well. In addition, certain bacteria, notably Helicobacter pylori, can also trigger such modifications.

These alterations in gene expression can increase the risk of cancer.

Nature vs. Nurture: Can Lifestyle Choices Override Genetic Predisposition?

Yes, lifestyle choices can significantly lower cancer risk, even in people with genetic predispositions. This is according to several studies conducted among individuals with a genetic predisposition to cancer.

A 2020 study on the Association of Nongenetic Factors With Breast Cancer Risk in Genetically Predisposed Groups of Women in the UK Biobank Cohort discovered that women who maintain a healthy lifestyle, like engaging in regular exercise, limiting alcohol intake, keeping a healthy weight, and avoiding hormonal therapy, had a lower incidence of cancer, even when genetically predisposed.

Similarly, a 2021 study on the Genetic Risk for Overall Cancer and the Benefit of Adherence to a Healthy Lifestyle discovered that cancer incidence was reduced by 1.72% in men and 2.08% in women who practised healthier lifestyles.

These studies reinforce the role of lifestyle in cancer incidence regardless of genetic predisposition. So, even if you have a genetic predisposition to cancer, it doesn’t mean that you will have the disease, especially if you follow a healthy lifestyle.

The Role of Gene-Environment Interactions in Cancer

Each time a cell divides, it must duplicate its genetic material into its daughter cells. This division is tightly regulated by cyclins and cyclin-dependent kinases, with checkpoints and repair systems helping reduce-but not eliminate errors.

However, environmental factors can initiate the malfunction of this tightly regulated process, which can lead to unregulated proliferation of cells.

The development of cancer is a multi-stage process which includes initiation, promotion, and progression. The first stage can be induced by environmental factors such as arsenic or benzene, or other environmental factors that may lead to genomic instability or disruption of cellular metabolism.

Additionally, the environment can interact with genes by causing epigenetic changes, which can lead to tumorigenesis as well.

How to Assess Your Cancer Risk: Genetic Testing and Environmental Exposure

Cancer risk assessment is a process of identifying individuals at increased risk for hereditary cancer and tailoring preventive and screening strategies that differ from those offered to the general population.

Some of these risk assessments include:

• Genetic testing for cancer: If you have a family history of certain cancers, tests for the BRCA1 and BRCA2 gene changes can be done to detect mutations linked to cancer.
• Genetic counselling: A genetic counsellor helps you understand your cancer risks, decide on genetic testing, and interpret the results.
• Use risk calculators and prevention checklists: Use credible sources like the National Cancer Institute’s cancer risk calculator and review fact sheets on carcinogens to assess your risks. You can then discuss your concerns with a healthcare provider.
• Screening tests: Tests such as the mammograms, colonoscopy, and Pap tests are screening tests to help detect cancer early and in some cases prevent it.

Your risk is determined by what you inherit, what you are exposed to, and how you live. Regular checkups are a way to help you reduce your risks.

Strategies for Prevention Based on Genetic and Environmental Insights

Studies show that environmental factors and genetic mutations, especially with age, influence cancer risk. To reduce this risk, scientists and stakeholders must adopt innovative, multi-level prevention strategies based on current knowledge.

Key approaches include:

• Vaccination: This approach is based on the discovery that certain viruses, such as the human papillomavirus and hepatitis B virus, can cause different types of cancers.
• Chemoprevention: The rationale behind this strategy is based on targeting high-risk individuals that have a higher risk of cancer than others. Therefore, chemoprevention with drugs such as tamoxifen slows down cancer progression in individuals with inherited mutations linked to cancer.
• Policy approach: Policies such as the protection of non-smokers from secondhand smoke have been implemented in recognition of the fact that secondhand smoke kills thousands of lung cancer deaths each year.

As scientists continue to make groundbreaking findings on the preventive strategies and causes of cancer, we can make the best out of the findings that have been made already to reduce our risk of cancer.

What the Latest Research Says About Cancer’s Dual Origins

Recent cancer research strongly supports a dual origin for most cancers, where inherited and acquired genetic factors interact with environmental exposures and epigenetic changes to start and drive cancer.

Below are some of the latest findings on this dual origin:

• Genes and environment usually act together: Large reviews and gene-environment interaction studies show that many cancers arise when genetic susceptibility and environmental triggers combine to set off cancers.
• Specific exposure causes cancer-driving mutations: Some tumour profiling and sequencing studies have linked air pollution to mutation signatures and driver mutations like TP53, providing mechanistic proof that environmental exposures can produce the same DNA damage mainly attributed to smoking, improving our understanding of cancer diagnosis.
• Environmental exposure leaves molecular marks that mediate risk: Pollutants, diet, infection, and other exposures alter DNA methylation and histone marks-changes that can turn genes on or off and promote cancer without affecting the DNA sequence, offering new leads for targeted cancer treatment options.

These insights have provided scientists with a wealth of knowledge to which they are shaping prevention strategies and guiding the creation of better medications for the treatment of cancer.

Final Thoughts: Embracing a Comprehensive View of Cancer Risk

Cancer genetics reveals how inherited mutations interact with environmental exposures, with lifestyle and epigenetic changes acting as key mediators in its development.

Understanding this dual nature empowers individuals and policymakers to adopt targeted prevention strategies.

While we can’t control our genetic inheritance, we can influence how environmental exposures affect our long-term health. Minimizing contact with toxins, eating well, and supporting the body’s natural detoxification systems are all practical ways to lower risk and strengthen resilience against chronic disease.

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Frequently Asked Questions

What cancers are more difficult to treat?

Some advanced cancers, like pancreatic, brain, or liver cancer, are often difficult to treat due to late diagnosis and limited treatment response.

What are the top 3 deadliest cancers?

Lung, colorectal, and pancreatic cancers cause the highest number of cancer deaths worldwide.

What cancers can you live the longest with?

Thyroid, prostate, and testicular cancers generally have the best long-term survival rates.

Why are some cancers inoperable?

Cancers may be inoperable if they are too widespread, located near vital organs, or if surgery would cause severe harm.

What role do epigenetics play in cancer risk?

Epigenetics can switch genes on or off without altering DNA, allowing environmental factors to increase or decrease cancer risks.

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