Is Cancer Genetic or Caused by Lifestyle? The Surprising Truth Explained

SINGAPORE – Statement of fact: Cancer is often hereditary in nature. This would imply that cancer is “inborn”.

Another statement of fact: Cancer is frequently caused by modifiable factors such as lifestyle and environmental influences. This would suggest that cancer is “acquired”.

So, how do we resolve this apparent contradiction? Can a rich man be born into a wealthy family, yet still be self-made?

Many theories in popular culture attempt to explain this contradiction.

One of the more commonly circulated ideas: You harbour dormant cancer cells in your body. Whether you eventually develop cancer depends on whether certain factors provoke these cells to awaken from a hibernating state.

The notion that cancer is somehow inherent may be a convenient way to explain why more than one in four Singaporeans are destined to be diagnosed with cancer in their lifetime. According to figures from the Singapore Cancer Registry for 2019 to 2023, about 50 people on average are diagnosed with cancer every day in Singapore.

However, cancer is fundamentally an acquired condition.

The key driver of cancer formation is genetic mutation. The genetic code of a cell functions as a code of conduct that governs its behaviour.

A normal cell is regulated, orderly and cooperative – much like a law-abiding citizen in society. Cancer arises when this code of conduct is corrupted.

In that sense, the transformation of a normal cell into a cancer cell is analogous to a normal citizen turning into a terrorist. Cancer cells harm the body in much the same way that terrorists harm society.

Just as no baby is born a terrorist, no one is born with cancer cells. The corruption of a terrorist’s mind is an acquired event. So, what causes a similar “corruption” in cells?

Factors that introduce errors into the genetic code – a process known as mutation – are necessarily acquired, although they are not always modifiable.

Modifiable factors that trigger cancer-causing mutations are often lifestyle-related. Tobacco use alone accounts for about 25 per cent of all cancers worldwide. Dietary factors and obesity contribute another 35 per cent.

Certain infections also cause cancer, likely accounting for about 15 per cent of cases. While not strictly lifestyle-related, these risks are modifiable through vaccination.

Hepatitis B infection significantly increases the risk of liver cancer, while the human papillomavirus (HPV) is an obligate factor in cervical cancer. Both infections can be prevented through vaccination prior to exposure.

Lottery of genetic mutations

How, then, do we explain the occurrence of cancer in individuals who have no known exposure to any defined risk factors? Is it simply bad luck?

In a sense, yes.

More than 50 per cent of genetic mutations occur randomly. The human body is a dynamic, living system with constant cellular turnover. Old cells die when they reach senescence, and new cells are formed to replace them.

Each newly formed cell requires its own genetic instruction manual, which must be copied from an existing template. It is during this repeated copying process that random errors are introduced.

Consider the party game Chinese Whispers (also known as Broken Telephone). A phrase is whispered from one person to the next down a chain. By the time it reaches the final participant, it often bears little resemblance to the original, frequently becoming nonsensical or humorous.

In a similar way, repeated genetic replication introduces cumulative errors, some of which may eventually become cancer-causing mutations.

Importantly, cancer is rarely triggered by a single mutation. Rather, it arises from the accumulation of multiple mutations that together result in loss of cellular control.

Of course, nature has evolved safeguards against such corruption.

Genetic replication includes built-in “proofreading” mechanisms that detect and correct errors before they cause harm. However, some individuals inherit defects in these self-correction systems. In other words, they have an innate tendency to accumulate mutations. This brings us to the topic of hereditary cancer.

In families with a strong history of cancer, individuals do not inherit pre-formed cancer cells. Instead, they inherit a predisposition to developing cancer.

In most cases, this involves the inheritance of a defective tumour-suppressor gene. As the name suggests, these genes act as safeguards against cancer. They are the brake pedals that prevent cells from spiralling out of control. Such mutations are known as loss-of-function mutations.

More rarely, individuals may inherit a defective “gas pedal” instead – an oncogene that actively drives cancer formation. These are known as gain-of-function mutations.

Well-known examples of inherited tumour-suppressor genes (more specifically, DNA repair genes) are BRCA1 and BRCA2, made famous by Hollywood actress Angelina Jolie. In 2013, at age 37, she underwent a preventive double mastectomy after learning she had a very high risk of developing breast cancer due to a defective BRCA1 gene.

Mutations in these genes impair the cell’s ability to proofread and repair genetic errors, resulting in a markedly increased risk of breast and ovarian cancers, among others.

Role of chance

So, how do we explain siblings who inherit the same defective gene, yet only some go on to develop cancer?

Despite genetic inheritance, chance still plays a role. This is explained by the two-hit hypothesis.

Every gene in the body exists in pairs – one inherited from each parent. If an individual inherits one faulty copy, the remaining functional copy can still suppress cancer. However, this creates a lifelong vulnerability. Cancer develops only when the second copy is lost – the second hit.

Cancer formation therefore requires cumulative mutations, a process known as multi-step carcinogenesis. Individuals without inherited cancer syndromes generally take longer to accumulate the necessary mutations and thus tend to develop cancer later in life. Those born with a defective tumour-suppressor gene start with a disadvantage and reach the critical threshold much earlier, often developing cancer at a younger age.

In summary, individuals do not inherit cancer itself, but they may inherit an increased tendency to develop it. Inherited defects in cancer-suppressor genes give cells a head start towards malignancy by weakening their brake pedals.

Ultimately, however, there remains an element of chance. Even with faulty brake pedals, a random event must still disable the “handbrake” before the system completely loses control.

Cancer, therefore, is not inborn. But for some, the odds are stacked from the very beginning.

• Dr Wong Seng Weng is the medical director and consultant medical oncologist at The Cancer Centre.

Article repurposed from The Straits TImes.

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