Why some smokers get cancer and others don't – scientists have found an explanation

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Tengrinews.kz — For the first time, scientists have obtained evidence that inherited genes can influence cancer risk and the specific way a tumor forms. The results of the study, published in the journal Nature, help explain why individuals exposed to the same conditions react differently to identical risk factors.


Why cancer does not develop in everyone

According to the study's authors, cancer develops when mutations accumulate in a cell's DNA. This causes them to grow faster and stop responding to the body's signals that normally trigger damaged cells to die.

The extent of DNA damage can be influenced by external factors, such as cigarette smoke or sunlight. Inherited genetic changes can influence how many mutations accumulate within cells.

However, the researchers note that not everyone exposed to the same environmental risk factors develops cancer:

"Most smokers do not develop lung cancer, yet some non-smokers do," the paper states.

The authors of the new study believe the answer may lie in inherited genetics.

"While many scientists suspect that inherited genetic differences influence cancer risk, proving this link is difficult because individuals within and across human populations differ in lifestyle, environment, and exposure history," the article says.

How the study was conducted

To test their hypothesis, scientists bred four strains of mice with different genetic predispositions to liver cancer. All animals, at the same age and under identical conditions, were administered the same dose of diethylnitrosamine (DEN)—a carcinogen found in tobacco smoke and certain processed foods.

This substance damages the DNA of liver cells, which can lead to mutations and trigger tumor growth..

Because all mice were kept in identical conditions, researchers were able to exclude the influence of external factors and focus specifically on the role of heredity.

The scientists then studied the genomes of nearly 600 tumors, analyzed gene expression within them, and compared the results with mice that had not been given the carcinogen. This allowed them to trace how each tumor progressed—from the initial mutation to the formation of cancer.

The researchers discovered that the consequences of a single mutation depended on the mouse's genetic profile. In some cases, it activated alternative cancer development mechanisms and caused whole-genome doubling—where a cell acquires an extra copy of all its chromosomes.

Potential impact

Scientists believe these findings could impact the development of personalized medicine, prevention strategies, and early detection programs for oncological diseases.

According to the study’s lead, Professor Duncan Odom, this is the first time scientists have been able to directly demonstrate how much genetic background influences both mutation processes and the pathways leading to tumor development.

"Cancer does not occur entirely by chance. Although tumors often reach the same biological endpoint, the path to that endpoint is determined by an individual's genetic background," he emphasized.

The authors noted that since the study was conducted on mice, the results have yet to be confirmed in human trials.

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