Genetic tests can reveal a person's predisposition to cancer, but having such a predisposition does not mean that developing the disease is inevitable. According to geneticist Dmytro Mykytenko, in an interview with RBC-Ukraine, the key factor is the degree to which the function of the genes responsible for protecting cells and correcting errors in DNA is impaired. It is the efficiency of these mechanisms that determines whether the disease will manifest and at what age.

Sporadic Mutations vs. Inherited Forms

In most cases, cancer arises as a result of a spontaneous mutation that disrupts normal cell function and leads to its uncontrolled growth. However, as Mykytenko explained, approximately 10–30% of tumors may be linked to familial hereditary forms — depending on the location of the disease. "Inherited familial forms are not tumors in themselves, but they create conditions under which the error-correction system works poorly," the geneticist emphasized. Thus, heredity does not form the cancer itself, but rather the environment in which mutations accumulate faster and are more likely to lead to a pathological process.

Age of Onset Depends on the Degree of Impairment of Protective Mechanisms

The geneticist detailed how the efficiency of the cell protection system affects the timing of disease onset. If the protective mechanism does not work at all, cancer may manifest at a very early age. With moderate efficiency of the system, failures may occur at the age of 30–40. If the impairments are minor, mutations accumulate much more slowly, and the disease may not show itself until the age of 60–70. This means that even in the presence of a genetic predisposition, the prognosis regarding the timing and likelihood of developing cancer is highly individual.

BRCA and TP53: Genes with Different "Ranges of Action"

As a clear example, Mykytenko cited the BRCA gene — one of the key components of the DNA error-correction system. It is traditionally associated with breast and ovarian cancer in women, as well as prostate cancer in men. However, there are also genes that are not tied to a specific organ. In particular, TP53 is supposed to trigger the cell death program if a mutation has already been detected in the cell. If this mechanism is impaired, the cell continues to divide, and a tumor may arise in a wide variety of organs. This is why, within a single family, cancer may be diagnosed in different members with different locations — such a situation is known in medicine as a familial cancer syndrome.

Genetic Predisposition Is Not a Sentence

It is important to emphasize: the presence of a genetic predisposition in itself does not mean a 100% likelihood of developing cancer. The risk always remains probabilistic, not deterministic. Nevertheless, awareness of one's own genetic profile allows a person to pay closer attention to prevention, undergo targeted screenings, and seek specialist care in a timely manner. The geneticist also noted that if a person is aware of their cancer predisposition and is planning a child, modern reproductive technologies make it possible to test embryos for the presence of the mutation. "We can test the embryos and choose one that will not carry this predisposition," Mykytenko said, pointing to the real possibilities of genetic counseling in the context of family planning.

Contradictory Data

No direct contradictions in figures or the date of the interview were found in the provided fact-checking sources. Both sources (RBC-Ukraine and novosti.ua) refer to the same interview with geneticist Dmytro Mykytenko and reproduce identical estimates: the 10–30% range for hereditary forms, and the age ranges of 30–40 and 60–70 years. The only caveat is methodological in nature: the phrase "approximately 10–30%" is a generalization and, according to the geneticist himself, depends on the location of the tumor, which makes the exact percentage conditional for a specific patient.