The “healthy” genes we inherit also influence the occurrence of cancer and its prognosis.

Research at Stanford University School of Medicine has shown that certain genetic sequences inherited from parents And benign They are associated with a greater susceptibility to cancer for decades to come. This connection has been demonstrated after analyzing thousands of cases mammary cancer whose appearance was regarded as spontaneousbecause the patients did not have a specific genetic risk marker.

Conclusions of your published work The science They contradict the traditional view that, in the absence of a specific hereditary risk, cancer arises as a result of random mutations that accumulate throughout life. However, as new research shows, the immune system’s predisposition to recognize and destroy potentially cancerous cells This is determined by certain genetic sequences. acquired from our parents.

According to their results it will be tens or even hundreds of genetic variants In healthy people, this could explain why some resist seemingly random mutations and remain healthy throughout their lives. “Our results indicate not only what specific subtype of breast cancer whether the patient is predisposed to suffer, but rather we are told How aggressive will it be and how prone to metastasis will it be?“.

(They discovered a hundred proteins that can detect cancer 7 years before diagnosis)

“This research is of excellent quality, and breaks the paradigm“, Explain Ramon SalazarHead of the Department of Medical Oncology and Director General of the Catalan Institute of Oncology (ICO) Scientific Media Center. Until now, it was believed that in sporadic non-hereditary cancers, the presence of somatic mutations is not associated with hereditary non-pathological functional genetic variants. “The authors destroyed this principle“.

Each gene contains hundreds of physiological genetic variants, Salazar continues, that can determine whether peptides or protein antigens that encode are present “more or less noticeably”—that is, detectable—to the immune surveillance system. T lymphocytesThus, immune cells capable of responding to a tumor will have greater or lesser sensitivity to antigen presentation receptors on the cell membrane. “The genetic makeup of this major histocompatibility system (HLA) is also highly variable,” he warns.

The researchers studied about 6000 cases of breast tumors in different phases of the disease to identify their relationship with genetic variants of oncogene sequences. Depending on each person’s genetics, genes will produce more or fewer copies antigens or epitopesincluding oncogenes which cause cancer. “When they present themselves a lot and very well, it is unlikely that cancer develops secondary to this oncogene“Salazar warns.

However, the operation of this system is paradoxical. First, the generation of multiple epitopes has a protective effect against cancer because the immune system becomes more sensitive to tumorigenesis and more effectively eliminates emerging tumors. But in the long run Tumors that manage to break out will be more aggressive and prone to metastases.favoring the progression of cancer.

The authors define it as a kind of tug-of-war game in which the immune system has the upper hand, but tumorigenesis may tip the balance in cancer’s favor. “We have clarified this opaque process and this may help us make decisions about When is the best time to intervene? therapeutically, or how to “warm up” a “cold” tumor, making it sensitive to treatment,” the report says. Christina CurtisProfessor of Medicine, Genetics and Data Science.

However, this finding was only confirmed for breast cancer mediated by oncogenes such as HER2 or MYC. “They’re trying to replicate it in other tumors and with other mutations,” Salazar says.