A group of researchers from the University of Helsinki and the Helsinki University Hospital have developed a genetic test that makes it possible to identify patients with ovarian cancer who would benefit from treatment with PARP inhibitors, substances that have been shown to repair the DNA they have obtained. excellent results as maintenance treatment of ovarian cancer after surgery and as cytostatic therapy in newly diagnosed ovarian cancer.
The genetic test, optimized according to the characteristics of the Finnish population, has been clinically approved at HUSLAB and is used to test all ovarian cancer patients in Finland. In 2022, the Finnish Social Security Institute (Kela) added PARP inhibitors to its list of medicines for which costs are reimbursed based on genetic testing, as this therapeutic alternative has been associated with potentially serious side effects.
For researchers, the modified genetic test helps identify patients who do not benefit from the drug, thus avoiding unnecessary treatment and associated adverse effects. From an economic perspective, at least in this case, it also represents savings of millions of euros from public funds that can be used for other government strategies.
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Machine learning, the secret to success in precision medicine for ovarian cancer
This genetic test was designed with the help of automatic learning, an essential tool to facilitate the identification of those affected with ovarian cancer whose tumors present certain genetic defects typical of this oncological pathology.
To do this, they carried out a study published in the scientific journal npj Precision Oncology, in which it was shown that each type of cancer is associated with different characteristics of genetic lesions related to HRD. As has been shown in several previous investigations, the lesions caused by this type of cancer are caused by a deficiency in the homologous recombination DNA repair (HRD) pathway; therefore, they are tumors sensitive to PARP inhibitors.
“About half of ovarian cancers have a deficiency in a specific DNA repair pathway. Cancer cells with this deficiency are unable to accurately repair DNA double-strand breaks, leading to the accumulation of DNA lesions.”explained doctoral researcher Fernando Pérez Villatoro from the University of Helsinki, in a press release from the institution.
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