An international scientific team from the Spanish University of Vigo (Uvigo) discovered a new molecular mechanism capable of restricting the capacity of tumor cells to repair their DNA, the main form of defense against drugs, reports the aforementioned academic center.
Research, fruit of more than seven years of work and published in the scientific journal Nature Communicationsidentifies the connection protein 43 as a new and powerful therapeutic target capable of curbing the growth of tumors and avoiding the appearance of resistance to treatments and even reversing it when it has already occurred, according to a statement from the Uvigo.
The advance is focused on tumors with a mutation in the BRAF gene, present in more than 60% of cases of melanoma and in certain cancers of colon, lung or breast.
This mutation activates a route that triggers the uncontrolled proliferation and survival of the tumor cells that possess it, according to the study led by Dr. María Mayán of the Research Center in Nanomaterials and Biomedicine of the Uvigo.
There are currently therapies directed against this type of pathologies, such as Braf/Mek inhibitors, “which have supposed a before and after on an oncology,” says Dr. Mayán.
However, with them “we do not reach all patients, because a high percentage are resistant to these therapies and, of which they respond, between 60 and 80% they also end up developing resistance,” he adds in the note.
To deal with this problem, the group of researchers launched a multidisciplinary and international project aimed at finding a solution to this resistance and evaluating strategies that allow it to avoid it.
You may be interested: The first Barbie doll with type 1 diabetes comes to give visibility to the disease
They discover vulnerability to overcome drug resistance of certain cancers
Twenty European research centers collaborated in the project, which have discovered a mechanism that makes the most vulnerable tumor cells.
The study had the European financing of the Horizon 2020 program.
The work reveals why these tumor cells get rid of the connection protein 43 to survive and how, when restoring it, they can “disarm” and lead to cell death.
The mechanism demonstrated to reduce tumor growth and prevent relapses in animal preclinical models.
This protein interferes with the main path that the cancer cell uses to repair the damage to its DNA. It acts as a brake, forcing the cell to use much less effective alternative repair routes.
As a result, the damage accumulates to an unsustainable point, causing the cell to enter a state of non -proliferation – senity – or directly dies.
This effect is multiplied by combining it with drugs that also damage the DNA of tumor cells, such as Braf/Mek inhibitors, triggering what is known as “synthetic lethality.”
The team generated an effective therapeutic strategy, demonstrated as proof of concept in this study, according to Mayán, and is now “looking for support to be able to transfer it and reach patients in the future.”
With EFE information.
Do you use more Facebook? Follow us to always be informed
