CONNEXIN 43 FOR USE IN THE TREATMENT OF A CANCER TYPE CHARACTERIZED BY THE ACTIVATION OF A MITOGEN-ACTIVATED PROTEIN KINASE

It provides a new strategy to avoid the resistance that patients develop to this type of therapy that is very effective in patients who respond to these treatments. Our elders Results indicate that increasing Cx43 could reverse resistance in the case of tumor cells that have acquired a phenotype resistant to BRAF/MEK inhibitors. The main handicap that hinders the definitive cure of cancer in general and in particular of cancer with mutation in BRAF, as is the case in more than 50% of melanoma cases, is the resistance that tumor cells generate toward treatments and toward targeted therapy. In the case of mutated BRAF, resistance to BRAF inhibitors appears after 6-8 months from the start of treatment. The treatment with the combination of BRAF and MEK inhibitors (dabrafenib with trametinib and vemurafenib with cobimetinib) is one of the alternatives to prevent the development of resistance. Still, the patients that respond to treatment develop resistance at 11-12 months, although there is a group of patients that supposes approximately 20%, of long survivors (at 5 years) that supposes an achievement historical. Today there is a need to develop new therapeutic strategies, which probably include the appropriate combination of drugs to prevent or avoid resistance and combat malignant melanoma in patients with BRAF mutations, also solving a key challenge in other types of cancer since it is estimated that 8% of all types of cancer have mutations in BRAF.