Therapeutic role of dabrafenib on thyroid cancer

Abstract. Thyroid cancer, which has a high prevalence of BRAF V600E mutations, is the ninth most frequent cancer worldwide, especially in the aggressive anaplastic thyroid cancer (ATC). The mutation causes continual activation of the MAPK pathway, resulting in unrestricted cell multiplication that leads to the development of tumors. The therapeutic potential of a selective BRAF V600E inhibitor, dabrafenib, has been approved in the treatment of thyroid cancer, especially ATC. The efficacy of dabrafenib was investigated by analyzing various in vivo and in vitro studies and clinical trials. The therapeutic role of dabrafenib on thyroid cancer has been approved in studies involving tumor growth, cell viability, apoptosis, and effects on cancer stem cells (CSCs). Notably, the combination of dabrafenib and MEK inhibitors such as trametinib. significantly inhibited tumor growth and induced apoptosis in thyroid cancer cells. Studies have shown that this combination therapy can reduce tumor volume and target CSCs, which are key to tumor recurrence and drug resistance. Clinical trials have reported improvements in patient status. Dabrafenib, especially in combination with other drugs, offers a better treatment strategy for aggressive thyroid cancer. It enhances the therapeutic effect by effectively targeting the MAPK pathway and CSCs. Future studies may focus on optimizing these combination therapies and exploring their effects and safety to further improve patient outcomes in thyroid cancer treatment.