The object of this thesis is the p53 protein, a tumor suppressor able to respond to various types of chemical and physical cellular stress by leading to mechanisms such as DNA repair, cell cycle arrest and apoptosis. Unfortunately, the transcription factor p53 gets mutated in nearly 50% of human cancer cells, resulting in the inactivation of the protein which will be unable to exercise its proper functions. Therefore, this leads to a facilitated cancer progression and negative consequences for patients. Studies identified in the protein’s DNA core domain six "hot spot" mutations, of which this thesis deals with the G245S one, a point mutation of the glycine in position 245 into a serine residue.