In 50 percent of breast cancer cases, a mutated protein, known as p53, is present. Previous research has indicated that when p53 is functionally abnormal, tumor cells are prolific and develop quickly. PRIMA-1, a small molecular drug, targets and returns normal function to the mutated p53, but PRIMA-1 alone is not enough to stop tumor growth. Proliferating blood vessels supply oxygen and other nutrients that the tumor needs to grow. However, a specific antibody, 2aG4, has the ability to destroy these blood vessels and prevent future growth. According to the MU research team, no one has previously tried to attack tumor cells by targeting mutated p53 and the tumor-associated blood vessels with this combination of PRIMA-1 and 2aG4. “Tumors are entities that want to live,” said Salman Hyder, professor of biomedical sciences in the College of Veterinary Medicine and the Dalton Cardiovascular Research Center. “They adapt under conditions that would cause anything else to die. In order to effectively treat tumors, treatments must attack the breast tumor cells and the blood vessels that supply nutrients to the tumor. Treatment strategies in our study that targeted both areas resulted in improved and more potent responses.”
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