Evolving Resistance: The Interplay of p53, Chemoresistance, and Metastasis in Cancer's Journey

Abstract

Cancer is a growing concern around the world with more than 20 million new cases confirmed and counting. This is partly caused by the overuse of Chemotherapeutic drugs against Cancer, leading to its potency. Cancer starts with an accumulation of genetic mutations in the genome, and the ignorance to cell checks by CD8 and NK cells. The Cancer cell utilizes its hallmark capabilities and uses one of its cells to metastasizes in other areas of the body either through the perineural, circulatory, or lymphatic system. p53 is a tumor suppressor gene which repairs the mutations of the cell by conducting cell cycle arrest and inducing apoptosis. However, cancer cells can increase the expression of SB100 which can inhibit p53. One solution is to combine PRIMA-1 and CDDP which restores p53 and it’s wild type functions to induce apoptosis. This effect is increased with the use of adenoviral DN-Akt since it could increase p53 phosphorylation at Ser15.