Changes to checkpoint enzymes can result in the loss of apoptosis during cell cycle checkpoints and lead to cancer. The p53 tumor suppressor gene regulates the cell cycle and is the most widely mutated gene in humans (Wang and Harris, 1997). This is supported by the fact that it is mutated in over 50% of all human cancers. p53 can activate DNA repair proteins when DNA has sustained damage, can hold the cell cycle at the G1/S regulation point if it spots a mutation, and can begin apoptosis if the DNA damage proves to be unfixable (Pietenpol and Stewart, 2002). Formations of cancer tumors can occur if this system no longer works. If the p53 gene is damaged, then tumor suppression is severely reduced. The p53 gene can be damaged by radiation, various chemicals, and viruses such as the Human papillomavirus (HPV). People who inherit only one functional copy of this gene will most likely develop tumors in early adulthood (Varley et al., 1997; Gu et al., 2001).
