These two types of genes are currently the subject of intense scrutiny by cancer researchers. In a healthy cell, the p53 tumor suppressor gene is active and able to fulfill its role of keeping cells noncancerous. In cancer cells, the reverse situation often exists. Antineoplastons appear to act as biochemical microswitches, turning off the oncogenes that cause cancer, while turning on the tumor suppressor genes that stop it. Thus, the purpose of Antineoplaston treatment is not to poison cells but, rather, to activate the cells' suicide program.
Cancer cells differ from healthy cells in that they are immortal.
Whereas healthy cells live for a time, die, and are replaced by healthy cells in an orderly process, cancer cells lack the ability to recognize when it is time for them to die. New cancer cells appear while the old ones live on, causing a riotous proliferation of these cells that eventually results in a tumor. Stanislaw R. Burzynski, MD, PhD, has used antineoplastons in his private practice of medicine since 1977. The NCI has called for further trials to determine the response rate, which provided the impetus for the current Phase II trials. Admission criteria vary depending on the type of cancer.