New cancer research published by UCSF Comprehensive Cancer Center members in this week's Nature challenges conventional wisdom about how an archetypal, protective "tumor suppressor" protein works to prevent cancer.
The p53 protein is a powerful tumor suppressor that prevents cells in our bodies from becoming cancerous. It does this by either killing or permanently shutting down cells exposed to stress or injury. Paradoxically, the UCSF study authors, led by Gerard Evan
, an international leader among scientists who investigate the origins of cancer, propose that new drugs be developed and tested with the goal of shutting p53 down -- at least temporarily -- at the time of cancer treatment. This is because, while p53 blocks cancer, it also is responsible for side effects of conventional cancer therapies.
By temporarily blocking p53, clinicians might be able to spare patients from many uncomfortable, harmful and dose-limiting side effects of chemotherapy and radiation therapy, the authors provocatively suggest. The researchers base their conclusions on experiments in mice exposed to DNA-damaging and mutation-causing radiation.
P53 is a sensor of DNA damage within cells. It triggers suicide among cells in which the damage cannot be repaired. It has long been believed that p53 prevents cancer by causing damaged cells to commit suicide -- before mutations triggered within the cells can drive uncontrolled cell division and tumor growth. The scientific term for the distinctive biochemical chain of events leading to cellular suicide is "apoptosis."
(Note that in November 2007 the UCSF Comprehensive Cancer Center was renamed the UCSF Helen Diller Family Comprehensive Cancer Center.)
Read more at Jeffrey Norris, UCSF Today