My excitement level just dropped after reading a bit on p53:
p53 has many mechanisms of anticancer function and plays a role in apoptosis, genomic stability, and inhibition of angiogenesis. In its anti-cancer role, p53 works through several mechanisms:
- It can activate DNA repair proteins when DNA has sustained damage. Thus, it may be an important factor in aging.
- It can arrest growth by holding the cell cycle at the G1/S regulation point on DNA damage recognition (if it holds the cell here for long enough, the DNA repair proteins will have time to fix the damage and the cell will be allowed to continue the cell cycle).
- It can initiate apoptosis (i.e., programmed cell death) if DNA damage proves to be irreparable.
I'm no molecular biologist (not even close, hated biology in school) but to me, it sounds like supressing p53 could lead to more cancer(s). Unless the drug specifically targets a mutated version of p53 that is.
Myc (c-Myc) looks more promising as it has been known to cause many cancers:
Myc (c-Myc) is a regulator gene that codes for a transcription factor. The protein encoded by this gene is a multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation.
A mutated version of Myc is found in many cancers, which causes Myc to be constitutively (persistently) expressed. This leads to the unregulated expression of many genes, some of which are involved in cell proliferation, and results in the formation of cancer. A common human translocation involving Myc is critical to the development of most cases of Burkitt lymphoma. Malfunctions in Myc have also been found in carcinoma of the cervix, colon, breast, lung and stomach. Myc is thus viewed as a promising target for anti-cancer drugs.