Application of stress to upregulate the p21 mechan

Application of stress to upregulate the p21 mechanism can result in pro apoptotic or anti apoptotic action. So - depending on mechanism that provokes the original upregulation - the result can be either enhancing apotosis or p21 protecting cells from apoptosis. This poster focuses on only one of the possible actions of p21 upregulation (when this occurs from stress to p53 mechanism. p21 also has mechanisms of action independent of p53) - the cytostatic effect. Kevetrin, with it's ability to restore function to damaged p53 gene, is also reportedly activating cell protective effects.

Up to 88% of all cancers with mutant p53 show reduced expression of p21. Increased levels of p21 thus indicate restoration of function to p53 - which includes protection of healthy cells and restoration of the cells ability to kill itself if it is cancerous. I do not know what the posters concern is re measurement of this expression in lymphocytes. The poster expresses concern that cell death pathway is activated in normal cells. Kevetrin restores function to cells with damaged (mutated) p53 gene. Doing so allows the cell to regain full function of p53 processes - which include both protective and apoptosis actions. This poster focuses only on one mechanism of action. Cellceutix focuses on many.

This posters statement that restoration of p53 function as evidenced by increased levels of p21 "would inhibit the growth of normal cells that are supposed to be growing" simply shows lack of knowledge of what that protein does. The poster, perhaps conveniently, ignores all of the protective functions of the protein when it is intact. This assumption by the poster leads him/her to then draw conclusions based on faulty information. So the conclusions are faulty too.

Even a nonscientific person knows that if a drug causes cell cycle arrest in healthy cells, and that process is genetically controlled, the the drug is toxic to that gene. A healthy cell won't kill itself without that gene being damaged. So the posters idea that a nongenotoxic agent will still cause genotoxicity is just....a little bizarre.

The poster has concerns re the animal preclinical side effects. There is nothing of concern that I can see there. The dogs had trouble tolerating it. The mice did not. They both showed that they received a drug. Their bodies reacted, but well within acceptable limits.