Review of P53 Research
Review of P53 Research
Ventura A et al. Restoration of p53 function leads to tumour regression in vivo. Nature. 2007 Feb 8;445:661-5.
“Loss of p53 function may not only play a role in the early stages of tumor development, but also be required for the continued proliferation or survival of an established tumor.” (Ventura 661) is an explicit hypothesis in this paper.
Increase in tumor volume can be predicted in tumors where p53 remains inactive. Tumor regression or cellular arrest due to the reactivation of p53 in mice with autochthonous tumors can also be foreseen. The importance of autochthonous tumors is that they originate in the organism and mimic real life events.
Collected data from this experiment support the conclusion that sustained inactivation of p53 is required for the maintenance of primary, autochthonous lymphomas and sarcomas. If p53 is reactivated in a tumor, then tumor regression may occur.
Data did support the conclusions and the hypothesis in this paper.
MRI images (Figure 2 d,e) show tumor growth in vivo where p53 was not reactivated.
These are the control and did not have Cre Estrogen Receptor.
An increase in tumor volume in both the sarcomas and lymphomas were observed in
mice that had inactivated p53. In Cre-ER positive lymphomas treated with tamoxifen,
apoptosis was verified by TUNEL staining (Figure 3,b 663).
CRE-ER positive sarcomas experienced senescence, marked by the presence of B-
galactosidase, with the treatment of tamoxifen.
Normal