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Shielding a Metastasis-Promoter

Conquest - Fall 2008

Efforts to protect the tumor-suppressor p53 could just as easily shelter a mutant version of the protein, causing cancer cells to thrive and spread rather than die, according to research by M. D. Anderson scientists.

Guillermina Lozano, Ph.D., chair of the Department of Genetics, stresses the importance of knowing which version of p53 is present in a patient’s tumor before treating it.

“As we develop therapies to restore the function of p53, we need to make sure we first know what version of this gene is present in a patient’s tumor and then decide how to treat it,” says senior author Guillermina Lozano, Ph.D., chair of M. D. Anderson’s Department of Genetics.

The research shows that attempting to restore normal expression of p53 protein by blocking another protein that normally degrades p53 can have the reverse effect of protecting mutated p53 and promoting metastasis.

The p53 gene is inactivated in many types of cancer. Its normal role is to halt the division of a defective cell and then force the cell to kill itself or deprive the cell of its ability to reproduce. Reactivation of p53 is thought to have great therapeutic potential.

Normally, p53 levels are low, but it springs into action in response to DNA damage or activation of cancer-promoting genes, or oncogenes.

Reported in the May 22 issue of the journal Genes & Development.


© 2014 The University of Texas MD Anderson Cancer Center