Research: Gene therapy with cellular guardian
Research using lab mice suggests that types of cancer can be forced into retreat by restoring the functions of a key guardian gene.
The spotlight is being placed on the p53 gene; the gene most commonly linked to cancer.
When functioning normally, p53 is alerted to the presence of an abnormal cell and unleashes one of two defensive processes -- apoptosis, in which the cell is instructed to commit suicide, and senescence, in which the cell's growth is arrested.
But inherited mutations in p53 can cause it to malfunction or it can be blocked by a protein called MDM2, and with this important suppressor out of the way, tumors then proliferate.
Two papers, published by the British journal Nature, used either gene therapy or a molecular technique called RNA interference to restore the function of p53 in mice with established cancer.
The tumors sharply regressed through senescence or apoptosis depending on the type of cancer cell. One of the studies, entailing mice with liver tumors, also found that inflammatory cytokines, a component of the immune system, were also unleashed to help clear the tumor.
The work "opens new therapeutic avenues against cancer," such as drugs to block MDM2 or other p53 inhibitors, and -- more distantly -- gene therapy to fix mutant versions of the p53 gene, a commentary in Nature says.
The papers are lead-authored respectively by Scott Low of Cold Spring Harbor Laboratory in New York and Tyler Jacks of the Massachusetts Institute of Technology (MIT).
Those authors sounded a note of caution about the success, saying that secondary tumors
sometimes emerged, apparently through resistance to the reactivated p53.
The spotlight is being placed on the p53 gene; the gene most commonly linked to cancer.
When functioning normally, p53 is alerted to the presence of an abnormal cell and unleashes one of two defensive processes -- apoptosis, in which the cell is instructed to commit suicide, and senescence, in which the cell's growth is arrested.
But inherited mutations in p53 can cause it to malfunction or it can be blocked by a protein called MDM2, and with this important suppressor out of the way, tumors then proliferate.
Two papers, published by the British journal Nature, used either gene therapy or a molecular technique called RNA interference to restore the function of p53 in mice with established cancer.
The tumors sharply regressed through senescence or apoptosis depending on the type of cancer cell. One of the studies, entailing mice with liver tumors, also found that inflammatory cytokines, a component of the immune system, were also unleashed to help clear the tumor.
The work "opens new therapeutic avenues against cancer," such as drugs to block MDM2 or other p53 inhibitors, and -- more distantly -- gene therapy to fix mutant versions of the p53 gene, a commentary in Nature says.
The papers are lead-authored respectively by Scott Low of Cold Spring Harbor Laboratory in New York and Tyler Jacks of the Massachusetts Institute of Technology (MIT).
Those authors sounded a note of caution about the success, saying that secondary tumors
sometimes emerged, apparently through resistance to the reactivated p53.
posted by gwg at 3:39 PM
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