Manipulation of a gene that normally protects against malignancy but is switched off in cancer cells could open up a promising new frontier in research.
January 25, 2007 (Press Release) --
Manipulation of a gene that normally protects against malignancy but is switched off in cancer cells could open up a promising new frontier in research, according to two new U.S. studies.
Whenever p53 was turned off, cancer cells in mice quickly went to work forming tumors, the studies found. But when researchers used high-tech tricks to switch the gene back on, "the tumor went away," said the leader of one of the studies, Scott Lowe, deputy director of the Cold Spring Harbor Cancer Center, in Cold Spring Harbor, N.Y.
"We would like to imagine that this would translate to human tumors," he said. "In such a system, you could have a very aggressive cancer that really depends on the continued inactivation of this gene to survive."
The study also uncovered surprising new insights into the power of the human immune system to "mop up" cancers weakened by reactivated p53.
Lowe's work and a related study were published online in the Jan. 25 issue of Nature.
"These studies indicate that this might be a fruitful path to explore from a cancer drug-development standpoint," said Dr. Ronald DePinho, a pioneer in this type of work and a professor of medicine at Harvard Medical School.
Although an actual drug for use in a clinical setting is still a long way off, "there are compounds that are now being directed toward the p53 kinase pathway that may enable re-establishment of p53 activity," said DePinho, who also authored a related commentary on the studies.
Almost all forms of cancer involve an inactivation of the p53 tumor-suppressor gene and its related biochemical pathway. So, the pathway has long been a favorite target of cancer research.
"What p53 does is help cells solve problems when they are stressed," Lowe explained. "So, if a cell is damaged in some way, it can make them stop growing, so they aren't dangerous and form a cancer. In fact, it can even kill cancer cells through a process called apoptosis," or programmed cell death.
Unfortunately, this cancer "safety net" is almost always switched off in tumor cells. Scientists have long known that shutting down p53 is key to triggering a cancer -- but what about maintaining its growth? Work by DePinho and others in the 1990s established that the genes that help start a cancer aren't always crucial to its continued survival.
Would that be the case with p53? To find out, Lowe's group used a highly advanced gene manipulation technique called RNA interference (RNAi) to first switch off p53 in cancer-prone mice and then switch it back on, watching to see what happened.
The results were heartening. Just like clockwork, the mouse tumors expanded in the absence of active p53, then shrank when the gene went back to work.
Lowe called the results "a nice proof-of-principle" that p53 inactivity is, indeed, crucial to tumor maintenance.
source: http://health.msn.com/
Whenever p53 was turned off, cancer cells in mice quickly went to work forming tumors, the studies found. But when researchers used high-tech tricks to switch the gene back on, "the tumor went away," said the leader of one of the studies, Scott Lowe, deputy director of the Cold Spring Harbor Cancer Center, in Cold Spring Harbor, N.Y.
"We would like to imagine that this would translate to human tumors," he said. "In such a system, you could have a very aggressive cancer that really depends on the continued inactivation of this gene to survive."
The study also uncovered surprising new insights into the power of the human immune system to "mop up" cancers weakened by reactivated p53.
Lowe's work and a related study were published online in the Jan. 25 issue of Nature.
"These studies indicate that this might be a fruitful path to explore from a cancer drug-development standpoint," said Dr. Ronald DePinho, a pioneer in this type of work and a professor of medicine at Harvard Medical School.
Although an actual drug for use in a clinical setting is still a long way off, "there are compounds that are now being directed toward the p53 kinase pathway that may enable re-establishment of p53 activity," said DePinho, who also authored a related commentary on the studies.
Almost all forms of cancer involve an inactivation of the p53 tumor-suppressor gene and its related biochemical pathway. So, the pathway has long been a favorite target of cancer research.
"What p53 does is help cells solve problems when they are stressed," Lowe explained. "So, if a cell is damaged in some way, it can make them stop growing, so they aren't dangerous and form a cancer. In fact, it can even kill cancer cells through a process called apoptosis," or programmed cell death.
Unfortunately, this cancer "safety net" is almost always switched off in tumor cells. Scientists have long known that shutting down p53 is key to triggering a cancer -- but what about maintaining its growth? Work by DePinho and others in the 1990s established that the genes that help start a cancer aren't always crucial to its continued survival.
Would that be the case with p53? To find out, Lowe's group used a highly advanced gene manipulation technique called RNA interference (RNAi) to first switch off p53 in cancer-prone mice and then switch it back on, watching to see what happened.
The results were heartening. Just like clockwork, the mouse tumors expanded in the absence of active p53, then shrank when the gene went back to work.
Lowe called the results "a nice proof-of-principle" that p53 inactivity is, indeed, crucial to tumor maintenance.
source: http://health.msn.com/
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