CHICAGO (Reuters) - Instead of killing off cancer cells with toxic drugs, scientists have discovered a molecular pathway that forces them to grow old and die, they said on Wednesday.
Cancer cells spread and grow because they can divide indefinitely.
But a study in mice showed that blocking a cancer-causing gene called Skp2 forced cancer cells to go through an aging process known as senescence -- the same process involved in ridding the body of cells damaged by sunlight.
If you block Skp2 in cancer cells, this process is triggered, Pier Paolo Pandolfi of Harvard Medical School in Boston and colleagues reported in the journal Nature.
And Takeda Pharmaceutical Co’s experimental cancer drug MLN4924 -- already in early-stage clinical trials in people -- appears to have the power to do just that, Pandolfi said in a telephone interview.
The finding may offer a new strategy for fighting cancer.
“What we discovered is if you damage cells, the cells have a built-in mechanism to put themselves out of business,” Pandolfi said. “They are stopped irreversibly from growing.”
For the study, the team used genetically altered mice that developed a form of prostate cancer.
In some of these, they inactivated the Skp2 gene. When the mice reached six months of age, they found those with an inactive Skp2 gene did not develop tumors, while the other mice did.
When they analyzed the tissues from lymph nodes and the prostate, they found many cells had started to age, and they also found a slow rate of cell division.
This was not the case in mice with normal Skp2 function.
They got a similar effect when they used the Skp2-blocking drug MLN4924 in lab cultures of human prostate cancer cells.
To see if this would work in mice, they transplanted the cells and treated the mice with the drug.
“We put human cancer cells into mice. We fed them with a drug and these cells do senesce (age),” Pandolfi said.
“The same mechanism of damage caused by the sun can be evoked pharmacologically in cancer cells.”
He said this Skp2-related aging pathway appears to be active in cancer, and not other cells. “We have no intention of aging the patient. But only the cancer,” he said.
Editing by Todd Eastham
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