Scientists in California have found a way to ”turn off” a gene that makes cancerous cells lethal. They eliminated aggressive, incurable liver tumours in laboratory mice in four weeks, they report in an advance paper in Nature on Monday.
The study, based on a gene called Myc, could lead to new ways of treating cancer.
Cancer Research UK scientists in Glasgow, working with colleagues in Seattle, last year worked out the details of how Myc cranks up the rate of growth of dividing cancer cells by sending one of the cell’s factories into overdrive. In cancer, cells divide uncontrollably.
The California team based their studies on mice with genetically modified liver cells. The type of cell that becomes cancerous is called an epithelial cell, and these form cancers in breast, colon and prostate. So the same approach might work in all of them. Liver cancer is common and difficult to treat.
”This is a terrible cancer. Anything that is encouraging in liver cancer may be important,” said Dean Felsher of Stanford University, who led the research. ”The exciting thing is that you can turn cancer cells into something that appears to be normal.”
The mice under study had a mutated Myc gene that was constantly on. It produced a Myc protein that served as a kind of conductor, sending a signal to cells to divide. Cancer cells produce too much Myc protein all the time, and are constantly dividing. Dr Felsher and his colleagues fed the mice an antibiotic called doxycycline, which turned the gene off, and stopped the protein flow.
As long as the mice had the antibiotic diet, they remained healthy. Once the antibiotic was withheld, they developed aggressive liver cancer in 12 weeks. When they were put back on the diet, all of them showed rapid regression: the liver cancer was eliminated, and liver cells seemed to behave normally. In effect, the scientists turned the Myc gene on and off like a tap, and turned cancer on and off at the same time.
They also found that some of the apparently normal cells retained the ability to become cancerous, which could explain why cancers often recur after chemotherapy. Cancer hits one person in three, and kills one in five. In recent years, researchers have concentrated on a number of new approaches. They have tried to cut off the blood supply to tumours, to halt their growth. They have tested search-and-destroy toxins, designed to make for and eliminate only cancerous cells. They have experimented with scalpels made of ultrasound, and they have tried to ”burn” cancerous cells with infrared radiation.
But cancer is, above all, a disease of the DNA, and British researchers have launched a cancer genome project to collect all the genetic mutations involved in the making of a cancer. There are more than 100. But the Myc protein seems to play a role in many cases of the disease.
The Glasgow study immediately suggested that it would be a good target. If researchers could find a drug that blocked the action of Myc, they could study its effect on cancer cases. The Stanford study shows that they were right.
But what works in mice may not work so well in humans. The next step is to hunt for a drug that would be safe for human patients, and yet have the same impact. – Guardian Unlimited Â