'Supermice' bred that resist cancer

[shamrock_uk]

http://news.bbc.co.uk/1/hi/health/3971103.stm

The supermice that resist cancer Scientists have bred a family of "supermice" that are highly resistant to cancer. The mice have three instead of two copies of genes that keep cell division in check. It might be possible in the future to make a drug for humans that would confer the same protection against cancer, the Spanish scientists hope. The team at the Spanish National Cancer Centre in Madrid report their findings in Genes and Development. Super resistant Cell growth and division is normally kept under control by a group of gatekeeper genes called tumour suppressors. In cancer, cells grow out of control and invade, erode and destroy normal tissue. Dr Manuel Serrano used DNA technology to breed mice that had an extra copy of part of the tumour suppressor genes called Ink4a/ARF locus. It might be anticipated that an extra working copy would reduce the risk of this disease Hazel Nunn of Cancer Research UK This locus controls the production of two proteins that together appear to stop most human cancer cells developing. These 'supermice' were found to be extra resistant to things known to trigger cancer, called carcinogens, in normal mice. When the animals were exposed to various carcinogens they developed tumours at a much lower rate than normal. What's more, the presence of the extra copy of the locus and increased cancer resistance had no apparent effect on the lifespan or fertility of the 'supermice'. Dr Serrano attributes the increased tumour resistance to the modest increase in the levels of the two proteins gained by the extra copy. He suspects some humans might inherit extra resistance to certain cancers. He said it might be possible to induce similar tumour protection in humans using a drug, although this would be some time away. He said: "This may translate in a big benefit regarding cancer susceptibility." Hazel Nunn of Cancer Research UK said: "As people who inherit a defective copy of this gene are susceptible to cancer, it might be anticipated that an extra working copy would reduce the risk of this disease. "This is exactly what the research has shown in mice. "It is very encouraging to have such clear confirmation on which to base future research into how this gene works. "Ultimately, we hope this knowledge can be developed for the benefit of the cancer patient." Story from BBC NEWS: http://news.bbc.co.uk/go/pr/fr/-/1/h...th/3971103.stm Published: 2004/11/02 00:19:50 GMT © BBC MMIV

[Davros]

And while we are on the topic of mice and genes - this story in from Australia today :


Mice hot to tackle obesity crisis
14:00 AEST Tue Nov 2 2004

Scientists in Sydney have discovered a gene they believe is responsible for obesity in mice, and which could have enormous implications for humans.

Mice with this gene, called C-CBL or Sybil, have a higher than average body temperature because they’re burning food faster. They even eat more than average mice, but don’t put on any extra weight.

“This discovery is so exciting [that] we are now working feverishly on this new avenue,” says Professor David James, from Diabetes and Obesity Research Program at Sydney’s Garvan Institute.

Sybil’s discovery came about by accident three years ago, when scientists discovered the gene’s contolling effect on metabolism. Since then, researchers at the Garvan have been working to find Sybil’s counterpart in humans. This three-year trial is the first major research done on Sybil and its effect on weight gain.

“We measured how much these mice ate, and they actually seem to eat more than a normal mouse but they still put on less weight,” says researcher Dr Greg Cooney.

The implications will be more than cosmetic. If researchers can make the leap from mice to humans all sorts of obesity-related diseases like diabetes, heart disease and stroke could effectively be treated before they became problems, saving countless lives.

“As the world is getting fatter the number of people with Type 2 diabetes is going up and up,” says Professor James. “So if we keep their weight down, we keep the increase in diabetes down.”