( . They are highly resistant to everyth...)New technique multiplies life span in simple organisms

Longo predicted that as molecular geneticists master the levers of aging, they will be able to design drugs that coax the body into entering chosen aspects of a starvation-response mode, such as stress resistance, even when food is plentiful.

If enough food is available, an organism might be programmed both to reproduce normally and to maximize its survival systems.

Longo urged caution in extrapolating the result to humans.

"We have been very successful with simple organisms," he said. "Naturally, mammals are complex, and it will be a great challenge to get major life-span extension."

A "really exciting" implication, Longo said, is that cells may be able to speed up their DNA repair efforts. All organisms have the ability to repair harmful mutations in their DNA, whether caused by age, radiation, diet or other environmental factors. Cancer often begins when DNA mutations outstrip a cell's ability to remain differentiated.

Many researchers believe DNA repair systems are already running flat out. The organisms in Longo's experiment say otherwise.

"In our paper, we show that age-dependent mutations increase at a much slower pace in organisms lacking RAS2 or SCH9 and at a remarkably low pace in organisms lacking both SCH9 and SIR2, raising the possibility that the mutations that cause human cancers can be delayed or prevented," Longo said.

"Notably, mutations that increase the activity of human homologs of the yeast SCH9 and RAS2 genes play central roles in many human cancers." Homologs are genes descended from a common ancestral DNA sequence.

Joining with researchers at the USC Norris Comprehensive Cancer Center, Longo is studying the feasibility of reducing or preventing the age-dependent DNA mutations that caus
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Source:University of Southern California