BAR HARBOR – How long can humans live? Can genetic studies lead to treatments that allow us to live more healthy lives as we live longer, too?

Scientist Kevin Flurkey, a researcher at Jackson Laboratory in Bar Harbor is hot on the trail to finding the definitive answers to such basic questions about existence.

“I do think maximum human life span can be increased,” Flurkey said. Most likely, drugs developed on the back of genetic discoveries might lead to as much as a 20 year increase in life span resulting in an average lifetime spanning more than 90 years in humans, he said.

More humans might live to 120, recognized as an outer limit today. Some scientists even believe 150 could be a possibility, the 53-year-old Flurkey said. To be sure, such developments are likely 20 years or more away, he said, but the footing for such advancements is becoming ever more solid.

Flurkey’s investigations center on the biochemical processes that may regulate aging and life span itself. Last week, he and colleagues at the University of Michigan and the University of Texas announced that they have isolated a gene in the Snell dwarf mouse that slows aging and dramatically extends life. The findings were described in The Proceedings of the National Academy of Sciences, published last week.

The remarkable news of a gene controlling aging in a mouse – a mammal genetically similar to humans – was hailed as another scientific step toward the understanding of how mammals age. But the findings of Flurkey and his colleagues may yield important clues about the genetic underpinnings of cancer as well.

Flurkey discussed in detail the implications of the study on cancer and aging studies in an interview in a laboratory crowded with equipment Friday.

Researchers found that Snell dwarf mice that lived one-quarter to one-half times longer than the control group of normal brown mice raised in the same cages, rarely died of cancer. When cancer was found during autopsies it was usually at an early stage – surprising because the mice’s life spans were already 25 to 50 percent beyond the control group. Non-dwarf counterparts, however, not only died earlier but also died of cancer about 85 percent of the time, Flurkey said.

“All the cancers these [long-lived] mice get is slowed,” Flurkey said.

Now, Flurkey is talking with colleagues about methods to determine the biochemical mechanism or mechanisms that delay cancer and aging itself.

Flurkey suspects there is a single mechanism responsible for development of a wide-range of cancers. If so, then a single intervention between a hormone and its action might slow or even prevent development of most age-related cancers like breast cancer, liver cancer and lymphoma, he said.

But it’s not clear if the biological pathway that delays aging and cancer and extends life span can be separated out from the overall deficiencies of hormones. That would be a problem because hormones have crucial biological functions as well.

The Snell dwarf mouse, for instance, only achieved its long life in a controlled environment because it has little resistance to infection. The dwarfs and the control mice in the study weren’t allowed to contract colds, flu or other normal illnesses.

“Anytime we talk about the benefits of hormone deficiencies we have to be talking about tradeoffs,” Flurkey said. “What’s lost here is the ability to survive in a normal environment.”

The immunological weakness is a tradeoff that creates skepticism about whether the genetic expression that extends life can be separated from the other crucial functions of the hormones.

For nearly 60 years, until 1990, the Snell dwarf mouse was actually considered to have a short life span, Flurkey said.

The Snell dwarf mouse is named after early Jackson Laboratory scientist George D. Snell. Snell acquired the mutant mouse in the 1920s from a British “mouse fancier,” a person who collects unusual mice as a hobby. In 1929, Snell was the first to publish information about the dwarf in a scientific journal.

The mouse is stunted, about a third smaller than a normal mouse, because it has a deficiency of growth, pituitary and prolactin hormones.

The Snell dwarf is one of 2,600 different mouse mutants sold by Jackson Laboratory to genetics researchers around the world. Last year the Laboratory sold 1.7 million mice.

Mice get the same diseases as humans and have remarkably similar genetic make-ups. Now, with workable maps of the human and mouse genomes available, the pace of genetic discovery is quickening. Findings are coming so rapidly that it’s difficult to keep pace.

Flurkey, 54, is excited as he talks about the possibilities of his work on aging and cancer.

“We want to look for genes and mechanisms that regulate all the functions of aging,” he said.

Flurkey’s interest in aging was kindled when he was 23 years old. The native of suburban Chicago was beginning to do student teaching in California with the goal of becoming an elementary school teacher when he concluded it wasn’t his life’s calling. At the same time, he’d begun to worry about features of his own development as he moved further into his 20s.

“I wasn’t getting bigger, stronger, faster [anymore],” he said. “You discover you’re not getting smarter every year – you’re not learning more.”

This led him to deeper questions about aging. When he contemplated how aging actually works he “decided that was an interesting question to devote my life to.” He turned his attentions to molecular biology.

When he made the decision in the 1970s to change careers, gerontology was still an area about which comparatively little was known, Flurkey recalls. Now, there’s much more information available and more people doing studies.

Flurkey said the latest findings by the team he has spearheaded are built upon his own work from the 1980s. He said it is still slow going because work with mice takes so long. An aging study takes three years to complete. By contrast, work with fruit flies or worms can be conducted in a matter of months – from hypothesis to findings, he said.

As a result, much of the groundbreaking work being done with such organisms is 10 years ahead of that in mouse models, he said.

In the latest study the team of scientists, which also includes John Papaconstantinou of the University of Texas, Richard Miller of the University of Michigan, and David E. Harrison of Jackson Laboratory, found signs of delayed aging.

Humans, like mice, have collagen throughout their bodies. The protein keeps our skin attached to our bodies and wraps organs. But as we age, the collagen loses its suppleness.

Snell dwarfs in the study developed stiffening about 50 percent more slowly and showed delays in other signs of aging.

“They look very healthy when most of their cohorts are dead,” Flurkey said.

Until recently, the only real extension of life seen in mice came from a restricted diet. That finding, made way back in 1935, has little use for humans because it’s impractical – mice had to eat only a third of a normal diet to see about a quarter to a third increase in life span, he said.

Now, the likelihood of a breakthrough drug to extend the years of quality life is a real possibility. For his part, Flurkey hopes he is laying the groundwork for such a discovery.

“I want to understand how aging works, and I don’t expect to succeed [myself],” he said.