SAN DIEGO (GenomeWeb News) – In a speech that touched on genomic research, translational research, and personalized medicine, Nobel laureate Sydney Brenner challenged conventional wisdom on Monday, proposing a “bedside to bench” approach to research and medicine.
Brenner made the remarks after receiving the AACR-Irving Weinstein Foundation Distinguished Lectureship award yesterday at the annual American Association of Cancer Research meeting. He received a standing ovation for the speech, in which he questioned the view of translational research as a way to apply basic research to clinical practice.
“What I’m advocating is: go the other way,” Brenner said. “Let’s go from bedside to bench.” Instead of compartmentalizing research and medicine, he said, the two should be integrated so that physicians, who are most familiar with human “phenotypes,” can inform the other arms of science.
Brenner, who was one of the 2002 Nobel Prize winners in Physiology or Medicine, helped discover messenger RNA. He also pioneered the use of the soil roundworm Caenorhabditis elegans as a model organism, opening the door for new insights into developmental biology, aging, and programmed cell death.
But these days he’s pushing a new model organism: humans. “We don’t have to look for a model organism anymore,” Brenner said. “Because we are the model organisms.”
As researchers unravel the genome, it’s easier than ever to evaluate human biology directly, rather than extrapolating it from research on other animals, he said. Human research happens all the time in society — in families and communities to governments and religions, Brenner mused, “Why don’t we now use this to try to understand our genomes and ourselves?”
He acknowledged that there are still challenges to interpreting genetic information. But Brenner argued that the extensive variation between individuals could hold a wealth of information. “It is the variation that has become the interesting thing to study,” he said.
Even so, completely analyzing the genetics of tens of thousands of humans remains technically impractical — and prohibitively expensive. Even as sequencing becomes cheaper, Brenner noted, interpreting the data will likely remain challenging.
“What we need, actually, is a view of all this that tests hypotheses all the time,” Brenner argued. This includes studying “human mutants” — something that may not be as difficult as it sounds given that, “We’re all mutants, basically. It’s hard to find a wild type.”
And humans’ interactions with their environment cannot be ignored either, Brenner said. Our “100,000 year-old genome” — the genome we acquired in ancient history when human biological evolution stopped and cultural evolution took over — is no longer suited to our environment, he said.
“We find we have a biological system now maladapted to an environment that the biological system has created,” he said. That means dealing with disease should not just involve patching biological problems, he argued, but also understanding biological-environmental interactions and using them to predict and prevent disease whenever possible.
“It is the responsibility of us to see that if there’s a way of preventing something — of not allowing it to happen — I think that we should follow that path,” Brenner said.