A Nobel Prize is just the beginning. Leading biologists are praising the selection of John Gurdon and Shinya Yamanaka for this year's Nobel Prize in Physiology or Medicine for their work on cellular reprogramming ? turning adult cells back to an embryonic state. But one of the laureates is worried that regulatory red tape could delay treatments based on the work.
While there's no real argument over the Nobel committee's choice, comments made by Gurdon after winning the prize point to an emerging bone of contention: whether caution from regulators may delay or prevent therapies based on reprogrammed cells from reaching patients.
"I think patients would be happy to take the risk of using their own cells given the choice," Gurdon told a press conference in London, criticising the US Food and Drug Administration for placing "immense conditions on approval".
Paradigm shifting work
Gurdon, who works at an institute at the University of Cambridge, UK, named in his honour, and Yamanaka, who divides his time between Kyoto University in Japan and the University of California, San Francisco, had been widely touted as possible winners. But there was also speculation that a prize might first go to Gurdon and later pioneers of mammalian cloning, whose work led to the creation of Dolly the Sheep, before Yamanaka got his turn.
In deciding to recognize Gurdon and Yamanaka together, the Nobel committee is acknowledging "paradigm shifting contributions", says George Daley of the Boston Children's Hospital in Massachusetts. "I think it's an inspired choice."
"I'd hoped for this outcome," agrees Jeanne Loring of the Scripps Research Institute in La Jolla, California, echoing the views of other biologists contacted by New Scientist.
Before Gurdon showed that you could create a new frog embryo by taking the nucleus of an adult cell and putting it into a frog egg, many biologists supposed that development happened by cells shedding unwanted genes. Gurdon's cloning experiments, published in 1962, revealed that development instead involves genetic switches being turned on and off ? a process that can be reversed.
A tour de force
In 1996, a team led by Ian Wilmut at the Roslin Institute near Edinburgh, UK used essentially the same technique to produce Dolly, the first mammal cloned from an adult animal.
"The legacy of Dolly was that it rejuvenated the reprogramming field and caught the attention of people like Shinya," says Alan Colman, a member of that team who now runs the Singapore Stem Cell Consortium. "In my view, the Dolly work was a tour de force in experimental perseverance but not so much in technical innovation."
Yamanaka changed the game again by showing in 2006 that similar reprogramming in mouse cells could be achieved using just four genes.
Speaking by video link between Kyoto and a press conference at UCSF, Yamanaka said he'd been inspired in part by experiments in fruit flies showing that a single genetic switch makes the difference between growing an antenna, or a leg. But most biologists thought he was wasting his time. "To succeed you have to have vision and you have to work hard," Yamanaka told reporters. "I really believe that."
From the lab to the clinic
One big question now is how quickly therapies based on Yamanaka's induced pluripotent stem (iPS) cells will reach patients. Gurdon's comments reflect a feeling among some biologists that the FDA and other regulatory agencies are being excessively cautious.
But the possibility of reprogrammed cells triggering cancer remains a big worry, and some biologists are anxious about the backlash that could result if safety problems emerged in a clinical trial.
"We have to be very, very careful to be safe, and to do no harm," says Deepak Srivastava, who works with Yamanaka at UCSF.
Nevertheless, the first clinical trial involving iPS-derived cells could begin next year. Masayo Takahashi of the RIKEN Center for Developmental Biology in Kobe, Japan, plans to use iPSCs to grow retinal pigment epithelium, which nourishes light-sensitive sensory cells in the eye, to treat a form a blindness called age-related macular degeneration.
If you would like to reuse any content from New Scientist, either in print or online, please contact the syndication department first for permission. New Scientist does not own rights to photos, but there are a variety of licensing options available for use of articles and graphics we own the copyright to.
Have your say
Only subscribers may leave comments on this article. Please log in.
Only personal subscribers may leave comments on this article
Subscribe now to comment.
All comments should respect the New Scientist House Rules. If you think a particular comment breaks these rules then please use the "Report" link in that comment to report it to us.
If you are having a technical problem posting a comment, please contact technical support.
sanctum the notebook duke basketball miranda july joe paterno near death joepa sc primary
No comments:
Post a Comment
Note: Only a member of this blog may post a comment.