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Last week, Shinya Yamanaka won a Nobel Prize for figuring out how to make adult stem cells revert to an embryonic (and much more medically useful) state. Within days, another scientist unconnected to Yamanaka, claimed to have produced such cells from human heart tissue and injected them back into human patients in a clinical trial. What's more, the researcher, Hisashi Moriguchi, claimed that a measure of his patients' heart function improved by 41.5% after the transplant.
It's hard to say which is crazier: The claims themselves, or the speed with which Moriguchi's story has completely fallen apart. Evidence suggests that these kind of re-programmed adult stem cells might be more likely to turn cancerous. Because of that, one of the first questions people asked was about the ethics committee that approved the research. Moriguchi said he worked for Harvard and that Harvard had signed off on his clinical trial.
And that's where things got nuts. Because Harvard had never heard of this study. And Moriguchi does not work there, anyway. In fact, this might not even be his field — the only professional affiliation that New Scientist could track down for him was as a visiting researcher in cosmetic surgery at The University of Tokyo. Also: The transplants may or may not have actually happened and Moriguchi might be plagiarizing images from other scientists. The worst part about this (from my perspective as a journalist) is that it was stem cell researchers who had to call out the fraud, after a major Japanese newspaper swallowed the story hook, line, and sinker.
You can follow the story much more in-depth at IPSCell.com, the blog of UC Davis stem cell researcher Paul Knoepfler.
Check out this post of Knoepfler's — written the day before the Moriguchi madness began — for more information on the risks of reprogrammed adult stem cells, the ongoing safety research, and proposed time-tables for when we will likely try these things out on humans for real.
The Nobel Prizes in science will be announced — one prize per day — between now and Wednesday. Today, the winners of the prize for physiology or medicine were announced. John Gurdon and Shinya Yamanaka will share the award for work related to cloning and our ability to manipulate the functioning of stem cells.
What's interesting here is that the research these two men are winning the Nobel for happened nearly a generation apart. Gurdon's work was crucial to the development of cloning. You'll recall that some embryonic stem cells can grow up to be anything, any part of animal's living tissue. Differentiated stem cells, in contrast, are destined for a specific job — for instance, they could grow into skin cells, or nerve cells, but not both. In 1952, other scientists had concluded that you could take genetic material from a very early frog embryo, inject it into the egg cell of another frog, and get that to grow into a living animal — a clone. But those researchers thought this process would only work up to a point. They didn't think you could clone an adult, or even an older fetus. Gurdon proved them wrong. In a series of experiments published between 1958, 1962, 1966, he worked with older and older donor cells, and produced more developed clones — eventually growing fully adult, fertile frogs from cells taken from the intestines of tadpoles.
Yamanaka, meanwhile, did his research in the early part of the 21st century, developing the methods that allow us to trick grown-up, set-in-their-ways cells into behaving more like embryonic stem cells. Yamanaka's work is linked to Gurdon's because it explains why Gurdon (and researchers after him) were able to successfully clone adult animals from cells that had fully differentiated.
The research history here is a little hard to follow, especially with Gurdon's work. The description of his findings I have here is what I've been able to piece together from several different sources, citing several different dates and specific achievements. To help cut through some of the confusion, here's a couple of links where you can get a good, reasonably detailed idea of what this research is, and why it matters:
• This article on the history of cloning from the Proceedings of the National Academy of Sciences is easily readable and interesting, especially if your awareness of this topic begins with Dolly the Sheep.
• In 2009, Gurdon and Yamanaka won the Albert Lasker Basic Medical Research Award. That organization has a good explanation of how both men did their experiments and how their work ties together.
Cancer researchers can sequence tumour cells’ genomes, scan them for strange gene activity, profile their contents for telltale proteins and study their growth in laboratory dishes. What they have not been able to do is track errant cells doing what is more relevant to patients: forming tumours. Now three groups studying tumours in mice have done exactly that. Their results support the ideas that a small subset of cells drives tumour growth and that curing cancer may require those cells to be eliminated.
It is too soon to know whether these results — obtained for tumours of the brain, the gut and the skin — will apply to other cancers, says Luis Parada at the University of Texas Southwestern Medical Center in Dallas, who led the brain study. But if they do, he says, “there is going to be a paradigm shift in the way that chemotherapy efficacy is evaluated and how therapeutics are developed”. Instead of testing whether a therapy shrinks a tumour, for instance, researchers would assess whether it kills the right sorts of cell.
Photo: (Nature.com/G. DRIESSENS). Researchers can now trace the cell lineage within a growing tumor. In this skin tumor, the red cells all originated from one stem cell.