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Michael West

National Institutes of Health, Dr Harold Varmus, has said that there is not a single area of medicine that these new technologies will not potentially impact. I think that’s probably an accurate statement, because they can potentially be made into anything.
David: How long do you think it will be before we’ll be able to use ES cells to grow any type of tissue or organ that we need?

Dr. West: I think it’s going to be a spectrum of opportunities. Some things will be relatively easy to do, and then other things are going to be harder to do. I guess some of the early applications of ES cells may be things like cartilage for arthritis, and blood cells for leukemia or other blood disorders. Maybe neurons for neurological disorders.

David: Like Parkinson’s disease?

Dr. West: Parkinson’s disease, certainly, is a classic disease where you simply need those cells back. But any disease where there is a loss of cell or tissue function is a clear target for this sort of thing. There are all kinds of other possible applications. In heart disease, when you lose heart muscle, you need to replace it. A lot of arrhythmias could be treated this way. With just a little imagination, you can see there are literally thousands of applications. Until last year, we never had the ability to make any cell type in the laboratory. So it’s obviously a very exciting development.

David: The discovery that the tips of our chromosomes–telomeres–become shorter with each somatic cell division may have important implications for our understanding of how we age. What sort of potential for extending human life do you foresee as being possible by preventing telomeres from being shortened during cell division?

Dr. West: We still do not know the real answer to that question. It’s amazing. I would put the blame for our lack of knowledge of this as simply the lack of funding that goes into aging research. As you know, Geron has been able to raise a fair amount of capital to promote aging research. Now, here at Advanced Cell Technology, we’ve been able to raise some money. The National Institute on Aging sponsors some research into aging.

But if you put all the biotech together, along with the federal government, it’s still a small fraction of what’s spent on AIDS, and, of course, the budget on AIDS is too small. We probably spend more in a week bombing foreign countries than we ever spend on aging research. That’s where I put the blame. We simply do not know. What we do know is that telomerase abolishes aging on a cellular level — what we call “cellular aging.” So, for cells at least, we’ve solved the problem of aging. The lack of telomerase is what causes cells to age. When the immortalizing telomerase gene (hTERT), which directs the synthesis of telomerase, is turned off, cells become mortal.

Since we’re made of cells, this should have an application to human medicine. I would bet that it does, but we simply don’t know what percentage of human aging is caused by cellular aging. If you pinned me down on it, I would say somewhere between five and a hundred percent of human aging. I don’t know whether it’s closer to five or a hundred, but it’s somewhere in that range. Recent studies point toward the higher end of that range. But even if it’s only five, it’s noteworthy that here we’ve tracked down the fundamental molecular cause of at least a part of human aging and have found a means of intervening in it and changing it. So even if it’s just a small piece of human aging, at least it’s some advancement.
David: Have you found that any genes trigger the release of endogenous enzymes that may be able to benefit us now through some type of supplementation?

Dr. West: No, I don’t know of any. There are some genes that have been reported that induce telomerase, but none of them give us any clues as to any supplementation  that would help — and that may be what you would expect. There are literally billions of people on the planet eating many different types of foods and supplementing their diet in many different ways. As of today, however, there’s no known case of anyone who has dramatically affected their life span–maybe because there is no dietary means of fundamentally altering this biology.

The reason that we think this biology is in place is that it may be a powerful antitumor mechanism. Cancer is a runaway cell — a cell that’s inappropriately growing without limits, like a runaway car that doesn’t stop for stop signs. But all of the cells in our body can only divide a finite number of times. So the “car” has only an eighth of a tank of fuel. That way, if it becomes a runaway car, it can’t go too far. Our bodies are actually littered with cells that have started to run away. If you look at your skin, you’ll see little moles and splotches, which often  represent some of the pigmented cells, where you can see the cells starting to run away in uncontrolled growth. But the mole, or the pigmented blotch on your skin, you’ll notice, grows to a certain size and then stops.

We believe that this is a reflection of the mortality of cells — that they have a finite life span. If there were a simple dietary means of unlocking a replicative immortality, it might allow those cells to just continue to grow. So the repression of telomerase may be an antitumor mechanism. Now that’s not the same as to say that telomerase would induce cancer. The ability to refuel the gas tank of a car doesn’t make it a runaway car. But it may be that allowing all the cells in our body to be immortal would raise the risk of cancer. Over the eons, natural selection has tended to “mortalize” the body, since in ancient times we rarely lived very long anyway. The average human being lived maybe 20 years in ancient times. So why would you need your cells to divide forever, when cancer or being eaten by a lion was much more of a risk?

David: Can you talk a little about the cloning research at Advanced Cell Technology?

Dr. West: What we’ve been working on here more recently is nuclear transfer or cloning. Having ES cells is great, but they’re not you–they’re somebody else.

David: I thought the whole idea was to use your own DNA?
Dr. West: Right, that’s what the nuclear transfer idea is. The ES cells that exist today came from embryos made during in vitro fertilization. That’s from taking a sperm and an egg and then making this little microscopic ball of cells we call a blastocyst. This contains the ES cells that can become anything. They’re sort of like a raw material for life in some respects. They can be grown in a dish and made into the cells and tissues in the dish. But those cells that exist today are not you. Your body will reject cells that are not your own.

So any cells or tissues that are made from an ES cell that’s not your own, your body would reject. But your body doesn’t have any ES cells — they’re long gone. So what we’re working on is a cloning technology to make ES cells for you. We just scrape some cells off your skin and put them back into an egg cell whose DNA has been removed. What you then get is this little ball of cells — ES cells that have your DNA. So what you’re doing there is cloning, but you’re not making an embryo that would be put in a woman. That would lead to a cloned copy of yourself. Rather, we’re proposing cloning stem cells.

You’re just making cells, not people. That’s called “therapeutic cloning,” as distinct from “reproductive cloning.” So we’re trying to make that work. The wonderful thing about this– which isn’t widely known–is that we’ve actually shown that you can take an old cell that’s at the end of its life span, and if you put it into an egg cell, it’s like taking the cell back in a time machine. The cell is actually made young again.

Dolly, the sheep that was cloned, was made from an adult animal but was obviously born young. In the same way that she wasn’t prematurely old (despite starting out as an old cell), we’ve shown that we can take old cells in a dish, and when we do this cloning technique, the cells we get are young: they have their whole life span ahead of them again. We believe that somehow, that step of putting the cell back into an egg cell winds the clock up again and takes the cell back to the beginning of life. So, theoretically, it looks as though we should be able to take a very old person and make new, young, transplantable tissue for that person, just like their own tissue when they were born.

David: And give them a new heart?

Dr. West: Potentially. Under certain conditions, we’ve observed ES cells actually forming complex tissues, such as intestines.

David: I read in Science that a dog’s bladder had been engineered.

Dr. West: That bladder was made using tissue engineering, which is a little different: it was manufactured. But the ES cells will actually form complex tissues themselves. They self-assemble into tissues like intestine that are obviously young. No matter how you think humans age, here is a technique that will allow us to create young, transplantable tissue. We honestly believe that we will be able to make new liver tissue, or maybe even young whole organs that are composed of your own cells, to replace the old worn-out ones. It’s a long-term project, and it’s years away from being available for most applications. But it’s an exciting prospect.
David: What are your thoughts about the rate at which our understanding of ES cells is progressing?

Dr. West: I’m happy to say that the field is advancing at a fast pace, despite the fact that there’s been very little federal funding for the research, and this is largely a

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