Human Limb Regeneration a Possibility?

SablKnight writes "This NY Times article (free reg. req.) says maybe. Apparently research is being done in parallel with the more controversial stem cell implantation to attempt to regenerate missing parts in humans. Though this has been a subject of mild interest for centuries, serious research started much more recently, when an experiment involving mice suffered a setback. 'A few years ago, Dr. Ellen Heber-Katz, an immunologist at the Wistar Institute in Philadelphia, was conducting an experiment with those mice, which develop a disease similar to lupus. As is common, Dr. Heber-Katz punched a pattern of holes in each mouse's ear to so she could tell which mouse was which. Three weeks later, she said, when she checked on the experiment, 'there were no ear holes.'' A quick google search reveals similar stories about Dr. Heber-Katz' research in other publications, such as the Science Daily and Nature."

Comments

stemcells

[virtualXTC]

Correct me if I'm wrong, but I though the idea behind current stemcell research was regeneration with out having to "graft" any thing on, such as spinalcord regenaration. I wouldn't think it would be practical to try to graft a whole arm on, unless you sample the patients DNA and encode the stemcells with it to oppose rejection problems.

Re:stemcells

[SablKnight]

I think a lot of current stem cell research is pointing at taking a mass of stem cells, most likely not from the patient, and forcing them to differentiate into the desired organ in a lab environment. This would then be treated like any other organ donation, including immune system suppression to avoid rejection.

The regeneration research here involvs more of a method of undifferentiating normal cells into stem cells where they are, which would avoid the whole rejection problem and surgery completely.

SablKnight

Re:stemcells

[Transcendent]

I wouldn't think it would be practical to try to graft a whole arm on, unless you sample the patients DNA and encode the stemcells with it to oppose rejection problems.

When they are creating the stem cells (specifically from embryos), they take a nucleus from your own body and make a "clone" of you to grow from, then they can continue manipulating the stem cells to grow into the organ/organs they want.

Just slapping on some stem cells on to the stub that used to be your arm doesn't do the trick...

Re:stemcells

[rickbrodie]

I seem to remember a story about a newly discovered plastic-like material which was not unlike cotton wool. It's remarkable property was that, when a stem-cell/nutrient solution was added, the new cells would grow around the outside of the fibres. In one demonstration, the material was pressed into the shape of a human ear, and cartilage cells were added. In a few days, the cells had grown into a new ear, and the fibre scaffold had dissolved. I think many people remember the image of a mouse with an ear growing out of it's back.

This is probably not new news to most people, but I wonder how many people knew that the same thing had been done with nerve cells. An experiment (sorry, no names or other pertinant details spring to mind at the moment) with mice showed that nerve cells can be regrown in-situ, and that further more, the new nerve cells actually connect themselves to existing cells.

In the experiment, the took some mice and severed their spinal cords by removing 1cm of nerve cells. Then, they filled the gap with this fiber soaked in the nerve cell solution. Several days later, the mice had a rudimentary spinal cord and limited use of their hind legs. I don't know about anyone else, but this sort of thing makes me really optimistic about the future of medical science.

Re:stemcells

[Sgt York]

Using nuclei from a differentiated cell in the cytoplasm of a stem cell kinda defeats the purpose of using stem cells in the first place.

The primary difference between stem cells and differentiated cells is that in stem cells, no DNA has been "packed off". If you take a nucleus from a host adult cell, you have to unpack it, so to speak, to make it useful in the sense that you describe.

It is more likely that you would make stem cells in that fashion, using unfertillized eggs as anucleate acceptors for the harvested, treated nuclei from the host.

Unfortunately, cloning is illegal in the US. As is the use of human stem cells (except CA).

Re:stemcells

[Anonymous Coward]

Just a shame bleeding-heart parent-hating liberal luddites would try to get such experiments banned.

Any man who would champion an animal's alleged 'rights' over the advancement of the human race is betraying the millions of years of evolution it has taken us to get this far.

Do society a favour. Kill a vegan.

Speaking of stem cells

[Anonymous Coward]

Heard an advert this morning from a company that wanted "blood donors". They tried real hard to portray the same context as the standard blood donation, but they were asking specifically for umbilical cords. Not once did they mention stem cells. But that is obviously something one would want to obtain from umbilical cords.

What are these people up to?

Tomorrows headlines...

[Chexsum]

Heartless man grows a heart!
Brainless child grows a brain!
Stomachless woman grows an appetite!?!

Re:Tomorrows headlines...

[docbrown42]

Heartless man grows a heart!
Brainless child grows a brain!

"Weeeeee're of to see the Wizard..."

Re:Tomorrows headlines...

[Anonymous Coward]

Judy Garland-loving Faggot.

Re:Tomorrows headlines...

[Gorm the DBA]

Brainless child grows a brain!
WASHINGTON, DC (Reuters--NOT!) George W. Bush today successfully went through an entire day without any malpropisms or misspoken phrases.

Presidential Spokesmen credited the benefits of Stem Cell Cloning Research.

Cancer link?

[SablKnight]

Does anyone know how much research is going into a link between stem cells and cancer cells? IANAB(iologist) but the only major difference I can see is a lack of control in cancer. If we can find a way to turn on stem cells, maybe the same switch could work to turn off cancer?

SablKnight

Re:Cancer link?

[tid242]

If we can find a way to turn on stem cells, maybe the same switch could work to turn off cancer?

Cancer is a very dynamic disease there is not, to the best of my knowledge, any way to just "turn off" cancer cells. The normal lifecycle of groups of cells consists of individual cells that "know" when to divide and when to die (aptoptosis), with cancer, cells may proliferate too rapidly, or cells, normal in all other respects, may simply not know when to apoptose. So there are many different facets of each individual cancer, and each patient with said cancer. For example: while some cancers may respond (by apoptosing) to genetic damage inflicted by cytotoxic chemotherapeutic agents, other cells may benefit from the mutation caused by said damage. Differnet cancers (and differnt populations of cancer cells in the same patient) may be driven by completely different mechanisms, especially as individual tumors evolve and adapt within their host, so again you'd be hard pressed to exact something from stem-cells that would/could just "turn it off."

the term "Cancer" is actually a pretty generic term used to describe hundreds of distinct diseases, much as "Infection" doesn't really tell you the nature of each individual infection (bacterial, viral, fungal, protazoal, parasitic, etc, etc - what kind of bacterial? G-, G+, acid-fast, hemolytic, coagulase +/-, toxin-producing, etc etc.). So when you say "cure cancer" or "turn off cancer" it's like saying "curing infection."

the only major difference I can see is a lack of control in cancer

this, again, is an over-simplification. it's much like saying the only difference i see with infectious disease and commensulistic/symbiotic bacterial colonization (such as your intestinal floura, which can cause infection if cirumstances are such) is that with infection your immune system can't keep them in check and they're in the wrong place, and with colonization this is not the case... or in more Geek terms: "the only difference i see between a PDA and an ULTRA-SPARC machine is that the ULTRA-SPARC box is faster"-it's just a lot more complicated than that...

Does anyone know how much research is going into a link between stem cells and cancer cells?

Contrary (i think) to what you were asking by this question, there is a school of thought that ties the two together. There was a paper published a short while ago which hypothesised that aging is the result of cancer suppression, and the two are almost inseparable. In other words the body's loss of regenarative ability is due to its control of accumulating genetic defects of stem-cells... i had just skimmed the publication and am not sure about its validity, but an interesting idea nonetheless... draw whatever conclusions from this as you like, but as i said i'm not positive of the validity of this report...

hmmm... that should be enough out of me :)

-tid242

Re:Cancer link?

[SablKnight]

Thanks for the clarification, I wasn't aware of the many subtleties involved. I don't know a lot about the subject, but what I did remember was that tumors are basically caused by a group of cells spontaneously (or not) losing their restrictions on differentiation and reproduction. It seemed like a natural tie-in to stem cells, which also reproduce quickly (or they would have to for medical purposes at least) and are undifferentiated.

I had heard of the link between aging and cancer before, but not in enough detail to tie that to stem cells.

SablKnight

Re:Cancer link?

[Sgt York]

Contrary (i think) to what you were asking by this question, there is a school of thought that ties the two together. There was a paper published a short while ago which hypothesised that aging is the result of cancer suppression, and the two are almost inseparable. In other words the body's loss of regenarative ability is due to its control of accumulating genetic defects of stem-cells... i had just skimmed the publication and am not sure about its validity, but an interesting idea nonetheless... draw whatever conclusions from this as you like, but as i said i'm not positive of the validity of this report...

Interesting idea, what journal was it in? I'd like to read it.

Re:Cancer link?

[Anonymous Coward]

Here's a semi-formatted News and Views (w/out figures) from Nature to get you started:

Nature 415, 26 - 27 (2002); doi:10.1038/415026a

Ageing: The price of tumour suppression?

GERARDO FERBEYRE AND SCOTT W. LOWE

The p53 protein works to suppress cancer, so one might think that bumping up the levels of this protein would be a good idea. But this isn't so -- mice with too much p53 age prematurely.

The p53 gene is often touted as 'the most frequently mutated gene in human cancer'. As a result, a great deal is known about it. When fully functional, p53 works to suppress the development of tumours, and current thinking suggests that it does so by affecting how cells respond to damage1. p53 can be activated by many stresses, such as breaks in DNA, and in turn induces responses that keep cell numbers down, including cell death (apoptosis) and permanent cell-division arrest (senescence; Fig. 1a). When p53 is mutated, cells cannot respond correctly to stress and are predisposed to becoming cancerous.

Indeed, mice that lack p53 develop normally but rapidly succumb to cancers2, implying that, at the whole-organism level, p53 acts purely as a tumour suppressor (Fig. 1b). But on page 45 of this issue, Tyner et al.3 identify an unexpected aspect of p53 biology. They show that mice engineered to have high p53 activity are resistant to tumours -- but age prematurely. Their results raise the shocking possibility that ageing may be a side effect of the natural safeguards that protect us from cancer.

Tyner et al.'s findings3 were serendipitous. They were trying to engineer mice with a particular mutation in p53, and instead produced animals in which a large portion at one end of the p53 gene (the 5' end) was missing. The remaining portion, which they call the m version of the gene, is just the 3' end and encodes a shortened protein. Mice with one normal copy of the p53 gene and one copy of the m version were resistant to tumour formation, but even relatively young animals resembled old normal mice. By contrast, mice with one non-functional p53 gene and the m gene were indistinguishable from mice that lack p53 altogether. So it seems that a normal p53 gene is needed for the m gene to have an effect, hinting that the protein encoded by the m gene steps up the activity of normal p53. This seems remarkable, yet is consistent with the observation4 that short peptides encoded by the 3' end of the p53 gene can activate normal p53.

It is not yet certain that the features of ageing are only due to the mutant p53 gene. The authors could not detect the truncated protein in the mutant mice, and at least one essential gene near the p53 gene was also deleted. Still, a second p53-mutant strain also shows signs of premature ageing3. Of course, the definitive experiment -- showing that loss of p53 increases longevity -- is impossible, because p53 and cancer are so intertwined.

Tyner et al.'s results might simply reflect a highly abnormal, diseased state. But they may also reveal a role for p53 in normal ageing. What might this role be? The evolutionary theory of ageing suggests that organisms invest resources to ensure reproductive success early in life, at the expense of longevity. It is not clear how this works at the molecular level. One model proposes that loss of the normal mechanisms for quelling gene expression leads to genes being expressed incorrectly and, ultimately, to ageing. So, enforced expression of the gene-silencer SIR2 extends lifespan in yeast and worms5. Another model holds that non-reproductive cells have a clock that monitors how often they have divided (based on the lengths of telomeres, protein-DNA complexes that cap chromosome ends and erode gradually with each cell division). Short telomeres eventually trigger senescence. Indeed, mice with critically short telomeres age prematurely6.

In a third model, cellular damage leads to mutations or general cellular decline, ultimately producing the spectrum of age-related characteristics7. Support for this idea comes from the fact that radiation increases mutations and promotes premature ageing in mice8. Tyner et al.'s results add an interesting twist to this hypothesis -- they suggest that ageing may be due in part to cellular responses to damage, and not damage per se (Fig. 1b). These responses protect most people from cancer during their reproductive years, but they may come at a price.

All of these models can be loosely linked to p53. The SIR2 protein can suppress p53 activity in mammalian cells9, 10. Cellular responses to telomere malfunction involve p53 (ref. 11), and a lack of p53 can counteract some of the effects of a lack of telomerase (an enzyme that regenerates telomeres) in mice12. Finally, doses of radiation that promote premature ageing in mice activate p53 efficiently13. Despite these connections, p53 has been on the periphery of ageing research -- until now.

The new work3 also has other implications. The ageing of whole organisms has been linked to cellular senescence in vitro, a process that also involves p53 and was initially linked to the finite lifespan of cultured human fibroblast cells14. Senescent cells remain metabolically active but cannot proliferate; they also show changes in gene expression that could produce alterations at the tissue level15. 'Replicative' senescence is triggered by telomere erosion and can be prevented by telomerase. But the same events can also be produced in response to, for example, DNA damage, oxidative stress and suboptimal cell-culture conditions14; telomerase has no effect here. Confusion over the exact process has led to a semantic debate, but it is clear that senescence parallels apoptosis as a cellular response to stress. These facts, coupled with the new results3, suggest that tissue ageing in vivo results from many factors, not just telomere attrition as has been suggested.

It might seem paradoxical that overactive p53 suppresses cancer but promotes ageing, given that the incidence of cancer usually increases with age. But the problem can be resolved by the fact that cancer results from the malfunctioning of p53 in single cells, whereas ageing involves a tissue-wide process. So, cells with inactive p53 ultimately shorten lifespan because cancer develops. Conversely, cells with abnormally high p53 activity do not contribute to cancer, but instead undergo cell death or senescence. With time, these changes may compromise tissue physiology, shortening lifespan through ageing. So p53 activity must be tightly controlled to balance a predisposition to cancer (too little p53) and premature ageing (too much p53; Fig. 2).

Finally, Tyner et al.'s work3 could have ramifications for understanding and treating human diseases. For example, p53 might contribute to premature ageing syndromes or age-related disorders in humans. And although longevity is complex and involves many p53-independent factors, it is conceivable that variation in lifespan is influenced by variation in p53's response to cellular damage. The results also raise the disturbing possibility that the DNA-damaging drugs used to treat cancer in young people might prompt p53 into action and accelerate age-related disorders later on. This is a testable hypothesis, and the prospect alone underscores the need for less toxic anticancer drugs. But perhaps the most provocative implication is that, if p53 is involved in ageing, then drug-related approaches to interfere with this process may come at a price -- the disruption of our natural mechanisms for keeping cancer at bay.

References
1. Vogelstein, B., Lane, D. & Levine, A. J. Nature 408, 307-310 (2000).
2. Donehower, L. A. et al. Nature 356, 215-221 (1992).
3. Tyner, S. D. et al. Nature 415, 45-53 (2002).
4. Hupp, T. R., Sparks, A. & Lane, D. P. Cell 83, 237-245 (1995).
5. Guarente, L. & Kenyon, C. Nature 408, 255-262 (2000).
6. Rudolph, K. L. et al. Cell 96, 701-712 (1999).
7. Szilard, L. Proc. Natl Acad. Sci. USA 45, 30-45 (1959).
8. Curtis, H. J. Science 141, 686-694 (1963).
9. Luo, J. et al. Cell 107, 137-148 (2001).
10. Vaziri, H. et al. Cell 107, 149-159 (2001).
11. Karlseder, J., Broccoli, D., Dai, Y., Hardy, S. & de Lange, T. Science 283, 1321-1325 (1999).
12. Chin, L. et al. Cell 97, 527-538 (1999).
13. Komarov, P. G. et al. Science 285, 1733-1737 (1999).
14. Campisi, J. Trends Cell Biol. 11, S27-S31 (2001).
15. Shelton, D. N., Chang, E., Whittier, P. S., Choi, D. & Funk, W. D. Curr. Biol. 9, 939-945 (1999).

Re:Cancer link?

[Sgt York]

Thanks...I have a subscription to Nature...How'd I miss that?

A good read.

[Anonymous Coward]

The Body Electric by Robert O. Becker, MD.

This book describes the efforts of Becker to try to study human limb regeneration and how he was shot down at every opportunity by the establishment. A fine example of how university educated people turn into religious-style bigots.

I didn't RTFA, but I'm sure it's a typical example of how Becker ridkes his career to bring to light new evidence, but 20 years later someone else takes the credit.

Re:A good read.

[Anonymous Coward]

ridkes? risked .... Sorry... Kind of dyslexic today.

Re:A good read.

[Anonymous Coward]

If I could, I would try to study human limb generation too when I was shot down time and time again. Otherwise you would have no body left after a few times.

evolution?

[tid242]

Scientists wonder why the ability to regenerate has not spread more widely through evolution...

...the advanced immune systems of higher life forms may mistake rapidly proliferating cells for cancer and kill them.

i find this a really interesting idea. Especially given that most cancers are not seen until after people are at an age where they generally have children (you've passed your genes on before you die of cancer). If you were to look at our pre-historic counterparts: if their life-expectancy were 20 years old and they had most of their offspring starting at 10-12 (these numbers are mostly guesswork on my part) then i would tend to think that evolutionally being able to regrow lost arms and legs would outweigh the ability to ward off cancer that doesn't strike until they're 25...

This is much the same as the differences between the rates of Progeria and Huntington's disease in people (people with Progeria don't have kids, but people with Huntington's do as the onset isn't until their 40's) even though, they're (apparently) similiar genetic abnormalities (ie in population genetics not taking into accout inheritence, their incidences should be equal)...

But getting back to regen/cancer: Of course there would be a fine balance between the two and figuring this out would involve lots of statistics and things my noggen doesn't compute so well, but i do find it interesting that there's so little regeneration in people.

conversely to my first point, since most regeneration would have probably been selected for, to take place before child-bearing age, and as we've advanced culturally and civically (child-bearing age) has markedly increased, and it's doubtful that missing a leg destroys your chances of having offspring if you live with a family in a cottage as opposed to running through savannas away from man-eating beasts and the like, maybe all this makes sense... (did you understand my convoluded run-on sentence?).

-tid242

Re:evolution?

[tid242]

oh yes, and would this theory then lead us to believe that our ancestors regenerated better than we do today?

that was the original conclusion of my previous post, but somehow i forgot to include it! - damn the brain..

-tid242

Re:evolution?

[Anonymous Coward]

For me, progeria, a tragic disease where children have all the symptoms of advanced aging, has always been proof that death is programmed, 'aging' is programmed and that immortality with perfect health is possible.

There's no reason for age to mean anything other than triggered genetic progams leading to self destruction. The information that is required to keep the organism young IS there. An old man can still father a child who will be young.

Re:evolution?

[Scrameustache]

Especially given that most cancers are not seen until after people are at an age where they generally have children (you've passed your genes on before you die of cancer).

I've know 2 kids that died of cancer. One of 'em had reached puberty, the other had not.

I'm trying to to loose my cool because this being an emotional issue for me, I take offense at what you said.

So, what I'm saying, is that your ideas are based on faulty data, and therefore your conclusions are equally flawed.

And BTW, small children (up to around 3yrs old) can regenerate small bits (finget tips). Older kids cannot, and adult of course cannot. Yet the liver always regenerates...

Re:evolution?

[ktulus cry]

While it is correct that in today's aging population, the majority of cancers effect the elderly that did not exist over the course of evolution, cancer still affects the young. It makes more sense for the body to develop defense mechanisms guarding heavily against rapid, unchecked division of cells (apoptitic triggering proteins and the like), since you can still live and reproduce without a limb. Regeneration would also tax the body's resouces like little else could - liver regeneration and such are one thing, but the reformation of bone and tissue, including neural cells, would be extremely difficult for an adult. A child has the ability to sit and heal, and thusly can regenerate small damages. Basically, it just makes more sense physiologically to guard against cancer than the loss of a limb.

Re:evolution?

[tid242]

I've know 2 kids that died of cancer. One of 'em had reached puberty, the other had not.

I'm trying to to loose my cool because this being an emotional issue for me, I take offense at what you said.

i am a bit taken aback by this, what i said was by no means to insinuate that children do not develop cancer, nor surely to offend anyone. i think the key words here are "most cancers" this does not mean the same thing as all cancers. point of fact (US 2000 cancer stastics):

incidence:
male: Prostate (30% of all cancers), Lung (14%), Colon/rectum (11%), Bladder, Melanoma (5%), etc, etc, leukemia (3%),

female: Breast, Lung, Colon, Uterine, etc. etc. (leukemia isn't even listed as one of the most common female cancers)

cancer deaths:
male: Lung(31%), Prostate (11%), Colon(10%), all others equal to or less than 5% (leukemia = 4%)

female: Lung (25%), Breast(15%), Colon(11%), pancreaus (6%), all others less than 5% (leukemia = 4%)

these stastics exclude non-melanoma skin cancers

of cancers Leukemias (especially fast-growing leukemias such as ALL, which are amongst the most easily treated of all cancers, if this be any comfort for you) account for 30% of all childhood cancers (and i think neoplasms represent usually w/i the top 5 childhood killers, while the nation's non-age-adjusted 2nd largest killer only behind heart disease), leukemia is 10 times more common in adults than it is in children...

all and all survival rates are higher in children than they are in adults, many times because of cancers specific to children, but also lending to a better chemotherapeutic/radiation tolerance in children allowing health-care providers to "push the dose..."

while cancer does certainly present in children, the fact remains that children constitute a much smaller cancer population, (even when statistically adjusted for population-size).

as i said before, it was not my intent to offend anyone, but the fact remains that general population trends show that cancer incidence increases with age (possible curtailing of the curve could be accounted for by genetic predispositions of cancer). Also, reember that personal experience is not necessarily indicitive of population trends. And likewise population trends does not necessarily reflect cancer incidence in your particular state, country, neighborhood, family, circle of friends, etc. So my original comment was not direct toward people you know, but toward the greater human condition. i am also painfully aware of the differences between statistics and the effect illnesses have had on my life and my family.

my source (american cancer society).

-tid242

Re:evolution?

[Scrameustache]

while cancer does certainly present in children, the fact remains that children constitute a much smaller cancer population, (even when statistically adjusted for population-size).

Really? I thought it was because of the population size, or the fact that it takes a while to accumulate carcinogens.

as i said before, it was not my intent to offend anyone

Yeah, sorry about that...

Re:evolution?

[Tablizer]

(* For me, progeria, a tragic disease where children have all the symptoms of advanced aging, has always been proof that death is programmed, 'aging' is programmed and that immortality with perfect health is possible. There's no reason for age to mean anything other than triggered genetic progams leading to self destruction. *)

But the *reverse* has never happened (documented). Nobody has ever had a desease which allowed them to live to say 500. This suggests that large-scale life extension is probably not possible (without artificial micro-correctors). Mutations tend to build up over time and get you one way or another. Aging is probably the slowing of matabolism to reduce mutation rates. If you undo this, then cancer may be more likely.

Thus, somebody with a desease that kept them from the regular aging cycle would probably die of cancer rather early in their life, so we would not notice that their aging clocks were not functioning.

Re:evolution?

[spike hay]

One guy in the 1950's died at over the age of 150. (Doctors in New York were sure he was this old)

It is hypothesized that there is a certain gene that caused him to live this long.

Re:evolution?

[Tablizer]

One guy in the 1950's died at over the age of 150. (Doctors in New York were sure he was this old)

I heard that his records were suspicious.

Re:evolution?

[Sgt York]

able to regrow lost arms and legs would outweigh the ability to ward off cancer that doesn't strike until they're 25...

Perhaps the reason our ancestors did not develop cancer until after age 25 is because of the inherent mechanisms of prevention. Loss of these mechanisms would allow regeneration to be possible, but would increase the risk of death due to cancer at a younger age; say, 15 or 20. That would mean you'd die about the time your kids are 2 or 3. Of course, they would die shortly after.

(did you understand my convoluded run-on sentence?).

Maybe.... Loss of a leg and the subsequent regeneration would take, at the very least, several weeks, if not many months. This downtime would probably result in the person's death. Loss of a leg means no walking or running. Loss of an arm means you can't hunt or gather (not effectively, at least). That may reduce the selective advantage

Another interesting note is that of the organisms that can regenerate on a large scale, I don't think any of them have a closed circulatory system. A closed circulatory system could introduce problems from a development standpoint (think about how a closed circ system is made in the embryo), and from the "oh-shit-where's-all-my-blood-going" standpoint.

Re:evolution?

[Turing Machine]

But the *reverse* has never happened (documented). Nobody has ever had a desease which allowed them to live to say 500.

On the other hand, no rat has ever had a disease that enabled it to understand calculus, yet human beings can do it just fine. What's different? The genome.

Mayflies live only a day (in their adult phase). Humans can live for a century. What's different? The genome.

Re:evolution?

[vrt3]

i am a bit taken aback by this, what i said was by no means to insinuate that children do not develop cancer, nor surely to offend anyone. i think the key words here are "most cancers" this does not mean the same thing as all cancers.

Obviously, children do develop cancer to a certain defree. In an attempt to answer your question why evolution provided us with quite an amount of cancer protection, maybe it is because otherwise even children would develop much more cancer than they do now? Perhaps that would result in even less chance to reproduce than the gained advantage of regenerating lost body parts.

Re:evolution?

[Kintanon]

If you go out on a limb and take some of the religious records (Biblical and otherwise) at semi face value some people can be recorded as living around 250-300 years. As far as I know those numbers were arrived at by counting up generations of there children and assuming birth at 13. So 10 generations would put you at 130, and if you were still alive after 29 generations (Methuselah supposedly) you would be almost 300 years old. I'm not saying any of this is definately true, but there are certainly historical examples of people who supposedly lived a very long time for one reason or another.

Kintanon

Re:evolution?

[Tablizer]

(* On the other hand, no rat has ever had a disease that enabled it to understand calculus, yet human beings can do it just fine. What's different? The genome. *)

There is a difference between adding a mechanism(s) and breaking an existing one.

Regeneration could be bad

[pandrew]

Regeneration has been tried before,

remember in spiderman? doctor with no arm uses techniques of regeneration only to backfire and he becomes a mean lizard man?!?

i say leave well enough alone

Things that grow

[Anonymous Coward]

I imagine Mr. Bobbitt would be keenly interested in this new technology...

Re:Things that grow

[Anonymous Coward]

(* I imagine Mr. Bobbitt would be keenly interested in this new technology... *)

Hell, why not buy 2.

re cnacer in children

[Anonymous Coward]

Do you have any statistics to counter the claim that most cancer cases occur in adults over (say) 25?

It's truly sad that some children do die of cancer, but that doesn't mean that the original statement isn't true.

As for children 'regrowing' fingertips, consider that in a child, the finger has a lot of growing left to reach adult size, and that may be the source of the 'regrowth'

Re:re cnacer in children

[j_w_d]

The claim can't be countered. Cancer statistics for the US can be acquired at http://seer.cancer.gov. A google search for "cancer incidence" will bring up. As regards the assertion that cancer becomes more prevalent with age, that is true. Cancer in children is tragic, but uncommon, about 22 in 10,000. It is sad, but pointless to rant about it.

Also, anyone who has spent any time around hospices and hospitals should have noticed that there are far more elderly there, dying of cancer than there are young. My 96 year-old grandmother is one.

The following figures are generated from the "seer" page:

AGE INCIDENCE
0-15 years p=0.22%
15-30 years p=0.55%
30-45 years p=2.08%
45-60 years p=8.85%
60-75 years p=21.75%
75-90 years p=25.82%

If you are familiar with typical population mortality profiles in traditional and "pre-medical" societies, then you are likely aware that the expected longevity is about 35 years. Only the advent of modern medicine and dentistry seem to affect this figure, regardless of the stories of extraordinarily long-lived people in Central Asia. All societies, regardless of medical technology do have some individuals that lived a long time, even by our standards, but that is simple chance.

The correlation between the increase in cancer and increased age is striking, and almost certainly is due to the effects of evolution, especially the jump between 30 and 45. This is just as the poster suggested.

*RE* generation? What about those born without em?

[yerricde]

Even if biomed engineers manage to create a way to regenerate natural limbs, would such a technique work for people born without legs?

There is no real link...

[tlambert]

There is no real link there.

Stem cells are cells which have arisen following gametogenesis. Cancer cells, in at least 80% of cases, are cells that have started production of telomerase independently. Stem cells do not have telomerase, which is normall present only during gametogenesis, and in cancers.

A good company web site to look at to see how these things relate to each other, specifically dealing with oncology (the study of cancer) and limb regeneration, amon other topics, is:

http://www.geron.com/

The specific fram page with a discussion of their cancer research is:

http://www.geron.com/03.01_oncology.html

Intentional telomerase activation is generally only useful in wound healing therapies; this is because the cells in which the telomerase would act in this case have already specialized.

It's not know whether or not telomerase could act on stem cells directly, permitting "farming" of stem cells (an interesting idea, raised by your question). My gut feeling on this would be "no", based on the existance of teratomas, but I'm willing to be wrong (particularly if it ends up making me immortal... 8-)). The regenerative medicine page is at:

http://www.geron.com/03.03_regenmed.html

Note that Geron (the company whose site this is) has the patent on the genes coding for human Telomerase, owns the patents that led to "Dolly the sheep", and is interesting for other reasons.

The company was originally founded -- and their web page used to claim this -- to find a cure for human aging. They have a more mainstream message, these days, but they are certianly making progress on their original goal, even if they are getting a lot of products out of the intermediate work.

-- Terry

misplaced mice?

[iggymanz]

And in a related story, Dr. Futzup, who works in a room adjacent to Dr. Ellen Heber-Katz, was feeding Nutrasweet to a group of mice for 3 weeks, and one morning when his lab assistant brought in the cage he noticed "three holes had appeared in all their ears!". Also, he noted "the cage had changed color!"

NP

[tid242]

Yeah, sorry about that...

NP, i just feel bad when i make other people feel bad (innocent people anyway)..

If you're interested here's a breakdown of causes of death by age provided by the CDC, it's actually pretty interesting... starting on page 13 or so: cdc.gov...pdf :)

take care,

-tid242

I KNEW NUTRASWEET WAS BAD STUFF!!!!

[Anonymous Coward]

I just knew it.

Re:*RE* generation? What about those born without

[drik00]

It seems to me that the main challenge in growing whole limbs would be the initial attachment of the new limb. Connecting nerves and tiny blood vessels is very difficult and fairly inexact as it is.

Secondly, what about the nerves? You spend the first couple *years* of your life learning motor coordination and skills. I would imagine that it would be very very difficult for an adult to learn to use appendages he/she never had to begin with. We know that certain parts of the brain are more hardwired than others, and that rewiring can occur, but that, as well, is something we've only begun to dabble in.

We still have a long way to go.

J

This isn't new

[RedWolves2]

Have you ever gotten your ear peirced and didn't leave the ear ring in your ear long enough. It will grow over the hole filling the hole back in. If that is her only evidence that holes in mice ears are regenerating then I would have to say "Big Deal!"

Now I guess what I might be missing is do mice ears regenerate like human ears or is it expected that the holes don't grow back?

Re:This isn't new

[Sgt York]

or is it expected that the holes don't grow back?

They normally don't grow back. The holes used in the ears of mice are an inventory mechanism. The holes are pretty big; the tool I use makes little semicircle notches about 1cm in diameter; quite a bit bigger than the holes in peirced ears for us.

Re:This isn't new

[c.emmertfoster]

"little semicircle notches about 1cm in diameter; quite a bit bigger than the holes in peirced ears for us"

Ummm... have you been to a big city recently? The neo-tribal thing is "in" now, at least with a particularly degenerate crowd.

Hopefully their inheritance will cover the price of a good plastic surgeon.

10 to 12????

[doublem]

That's sick.

Pervert.

Seriously though, that's below the age range where the average human is capable of reproducing. The other points are interesting, but that age guess is way out of wack.