Tumor-suppressing Gene Contributes to Aging 145
Van Cutter Romney writes "Scientists have discovered a tumor suppressing gene which also leads to aging in stem cells. The gene also known as p16INK4a when removed from 'knockout' mice resulted in older mice having organs as healthy as younger ones. However they didn't live any longer than normal mice. The new study was confirmed by three independent researchers from Harvard, UNC Chapel Hill and University of Michigan."
Cancer, aging. (Score:4, Informative)
Cancer, then, is an anti-aging program.
The article basically states that when they turned off the flow of ink-4, embyyonic stem cells were free to divide without check. The mice without the ability to produce ink-4 developed cancer within a year and died. This behavior cannot be reliably reproduced in aged stem cells, and ink-4 production naturally increases exponentially with age.
The main news I see here is either a possible avenue for cancer research, or a good supporting argument to lift bans on exploiting new strains of embryonic stem cells (over adult stem cells). This does not represent a specific breakthrough, but yet another amazing revelation of stem cell capabilites has come to light.
I support the ban on cloning, I disagree with the ban on new stem cells, I am relatively opposed to mass abortion, but banning it would be stupid. I think this story's new information supports these views.
Principle of Hardy-Heisenberg-Jagger (Score:3, Funny)
The article basically states that when they turned off the flow of ink-4, embyyonic stem cells were free to divide without check. The mice without the ability to produce ink-4 developed cancer within a year and died.
There's a famous principle in Mathematics & Quantum Mechanics, first discovered by the British mathematician GH Hardy, and then refined by Heisenberg, which states that both a function & its Fourier transform cannot decay too rapidly [otherwise the function is identically zero].
Or, as Mi
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I forget, was it spaghetti or ramen he created on Day 5?
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Their Satanic Majesties Request (Score:2)
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Sure, he can use it as a further argument for ID. And the rest of the world can, as they always have, either ignore his dumb ass, or feed the academic troll (which is where I feel it best to place IDers in the for
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Which he doesn't. Come on! Doesn't anyone read the post they're responding to anymore? Someone mentions "The Designer of the Universe" in a joke and everybody is assuming he's advocating Intelligent Design?
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Meanwhile, I've found that the ability of Slashdotters to smell sarcasm seems to have a very high standard deviation (i
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Cancer, then, is an anti-aging program (Score:4, Funny)
Yes, when cancer works, you stop getting older.
Q.E.D.
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Sounds to me like Planned obsolescence [wikipedia.org]... that is, if you believe in a higher power.
Why is it that back in Biblical times, people like Abraham & Moses used to live several hundred years? Did they all have cancer? (Assuming that cancer is an anti-aging program)
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Biblical old dudes (Score:2)
Perhaps you're thinking of the antediluvian patriarchs. Noah was one of the younger ones at like 600.
Re:Cancer, aging. (Score:4, Interesting)
You don't have to believe in a higher power for that. Sounds to me like a natural function of the balance between being able to repair yourself and exploding into a ball of disorganized meat (ie: developing cancer in every cell). Based on the amount of damage your body takes, it automatically determines how much it needs to be able to redivide its cells.
"Why is it that back in Biblical times, people like Abraham & Moses used to live several hundred years? Did they all have cancer? (Assuming that cancer is an anti-aging program)"
Nah. I would guess it's because of a trans-generational game of 'rumour' that happened before any of it got written down. Don't get me wrong; much of Exodus actually happened (the plagues, parting, etc, are easily explained by a volcano eruption that happened as moses returned to Egypt; I can't blame him for using it as a way to extort pharoh and reinforce judaism - we all have our agendas, after all, and they're almost always good in our eyes). But Genesis... it all sounds a bit like stories passed from father to son that eventually got written out.
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It's really quite simple. The early people had nearly perfect genes (you know, made in God's image and all that), but since God only really created two (and the second one was basically a clone of the first one but with the Y chromosome taken out and the X duplicated again) there was a LOT of inbreeding going on. Which isn't
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Re:Cancer, aging. (mistake) (Score:3, Informative)
How this supports embryonic stem cell research is: we now have evidence that adult stem cells will not be effective when used as treatment because they will be naturally suppressed. Thus to get stem cells that will divide and provide therapy, we mus
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Extracellular signalling pathways, such as G-coupled protein receptor pathways, may be key to INK4 expression levels. If that is the case, embryonic stem cells would likely undergo the same INK4 suppression as adult stem cells, whether they be transplanted or naturally occuring.
The key is then not the source of the stem cells but modulation of protein expression in the stem cells you have.
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You will find that the distribution of ignorance, indifference, stupidity, pandering, sloth, envy, ambition, hatred, disgust, and pretty much any adjective--positive or negative--can be applied universally to any politician or political person regardless of affiliation.... PLEASE PLEASE PLEASE don't let (force) a really good discussion that
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But, it has been partisan politics that has interfered greatly with science for quite some time now. In particular, politicians have been bent to the will of religious groups. Yet these same groups daily depend on the fruits of s
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About the other point. I'm sure Frist was a wonderful heart-surgeon. But he's not the type of doctor that I want operating on my heart, considering he renders life or death medi
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Perhaps I should have paid better attention in English class.
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Sorry, but when the subject of your point ('of these Republicans') can be easily replaced with an asterisk, your point suffers. For example, I could replace it with 'inteliigent designers', 'radio pundits', or 'of the citizens of pennsylvania', and it would still be true.
That doesn't make it a point. It makes it astroturfing.
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Republicans and conservatives generally tend to fall into the middle intelligence range. The stupid tend to be poor and want someone to take care of them, which is not Republican politics. The very smart tend to be highly educated; tho
Old news... (Score:3, Interesting)
Re:Old news... (Score:5, Informative)
Slight mischaractarization (Score:5, Interesting)
If I understand it correctly, this is a SLIGHT mischaracterization. It's not about risk of creation of cancer cells so much as it is about limiting tumor size - generally in malfunctioning differentiated cells - and limiting stem cells is an undesirable side-effect of how it's done (though it WOULD also limit a stem-cell tumor, if such exist).
The mechanism (or set of mechanisms) is a limit on how many times a non-gamette cell may replicate. Thus when a cell mutates so that it, and its progeny, continue to replicate (ignoring their normal limits), the resulting tumor reaches a maximum size (say-pea sized) and stops growing. (It may even die off, as cells die TRYING to replicate with an "expired meter", or are no longer replaced fast enough to stay ahead of immune-system attacks).
The smaller the tumor when it hits the limit, the better (and the less likely some cell within it will acquire the ADDITIONAL mutations necessary to escape this limit, founding an "immortalized" tumor cell line). But there's the downside that the limit also results in cellular senescence - inability of the body to replace tissue in late age, because the "counter" in the otherwise-fine cells is running out.
So the limit apparently evolves with the typical lifespan of the population, allowing enough replication that cellular senescence doesn't begin to occur in normal inividuals until virtually all of them would be dead (or otherwise no longer an asset to the species) due to other causes. (I vuagely recall reports of research suggesting the typicall setting is something like twice as many cell replications as are necessary to avoid senescence by the age where about 95% of the population would be dead.)
Meanwhile other protective mechanisms (such as the metabolically-expensive production of antioxidant enzymes) co-evolve to trade off keeping the cancer rate down against resource consumption, given the typical lifespan due to risks and the cell-reproductive limit setting. (THESE are the "twiddle settings" that trade off CREATION of a cancer cell against other life-shortening factors.)
The settigs of these protective mechanisms apparently evolve quite rapidly, so they tend to closely track the lifespan-due-to-circumstances of most species that have been in their niche for a while. But the human lifespan has been drastically extended in a period that is evolutionarilly VERY short, thanks to weapons (protection against predation and improved hunting success), agriculture, animal domesitication, lore transmission, medicine, and other technological and cultural improvements in lifestyle. So plenty of people live to the "threescore and ten" or so years when the current setting of the cell replication limit tends to cause fatal system failures.
Research such as this, identifying the details of the mechanisms, should lead to interventions to compensate for the now incorrectly-low setting of this "tuning knob" in the human genome.
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This is known as the Hayflick limit, and is related to what the great-grandparent post brought up- telomeres. When normal differentiated cells divide, an issue with the way our DNA polymerase works causes a bit off the end of the DNA strand to not be replicated- your DNA gets shorter with each cell division. To counter this, there are sequences of repeating nucleotides at the end called telomeres. The te
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Possibly. But they'd also be completely unable to repair themselves. You'd get a population much like the late Brunnen'gee.
What springs to mind... (Score:5, Interesting)
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Ideally, you would be able to turn it on and off at will. Turn off aging when you reach a certain age. Then if you contract cancer, turn it on really quick to help kill off the cancer, and then when you recover from cancer, turn the "aging" process back off.
Not that we could do anything of the sort anytime soon, but
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Hmm. (Score:3, Interesting)
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You say flawed methodology, I say.... progress!
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Re:Hmm. (Score:5, Insightful)
There is only one catch and that is Catch-22, which specifies that turning off p16INK4a for one's safety of your organs in the face of dangers that are real and immediate will cause cancer. Giving yourself cancer is not the process of a rational mind.
The trick might be to turn off the expression of the gene temporarily to rejuvenate aging organs, then switch it back in again to suppress cancer. That way, maybe Yossarian can have is cake and eat it too...
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Only to be killed at a zebra crossing right after the procedure.
Re:Hmm. (Score:4, Insightful)
Wishful thinking. As much as people would love to blame the cause of aging on one particular gene or process, the truth of the matter is that aging is a complex and multi-factorial phenomenon that can't be addressed that easily.
Sure, stopping this particular gene might allow for more somatic cell repair but what does that do for the damaged mDNA due to free radicals in the mitohondria [nature.com]? And what about the telomeres protecting the ends of your chromosomes which would decrease with every replication [utah.edu]? And what about damaged cells whose replication could cause the very cancer this gene was probably "designed" to prevent?
Not to be discouraging of this kind of research, but really it is just pie-in-the-sky type of stuff and should be regarded as such; the science just isn't there yet. And the irony of it all is that immortality most certainly won't be obtained in our lifetimes. Joseph Heller has to be smiling somewhere about that one.
-Grym
I think they're just hyping this with that title (Score:1)
Re:I think they're just hyping this with that titl (Score:3, Insightful)
Think of it like social behavior. Ideal
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Re:I think they're just hyping this with that titl (Score:1)
This is probably why a handful of humans had deseases causing them to age far too prematurely, but NEVER the opposite (at least not on a signif scale). Thus, entropy is innevitable it appears. Errors happen. Either we slow down to death or get i
Re:I think they're just hyping this with that titl (Score:2)
Re:I think they're just hyping this with that titl (Score:5, Interesting)
The immune system is handicapped by the fact that with at least some types of cancer, there is comparatively little difference between the malignant and healthy cells. If it can't tell them apart, it can't stop the cancer from developing or spreading. You're right in that the immune system can sometimes stop cancer, but from a survival standpoint it's better not to get it in the first place.
So we have genes in place to limit cell replication. It's been suggested that aging is an inevitable side effect of these limits (take a look at telomeres for instance). Just the immune system by itself, or just the genetic protections by themselves, isn't enough; you really want both defenses.
Oversimplified, the genetic element is why some cancers run in family lines, and the immune element accounts for why some cancers develop when the immune system is weakened (like KS in AIDS patients).
Genetic Safeguards are way more important... (Score:5, Informative)
The first thing that needs to fail is the proofreading enzymes, so that a gene or two are damaged without being repaired.
Then the "self destruct" needs to fail to activate in a cell, The self destruct is almost always armed and ready to go, unless it gets knocked out by a "lucky" mutation.
Even if the self destruct fails, the cell sensing needs to fail in order to grow beyond a few cells. Then the telemorase halting needs to fail in order for the cancer to reach something larger than a mole.
The immune system is a last resort, and not a very good one in comparison.
Storm
Re:I think they're just hyping this with that titl (Score:2)
That has very little to do with the immune respose issue you mention, which comes in significantly later, when tumors have actually started to form. The oncogene / tumor suppressor interactions are part of the balance tha
Age mutations versus cell division mutations (Score:4, Insightful)
Does the same thing apply to a cell?
In other words, as a cell ages is it more likely to have a cancerous mutation? And how does this likeliness compare to the chance of having a cancerous mutation through a cell's reproduction process? (these are for the biologists out there)
If you have a greater chance to have the mutation a cell reproduces then you'd want cells to live along time so they have to reproduce less. If you have a greater chance as the cell sticks around (ages) then you'd want more reproduction and a shorter life span (even though this would be less energy and resource efficient, but maybe more efficient than fixing/killing cancerous cells).
Re:Age mutations versus cell division mutations (Score:4, Interesting)
Look at this statistically.
Everytime a cell divides there is probablitly P that the cell mutates.
Everytime a cell ages 1 day there is a probability Q that the cell is damaged.
Since we must maintain a constant number of cells we assume that everytime a cell divides the "Old" cell dies.
If we make the simplified assumption that all cells must divide at the same time then we must choose to either (1)let the cells divide or (2)let the cells age one more day.
There is an obvious strategy to keeping the greatest ratio of healthy cells in the body. We will choose whichever action results in the least expected number of unhealthy cells.
If P Q (which it should be) the strategy would be to divide every chance you get until the probability of getting a mutation is greater then the probability of having cell damage. You will then alow the cell to age and the ballence will swing back in the other direction.
As you continue this pattern you will find that it is optimum to have cells divide less and less frequently. Eventually the probability of mutation will be so high that the best strategy is to simply stop cell division all together although it is unlikey that anything will live long enough to reach thsi point.
This is an oversimplification but the point is still valid. The best strategy for survival changes constantly.
the gambler's folly (Score:2)
Perhaps OT, but your example doesn't accurately characterize what I think it is you're saying. Consider a coinflip. Assume the chance of the coin landing heads-up is 1:2, as is the chance of it landing tails up. Assume you're going to flip the coin once. What are the chances of a heads-side-up landing? 1:2, of course. What about if you flip 700 times? 1:2, still. The fallacy
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No, your parent post deliberately sidestepped the Gambler's Fallacy. He clearly indicated that he meant "more likely" in the sense of "the odds of at least one tails after one flip is 50%; the odds of at least one tails after 8 flips is 99.6%", since the total number of tails/mutations accumulates. After a very long time, the probability of one or more mutations is nearly certain, even if the probability of each mutation occuring is constant.
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No... the odds of at least one tails flip (that is, the sum of exactly one tails flip, exactly two tails flips, exactly three tails flips, etc.) is the complement of exactly zero tails flips -- that is, all heads flips. The probability of 8 heads flips in a series of 8 flips is (0.5)^8 = 0.00390625; the probability of less than eight heads flips in a series of 8 flips (that is, the odds of one or more tails flips) is therefore 1-(0.5)^8 = 0.99609375. Please study some high school statistics.
aging / tumor (Score:2)
You can be young forever (Score:2)
Anti-ageing research is selfish (Score:1, Insightful)
Once the old people can no longer look after themselves, they will be put into a care home, and kept alive for decades using modern technology. I visited old folks homes for a while, and me playing chess with an old man for 1 hour a week was the highlight of his life, the highlight for another man was me rolling a ball back and forth on a table to his arthritic
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Nobody will take you seriuosly unless you live by example. Will you willingly die before you hit `old age' and become a `burden on society'?
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I'm 26 - how should I do that? Take up smoking?
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A very commendable sacrifice Citizen!
I don't know why Govs around the world complain about smoking etc, and worry about aging populations on the other.
Just tax tobacco at a reasonably high rate, educate citizens on the dangers of smoking. And if people still want to smoke, why make it so hard for them?
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Or you could just donate your organs.
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1) Those old people are generally able to end their own lives if they really wanted to - but they don't. Your generalisation that old people "don't want to live" is inaccurate. Many studies (check on PubMed with a few salient keywords) have shown that elderly people are just as happy (if not more so) than younger people. There is also no magic point at which people suddenly decide that life is not worth living - the vast majority of people will always want to live lon
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Babyboomers make up a significant proportion of the population. Thus, when they were young, they were listened to, and lots of changes (equality of women/non-white etc) occured. Now that they are old, almost all countries in the English speaking (winners of WW2) world have become very conservative.
Evolution occurs when a new generation replaces the old. A society where the old outnumber the y
Re:Anti-ageing research is selfish (Score:4, Insightful)
John Stuart Mill said, "I never meant to say that the Conservatives are generally stupid. I meant to say that stupid people are generally Conservative. I believe that is so obviously and universally admitted a principle that I hardly think any gentleman will deny it." Mill goes on to say that since there are undeniably a lot of stupid people, the Conservatives will always be a very powerful party. Perhaps this is closer to the explanation you are looking for.
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Why is everything assumed to be a tradeoff, or subject to some sort of cosmic balance or fairness.
Sometimes the very rich are also happy, smart, beautifull, wonderfull people.
Sometimes the poor are ugly idiot assholes who desrve worse than thier short miserable lives.
Life aint fair and sometimes you can have your cake and eat it too.
Mycroft
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Ummm... If you were 80 years old and had the body and the mind of a 20 year old... Well... I don't think there is going to be a need for you to retire... EVER!
Maybe a scary prospect having to keep a day job for the next 1,000 years, but I'd take that over having my mind rotting away and me crapping myself for a good 30 years in some rest home.
Cancer cure == indefinite lifespan? (Score:4, Interesting)
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It is a whole class of diseases. There are many many types of cancer, each with its own causes, mutations or cell environment changes.
If there is a "cure for cancer" its going to be a hell of a lot of cures.
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It may be possible in the future to prevent breast cancer ahead of time by genetic modification (before getting the cancer).
Sure, it may not be possible too, but you cannot rule that out.
As I said in the GP, I do agree that "curing all cancers" is a moot thing, but preventing a specific type of cancer by DNA modification sounds plausible. Ofcourse other side-effects might ensue.
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Not an expanded life.
Imortalty would be nice, but this is good to.
Article quoted the caloric-restriction bogosity (Score:3, Informative)
Unfortunately, caloric restriction only raises the life expectancy of rodents in the laboratory, not when exposed to natural conditions. While it reduces risk of cancer, it also drastically reduces the effectiveness of the immune system at fighting off infection (and the resulting stresses which, in turn, re-raise the cancer risk.)
This has been known for decades by those educated in food & nutrition science. Unfortunately, the news has apparently not spread widely in other fields.
So while there is a strategy that reduces both of these TWO problems, it does it at the cost of creating a third. Again no free lunch.
Though there may be useful insights from the lab results, life extention strategies based on caloric restriction in the real world seem unlikely to be successful.
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(Note that the main problem, of course, is death and disability from the infections, not the marginal cancer re-increase.)
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Well I know plenty of people who spend all day in the lab and barely take any time off to eat. But I'm guessing this will not increase their lifespan much.
It depends on your diet (Score:3, Interesting)
This has been known for decades by those educated in food & nutrition science. Unfortunately, the news has apparently not spread widely in other fields.
It all depends how you
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Another risk is B12 deficiency - it is NOT found in plants, humans and their intestinal flora don't synthesize it, and perma
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There are many different thoughts on Ayurveda. Some ayurvedic doctors recommend eating meat (usually due to p
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It is originally more of a scientific description of cause and effect. That if you pull the trigger while pointing at your toe, it will hurt alot
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Don't confuse low caloric with malnutrition.
Of course, if the only caloric intake you have is candy, pop and chips, you've missed the point.
Time to Live (Score:2)
a couple thoughts on biology of aging (Score:2)
This isn't really surprising. I think that JSB Haldane provided the mathematical framework for showing why this is the case.
First off, evolution is about amplification: the genes from an animal that has more children, younger, will be spread more than the genes from an animal that lives longer, so the successful strategy is to commit energy towards early maturation, rather than towards longevity.
Secondly, and this is the part Haldane wo
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Out of millions of sperm you get one and it goes with an egg, if the result is not good enough, poof, try again.
Otherwise, you get an embryo and all that cell division with chances of errors each time. If the end result is successful enough, you get either another millions of sperm thingy, or some few hundred thousands of eggs, and the process repeats.
If you have very very good error detection and correction, there won't be very much evolution.
However, if we are that point where we don't wa
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So, like the recent breakthrough in white blood cell modification to target cancer cells?