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Age A Byproduct of Cancer Defense?
A reader writes "The International Herald Tribune has an article which says, in brief: they have discovered that aging in mice seems to be a byproduct of the chemicals that prevent cancer" If true, that's quite a double edged sword - avoid death, to cause it later.
The average lifespan is only that long thanks to modern advances in medicine, disease cures, etc. Without them, the average human could expect to live maybe 50 years, although menopause might also come a little earlier.
But you can't think of those years as being wasted. After all, if a woman has children as late as 40, she'd certainly like to raise them to adulthood (and then help them learn to raise their own children) before she dies.
Not quite. Ender had no such affliction. In fact, Ender lived to be several thousand years old. Bean was the mutant.
-- Nerds on toast in the new millenium
that would be natural selection, operating at the cellular level, ultimately producing cells that are capable of working around the substantial machinery that is in place to identify and destroy aberrant cells.
...)
:)
however, avoiding cancer does not necessarily lead to death. biology reuses parts: p53 is involved in programmed cell death and cell-cycling, and probably other things i'm not aware of. fortunately, big proteins often have disjoint functional domains, meaning mutations can affect different functions discretely, meaning, we may be able to tweak p53 to keep the programmed cell death w/o the aging (which around here we're guessing is the result of interaction between p53 and TEP which is involved in telomerases which are like little timers ticking down in the cell
if we can't tweak p53, we'll selectively tweak whatever it's touching causing the aging problem, w/o disturbing its interactions in apoptosis.
cancer is tough, but in the long run there's no need for despair. don't you people watch enterprise? they cured metastatic interstitial lung tumors without breathing hard a few episodes ago
I've read that in cancerous cells, the telomeres don't shorten each time the cell divides, so there's no system in place to stop the cell from dividing forever (and all of it's children cells, etc.).
A reasonable hypothesis for why controlled growth through telomeres is necessary is to prevent mutations from a long series of copies (copies of copies, etc). This way, a "series" of cells only last for a fixed number of generations. After so many, the series stops. Then the stem cell(s) can take over and start a new "first generation" cell which can be the start of a new series of cells.
As we get older, perhaps the stem cells themselves start to degrade or become mutated (possibly causing cancer), and are no longer able to produce good "first generation" cells. As an example, this could be why we develop skin blemishes as we get older. Just imagine what's happening to other genetic attributes.
It's my personal theory that the process of aging is actually just the process of various parts of our body mutating to a small degree. For example, one little DNA pair mutated in a skin stem cell, and suddenly you have a freckle.
I always figured that given the knowledge that's taught in regular high-school biology, most people could figure out that the tradeoff of preventing aging is the increased risk of cancer (since cancer cells could go on forever if supplied with the nutrients necessary for cells to live).
*shrug* I dunno...
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I'm a 34 year old programmer whose been fighting cancer vigorously for the past 6 years, including losing 2/3rd of my liver, having a stem cell transplant, massive chemotherapy, radiation therapy, etc. If any or all of my treatments reduce my overall life span by 20 years, I'll gladly take that trade off. Simply living another 5 years and seeing my young daughter at her first school dance would be worth any amount of damage caused by my treatments.
That said, I can also pass on through my findings with various hospitals and oncologists, that it's not so much of if you might get cancer, but when will you get cancer. Given time and old age, the body begins deteriorating to the point that cancer becomes a fairly natural process, whether it is the more deadly forms or milder forms (such as treatable skin cancer). Of course, for those folks lucky enough to make it to 80+, considering radical therapys that have extreme side effects is usually not worth the agony just to extend life a year or two.
You have it backwards -- controlling runaway growth is vital, and our bodies have it at the cost of aging and senescence. Attempts to halt or reverse aging would likely result in runaway cancer.
What's new here, by the way, is the effect of p53. The tradeoff between aging and cancer has been clear for a while and suspected for decades -- Hemos reported on a project that supposedly beat the problem back in 1998.
What I'm listening to now on Pandora...
I'm speaking here as founder and president of what was the 2nd largest biotechnology company in the U.S. focused on the molecular biology of aging during the mid-'90s. So we will assume for the sake of improving the discussion I'm moderately well informed in this arcane branch of knowledge.
Point #1: If you read something scientific or technical in the "popular" press, never assume that they managed to interpret it properly. If reporters don't have an education in a particular discipline, they are not likely to understand the subtleties of what is being discussed. Always go back to the most scientific sources you can get access to. Most of the readers are presumably qualified to evaluate arguments on technical merits (this is the /. forum!). Learn the jargon and if you don't understand something find an expert and ask questions (or post to the forum -- you never know when an expert might be lurking).
Point #2: Never assume a /. poster knows what they are talking about (or has verified what they may have copied or concluded from popular press). Case in point: "aging in mice seems to be the byproduct of the chemicals that prevent cancer". The material under discussion is a mutant p53 protein which is the byproduct of a modified p53 gene. It is not by anyone familiar with discussions in this field a "chemical". The p53 protein weighs tens of thousands of daltons and has multiple "active" functions -- most molecules considered "chemicals" weigh less than a few thousand daltons and have few, if any, "active" functions.
From the Nature news report: "they created mice with a chunk missing from one copy of the gene". Translating this into "programmer" terms -- this is in effect replacing 1 of 2 instantiations of an essential subroutine in an ~30,000 subroutine system with a subroutine that has had some of its lines deleted. How do you draw conclusions as to what is going on in that situation? Unless you know what lines were deleted and what the purpose of those lines was you have relatively little hope of drawing conclusions that would allow you to debug the system (at least IMHO). You certainly cannot discuss what the situation means in any intelligent fashion.
All of that being said, I'll provide my "spin" on the results. The normal p53 protein is a "gatekeeper" protein. Its purpose is to determine whether or not DNA damage is present (i.e. whether your program has been corrupted). If too much damage is present it induces cells to commit apoptosis (cellular suicide). If less damage is present, it delays cellular replication (copying) until the damage that is present can be repaired (calling the ECC subroutines). So it acts as a brake on the replication of mutated/damaged DNA and an executioner for cells that are so far beyond the error-correction subroutines that they represent a threat to the entire organism. In larger organisms (which have more cells and are therefore at greater risk of developing a "mutant" program and therefore cancer [which is unregulated cellular replication]) it is important to constrain replication. So humans, in contrast to mice may have a p53 which strongly constrains cellular replication. { Alternatively they may have "redundant" subroutines like telomere shortening (mice have very long telomeres, humans do not) which function as "backup" programs that function to limit cellular division and therefore the development of cancer. (This is based on the concept that short telomeres inform cells to "stop dividing" just as "damaged DNA" [through the p53 protein] cause cells to stop dividing.) } The extent to which short telomeres may resemble "damaged" DNA (and therefore activate the p53 "subroutines") is unclear (to me) at this point. [This is a fairly hot topic of scientific debate.]
If we view cancer and aging as complementary ends of the see-saw -- allow too much cellular replication and one gets cancer -- allow too little cellular replication and those parts that wear out are not replaced, resulting in aging, and one may be able to interpret the results of this study. The part of the p53 gene that was deleted probably served to function to "remove" the block against replication or "enable" the replication function. So what may be occuring is that the mutant p53 gene may be detecting damage, blocking replication, but then when the damage is repaired the defective p53 may not be allowing replication to proceed. Thus you have very effective anti-cancer properties but as one gets older there are fewer and fewer cells available to replace those that are lost. Net result: accelerated aging.
Now, this result need not be pessimistic. As Tom Kirkwood, one of the world's leading gerontologists pointed out in the Nature article, "We could be able to pick a path through the molecular mechanisms of ageing without making cells more tumour-prone. 'There's no reason why you shouldn't get greater defence against cancer and greater longevity.'"
As a once upon a time programmer -- I encourage people in the software industry -- "View genomes as programs -- lets figure out where the bugs are and then lets go fix them."
It makes me think that if we find the cure for cancer, we find the key to immorality.
/.)
Its not that simple I think. (From memory I think I posted about this alot 2-3 months ago on
You can rest assured that there are many ways to die other than cancer however. These include accidents and trauma (mean time to death many hundred years), infections (major cause of death before antibiotics), vascular disease (still the leading killer), alzheimers (a good 10-15% of those who live long enough), respiratory failure (we get about 150 years worth of lung function at birth, accelerated decline with smoking etc). Not to mention non lethal problems such as cataracts and lens failure (age related long sightedness - presbyopia), macular degeneration - and these things only send you blind.
Not that I would want to stop you hoping. I'm hoping too. Its just that I am starting to get a feel for how complex the whole problem is - our entire bodies were selected to get us to old age, which was probably mid 50's back when average life expectancy was in the mid 20's. And precious little lasts alot longer than that.
I do believe that most of these problems are technical in nature, however, and there is hope in that.
Michael
There is no cryptographic solution to the problem where the intended receiver and the attacker are the same entity.