Cancer and aging cells

There have been a number of interesting studies of late and this one links a gene regulation mechanism inversely to aging as a means of fighting off cancers. Thoughts?


Gene fights cancer by aging us, studies find

Sept. 6, 2006
Courtesy Nature
and World Science staff

Bi­ol­o­gists say they’ve iden­ti­fied a gene that pro­tects against can­cer by sup­press­ing cells’ abil­i­ty to di­vide—making us age faster in the proc­ess.

The find­ings sug­gest that a fun­da­men­tal trade-off be­tween long life and can­cer pro­tec­tion is built in­to our bod­ies, the sci­en­tists said. The work also in­di­cate ag­ing may in some sense be pro­grammed, they added, which some re­searchers have the­o­rized be­fore.

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The con­clu­sions emerge from three pa­pers pub­lished on­line in the re­search jour­nal Na­ture this week.

The stud­ies were aimed at explaining why stem cells, “mas­ter” cells that can de­vel­op in­to a va­ri­e­ty of dif­fer­ent types, lose their abil­i­ty to di­vide and gen­er­ate new cells with age.

Ex­per­i­ments found that a mol­e­cule called p16INK4a, and a gene that pro­duces it, lim­its such cells’ re­gen­er­a­tive abil­i­ties, the re­searchers said. The ap­par­ent ben­e­fit of this is to head off can­cer, which in­volves run­away cell mul­ti­pli­ca­tion; the mol­e­cule was al­read­y known to sup­press can­cer.

The draw­back is that slowed cell di­vi­sion is as­so­ci­at­ed with ag­ing, ac­cord­ing to the sci­en­tists.

The au­thors of the stud­ies found that that the gene’s ac­tiv­i­ty in­creases as stem cells in three mouse tis­sues lose their abil­i­ty to self-re­new. The teams ge­net­i­cal­ly en­gi­neered mice that lacked p16INK4a and then ex­am­ined them when they got old. Pro­gen­i­tor cells in the ro­dents clung on­to their youth and did­n’t show the nor­mal de­cline in pro­lif­er­a­tion with age, they said.

Sean Mor­ri­son of the Uni­ver­si­ty of Mich­i­gan in Ann Ar­bor, Mich. and col­leagues stud­ied pro­gen­i­tor brain cells in mice. Nor­man Sharp­less of the Uni­ver­si­ty of North Car­o­li­na School of Med­i­cine in Chap­el Hill, N.C. and his team stud­ied pro­gen­i­tors in the pan­cre­at­ic islets that make insulin-secreting beta-cells. Da­vid Scad­den of the Har­vard Stem Cell In­sti­tute in Bos­ton and his group ex­am­ined bone mar­row cells that make blood.

The work al­so sug­gests type 2 di­a­be­tes might part­ly re­sult from a fail­ure of cells in the pan­cre­at­ic islets to re­new with age­ing, the re­searchers said. Thus, they added, block­ing this pro­tein in cer­tain tis­sues might com­bat cer­tain ef­fects of age­ing.

Gene Found to Switch Off Stem Cells During Aging

Switching off Aging in Stem Cells

Loss of Anticancer Gene Retards Aging in Stem Cells

Thus, they added, block­ing this pro­tein in cer­tain tis­sues might com­bat cer­tain ef­fects of age­ing.

Exactly. This is one of those great life-extension ideas that have never been tested although they could have been. Knock things like this out conditionally, in cell types thought to never get cancer (neurons, heart muscle), see what it does... Same about knocking telomerase in. Hope the selectivity is good enough %-)

p16INK4a like p53 and even telomerase belong to a group of genes that operationally can be broadly defined as being part an ever-vigilant quality control process that serves to protect the organism by eliminating dysfunctional cells. When we switch off these genes in cell cultures we find that senescence is delayed at the cost of genomic stability, which in an organism inevitably leads to cancer. The avoidance of cancer, however, need not come at the cost of aging. This is a system that evolution has designed according to the necessary constraints of energy expenditure and genomic plasticity. The cell will devote only so much energy to maintaining the integrity of its molecular structure against the factors that threaten it such as toxic metabolic byproducts and solar radiation. At the same time the cell has to allow the genomic information it carries to be able to be reshuffled at a rate that is in keeping with changes in its environment. If this reshuffling takes place too often the cell is unable to sustain specific characteristics long enough to be able to evolve into sophisticated multicellular arrangements yet if it is too slow then it may not be able to generate a sufficiently diverse range of characteristics to adapt to changes in its environment.

The take home point is that what evolution has designed in respect to these contraints does not apply when the contraints are removed, ie the pressure to conserve energy and the requirement for evolutionary diversity. It is very likely that in a few millenia we will evolve extended lifespans if we can ensure that our environment stays constant and there is no shortage of high quality nutition. Or, we can accelerate this blind, creeping process by making the changes ourselves.

first of all, the main reason of evolution is for the genes to replicate and multiply and to have descendants.

too little of our bodies are made for resistance on longterm, after the multiplying part (reproduction of the genes) was already done.

Then everything goes down, we are just the garbage that evolution throws away after reproduction was made.

So i personally find it hard to believe that this gene simply protects us in a bad way... because the genetical material deterioration happens anyway after age of 30-40 years old, usually when we already have descendants, so this "protection" has no meaning