Want to live forever?

[Taem]

While reading in the LA Times today, I found an interesting article about stem cells in adults. Here is a link from another site.

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 trade­off 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.

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 cell types, lose the 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 linked 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.

The article I read was basically saying if you turned off the p16-Ink4a gene, you *could* live forever, however you would most assuridly get cancer right away and always live with a high risk of getting cancer!

[Occhidiangela]

While reading in the LA Times today, I found an interesting article about stem cells in adults. Here is a link from another site.
The article I read was basically saying if you turned off the p16-Ink4a gene, you *could* live forever, however you would most assuridly get cancer right away and always live with a high risk of getting cancer!

Planned obsolescence at its most basic level.

See also white lab rats, all of whom eventually die of cancer.

Occhi

[Lissa]

While reading in the LA Times today, I found an interesting article about stem cells in adults. Here is a link from another site.
The article I read was basically saying if you turned off the p16-Ink4a gene, you *could* live forever, however you would most assuridly get cancer right away and always live with a high risk of getting cancer!

That fits quite differently from what I have seen other biologist say concerning cell division. There is something (Telemer?) that is attached to the genes in the cells that each time the gene is divided the portion lessens in lenght. Upon reaching a given length, the cell will no longer divide. This is why as people age skin and tissue will thin making it easier to injure and more difficult to heal from what I've read.

[Jester]

Wait, are you saying that if I want to live forever, I have to die of cancer?

Man, this immortality stuff is confusing.

-Jester

[Occhidiangela]

Wait, are you saying that if I want to live forever, I have to die of cancer?

Man, this immortality stuff is confusing.

-Jester

Small wonder the Noldor finally went west, they got tired of all the chemotherapy: hell on the hair.

Occhi

[Ell_man]

The first thing that came to my mind when reading the message title was... Alex Chiu! Didn't he used to title his spam posts on the dsf that way? When looking up Alex Chiu on Wiki, I saw he had a slashdot interview! It's not really that funny but just the thought of him being interviewed seriously brings me a good chuckle.

I find this extremely funny too. (taken from Wikipedia)

"Alex sells Bible Decoder software which can presumably predict the future by observing the implications of code in the Old Testament."

-Ell_man

[Bun-Bun]

That fits quite differently from what I have seen other biologist say concerning cell division. There is something (Telemer?) that is attached to the genes in the cells that each time the gene is divided the portion lessens in lenght. Upon reaching a given length, the cell will no longer divide. This is why as people age skin and tissue will thin making it easier to injure and more difficult to heal from what I've read.

I believe the term is "telomere".

[kandrathe]

That fits quite differently from what I have seen other biologist say concerning cell division. There is something (Telemer?) that is attached to the genes in the cells that each time the gene is divided the portion lessens in lenght. Upon reaching a given length, the cell will no longer divide. This is why as people age skin and tissue will thin making it easier to injure and more difficult to heal from what I've read.

Telomere shortening in aging would most affect skin, stomach and intestine linings and some other cells that divide most quickly. But, death of cells due to telomere shortening can be overcome with telomerase. My view is that a longevity key is in a rejuvenated endocrine system that can keep a healthy level of enzyme function, and youthful immune system levels that would prevent mutations from developing into cancers.

Normal human cells have a finite lifespan in vitro, after which they cease dividing and undergo senescence (1). Tumour cells, however, will often divide indefinitely in vitro, and hence have overcome the normal limits to proliferation and are immortal. The molecular basis of senescence and immortalisation is not well understood, but one hypothesis for which there has recently been a large amount of evidence involves the shortening of telomeres. Human telomeres consist of large tracts of the 6 bp repeat TTAGGG (reviewed in ref. 2), which diminish in size as somatic human cells age, both in vitro and in vivo (3–8). Germline cells,
however, do not exhibit telomere shortening (9–11), and have been shown to have active telomerase (13), an enzyme which adds telomeric repeats to telomeres (12). It has been proposed that the expression of telomerase leads to stabilisation of telomere length and is a requirement for the immortalisation of human cells.
The telomere lengthening mechanism in polomerase-negative immortal human cells does not involve the telomerase RNA subunit, 1997 Oxford University Press, Human Molecular Genetics, 1997, Vol. 6, No. 6