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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.


Lung can­cer cells in an image from a scan­ning elec­tron mi­cro­scope. (Cour­te­sy U.S. Centers for Disease Control)


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.


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Biologists say they’ve identified a gene that protects against cancer by suppressing cells’ ability to divide—but makes us age faster in the process. The findings suggest a profound tradeoff between long life and cancer protection is built into our bodies, the scientists said. The findings 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 answering a fundamental question about ageing in mammals: 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 new studies found that that the gene’s activity increases as progenitor 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.