Atleastbasedonstatisticsfromanimalsincaptivityin a massive 2019 genome, studymighthaverevealedwhy, in a paperpublishedinthejournalScience, researchersanalyzethegenomesofcertainspeciesofdeeralongwithdozensofrelatedspecies, andthegeneticchangestheyfoundinthedeerDNAgo a longwaytowardsexplainingbothhowantlersgrowsofastandhowthatgrowthdoesn't leadtocancer.
Moreoffusuallysellsgrowing, anddividingtoofastis a problem.
A tumorcanceriswhathappenswhenthoseuncontrolledcellsbecomemalignant, capableofescapingtootherpartsofthebodyandcausingextracelldivisionThere, too, withtheirsuperfastgrowthantlersbearsomeresemblancetotumors.
Infact, the 2019 studyfoundthatintermsofwhatgenestheyexpress, antlercellsaremorelikebonecancerthanregularbone.
AnycancerbiologistwilltellyouthatFossisreally, reallymeanddearstronglyexpressedfalseand a bunchofothergenesthatcanleadtocancer.
Butitturnsoutdearalsohavegeneticchangestokeepallthatextracelldivisionfromturningintocancer, mainlyinvolving P 53 sometimesknownasthemastertumorsuppressor, P 53 makes a proteinthatcheckssellsforDNAdamage.
Ifthedamageisflexible, the P 53 proteintellsthecelltorepairit.
Ifit's notfixable, itmakesthecellselfdestruct.
Elephants, whichalsohaveverylowcancerrates, haveextracopiesofthe P 53 geneintheirDNA.
Researchersthinkthat's a bigpartofwhatmakesthemlesspronetocancer.
Deardon't haveextracopies.
Instead, they'veevolvedmoregenestosupportwhat P 53 doesandhelpitalong.
They'vealsoevolved a bunchofothertumorsuppressorgenesspecificallyexpressedintheirantlers.