PROSTHODONTICS - American College of Prosthodontists
PROSTHODONTICS - American College of Prosthodontists
PROSTHODONTICS - American College of Prosthodontists
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tightregulation<strong>of</strong>transcriptionalevents.Aspreviouslymentioned,inanefforttoensurefidelity<strong>of</strong>thecellcycle,error‐preventionmechanismsarepresentTheSixHallmarks<strong>of</strong>aCancerCell1.Self‐sufficiencyingrowthsignalsInnormalcircumstances,foracelltoundergocelldivision,mitogenicstimuliintheform<strong>of</strong>proliferation‐inducingproteinsinteractwithcellsurfacereceptorstomanipulatekeyintracellularpathwaystobegincelldivision.Indeed,cellsrelyontheseextra‐cellularsignalstoproliferate.Indentistry,tissue‐guidedregenerationintheform<strong>of</strong>boneaugmentationisincreasinglymakinguse<strong>of</strong>proteinssuchasplatelet‐derivedgrowthfactors,insulin‐likegrowthfactorsandfibroblastgrowthfactorstoenhancecellularproliferationandhenceimprovetheaugmentationoutcome.Inaddition,theuse<strong>of</strong>plateletrichplasmaisbasedupontheassumptionthatthispreparationisespeciallyrichingrowthfactors.Cancercells,incontrasttonormalcells,acquiretheabilitytoproliferatewithlessdependenceonnormalextracellularsignals.Threemechanismscanbeemployed:increasedmitogenicsignalproductionbyadjacentcells(whichimpliestheabilitytocontrolnearbycells)orbythemselves;modifyingthenumberand/ortype<strong>of</strong>cellsurfacereceptorsthatareresponsivetomitogenicsignals;andpresence<strong>of</strong>intracellularoncogenesthatpermitbypass<strong>of</strong>theneedforextracellularsignalingtoinducemitosis.2.Insensitivitytoanti‐growthsignalsJustasthereareextracellularsignalsthatinduceproliferation,thereareextracellularsignalsthatpreventproliferation.Theseanti‐proliferationsignalscanbeeithersolubleproteinsthatengagespecificcellsurfacereceptorsortheycanbecell‐cellinteractionsorcell‐extracellularmatrixinteractions.Theneteffect<strong>of</strong>all<strong>of</strong>thesemechanismsistopreventcellproliferationeitherbyinducingpassagetoG0(quiescence)orelsebycausingdifferentiationtothepointwhereacelllosesitsabilitytoproliferate.Therefore,acellintendingtoproliferateuntowardlyneedstoovercomeeitherorboth<strong>of</strong>theseanti‐growthmechanisms.EmergencefromG1isakeyregulatorystepandpro‐proliferationandanti‐proliferationsignalsaffectthisemergencetoasignificantdegree.Some<strong>of</strong>themolecularmechanismsinvolvedinmaintainingtheG1statepertaintothefunction<strong>of</strong>theretinoblastomaproteinanditsassociatesthatactanti‐proliferatively.Disruptionorinactivation<strong>of</strong>retinoblastomaproteinpathwayfunctions“releasesthebrake”,asitwere,andproliferationcanoccur.Inaddition,whereasspecificoncogenescaninduceproliferationbybypassingtheneedforextracellulargrowthsignals,otheroncogenescanimpedeprogression<strong>of</strong>acelltothedifferentiated,andhencenon‐proliferative,state.Inparticular,thec‐myconcogeneappearscapable<strong>of</strong>releasingtherestraintsoncellproliferationduetoinduction<strong>of</strong>terminalcelldifferentiation.3.EvadingapoptosisApoptosis,programmedcelldeath,isavitalmechanismtoensurethatcells“pasttheirprime”areremovedfromthesceneleavingthehealthiest,andconsequentlythemostusefulcellstocarryoutfunctionsvitaltissues,organsandtheentirebody.Histopathologicalevidenceindicatesthatlowerrates<strong>of</strong>apoptosisareseenincancertumoursthaninneighboringunaffectedtissues. 172010 CDEL Re-recognition <strong>of</strong> the Specialty Report 201 <strong>of</strong> 279
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