The JAK2 V617F mutation in MPDs can be detected by a variety of methods. The simplest method is to isolate DNA from whole blood leukocytes and use PCR-direct sequencing. However, since the mutation is acquired and restricted to the myeloid lineage this method has a sensitivity of between 20 to 30%.NCBISkiptomaincontentSkiptonavigationResourcesHowToAboutNCBIAccesskeysMyNCBISignintoNCBISignOutJournalListUlsterMedJv.75(2);2006MayPMC1891745UlsterMedJ.2006May;75(2):112–119.PMCID:PMC1891745PMID:16755940JAK2V617F:ASingleMutationintheMyeloproliferativeGroupofDisordersDonalMcLornan,MelaniePercy,andMaryFrancesMcMullinAuthorinformationArticlenotesCopyrightandLicenseinformationDisclaimerDepartmentofHaematology,Queen'sUniversityBelfast,UFloor,BelfastCityHospital,LisburnRoad,Belfast,BT97AB,UKCorrespondencetoDrMcMullin.Email:[email protected]©TheUlsterMedicalSociety,2006ThisarticlehasbeencitedbyotherarticlesinPMC.Themyeloproliferativedisorders(MPD)areagroupofhaematologicalconditionswherethereisaprimarydisorderatthelevelofthemulti-potenthaematopoieticstemcellleadingtoincreasedproductioninoneormorebloodcelltypes.Thethreemaindisordersinthegrouparepolycythaemiavera(PV),essentialthrombocythaemia(ET)andidiopathicmyelofibrosis(IMF).PVischaracterisedbyanincreaseinredcells,whitecellsandplateletsandclinicallyaplethoricappearance,itchandsplenomegaly.Thediseasecanbecomplicatedbythromboembolicphenomenaandhaemorrhageandintheendstagescanprogresstomyelofibrosisandacuteleukaemia.ETischaracterisedbyanincreasedplateletcount.Clinicallyitisfrequentlyasymptomaticbutthethromboemboliceventsmayleadtodiseasedetection.Thereisasmallpropensitytoprogresstomyelofibrosisandacuteleukaemiawhichmaybeinfluencedbythetreatmentmodalitiesused.IMFisdefinedbyaleukoerythroblasticbloodpicture,splenomegalyandbonemarrowfibrosis.Thebloodpictureincludesanaemia,thrombocythaemiaorthrombocytopeniaandvariablewhitecellcounts.Thediseasefrequentlyprogressesinexorablytotransfusiondependentanaemia,symptomat

The JAK2 V617F is present in 95% to 98% of polycythemia vera, 50% to 60% of primary myelofibrosis (PMF), and 50% to 60% of essential thrombocythemia (ET).SkiptomaincontentSearchMayoClinicLaboratoriesMayoACCESSMayoLINKContactUsRegisterSignInTestCatalogAccountTESTCATALOGTestCatalogABCDEFGHIJKLMNOPQRSTUVWXYZ#TestInformationNewTestsTestUpdatesOrderYourFirstTestAlgorithmsTestsbyClassificationTypeNYStateInformedConsentTestsReferredTestsReferencesCriticalValues&ResultsPerformingLocationsTestPerformancePoliciesDownloadTestCatalogInterpretiveHandbookSpecialtyTestingAllergensCardiologyDrugTestingEndocrinologyFertilityGastroenterologyGeneticsHematologyMicrobiology&InfectiousDiseaseNeurologyNewbornScreening&PediatricsOncologyPathologyPrenatalRenalTherapeuticsORDERING&RESULTSMayoACCESSApplicationResourcesMayoLINKApplicationResourcesFrequentToolsAddTeststoanOrderOrderYourFirstTestCriticalValues&ResultsCustomGeneOrderingFormsFormListingNT/CRLDataFormPatientInformation&SignatureFormsMaternalScreeningLISResourcesNewTestsTestUpdatesCPTCode&TestClassificationUpdatesSetupFilesAOECodesUnitsofMeasureLOINCNYStateInformedConsentTestsSIConversionUnitsTestValidationSupportPDFReportsSPECIMENHANDLINGCollection&PreparationSuppliesInstructionsbySpecimenTypeMicrobiologyCultureTestsLightProtectionTestsUrinePreservativesPhlebotomistInstructionsShipping&LogisticsCustomizedInstructions&ShippingGuidesSpecimenTransportQuestionnaireCourierInstructionsTransportationRegulationsCategoryAInfectiousSubstancesCDCPermitDangerousGoodsTrainingCUSTOMERSERVICEContactUsPhoneNumbers&AddressesSalesRequestsPHISecureRequestsPatientRequestsBillingGeneralInternationalInsurancePriorAuthorizationCPTCode&TestClassificationUpdatesDEXZ-Codes™CMSDateofServiceReferencesQuality&ComplianceNewClientCenterFAQEDUCATION&INSIGHTSEducationalResourcesCaseStudiesConferencesDangerousGoodsTrainingOnDemandPodcastsWebinarsMLSCreditOurInsightsCOVID-19NewsPodcastsStoriesOutreachSolutionsTacticsArticlesEventsUtilizationManagementResourceCenterA

Background: The Janus kinase-2 (JAK-2) V617F mutation has been recently reported in patients with myeloproliferative disorders (MPD), which is believed to ...跳至主導覽跳至搜尋跳過主要內容PrevalenceoftheJAK2-V617FmutationinTaiwanesepatientswithchronicmyeloproliferativedisordersC.H.Lieu,H.S.Wu,Y.C.Hon,W.H.Tsai,C.F.Yang,C.C.Wang,Y.C.Lin,C.H.Shih,H.C.Hsu呼吸治療學系臺北醫學大學附設醫院胸腔內科臺北醫學大學胸腔醫學研究中心研究成果:雜誌貢獻›文章›同行評審10引文斯高帕斯（Scopus）總覽指紋摘要Background:TheJanuskinase-2(JAK-2)V617Fmutationhasbeenrecentlyreportedinpatientswithmyeloproliferativedisorders(MPD),whichisbelievedtounderliegrowthfactorhypersensitivitydisplayedbyhaematopoieticprogenitorsinthesedisorders.However,itsfrequencyhasbeenrarelydeterminedinTaiwanesepatients.Methods:ThefrequencyofJAK2-V617Fmutationinpatientswithpolycythaemiavera,essentialthrombocythaemiaandidiopathicmyelofibrosis(IMF)wasdeterminedintheDNAfromtheperipheralbloodleucocytesof108patientsbygenomicpolymerasechainreactionandrestrictionenzyme-basedassay.Results:TheJAK2-V617Fmutationcouldbedetectedin28of33polycythaemiaverapatients(85%),29of49essentialthrombocythaemiapatients(59%)and2of6IMFpatients(33%),butwasnotdetectedin11patientswithmyelodysplasticsyndromeoranother10withotherhaematologicaldiseases.ThepresenceoftheJAK2mutationwasassociatedwithspecificMPDdiseasesubtypes(P=0.007),longerdiseaseduration(P=0.005),splenomegaly(P=0.019),ahigherwhitebloodcellcount(P=0.002)andahigherhaemoglobinlevel(P=0.036).However,theoverallriskofthrombosisorbleedingwasnotaffectedbythepresenceoftheJAK2mutation(32vs17%;P=0.22).Conclusion:TheJAK2-V617FmutationcanbefrequentlydetectedintheTaiwanesepatientswithMPDdisordersandthereforeshouldbeincorporatedintotheinitialevaluationofpatientssuspectedofMPD.原文英語頁（從-到）422-426頁數5期刊InternalMedicineJournal卷38發行號6ADOIshttps://doi.org/10.1111/j.1445-5994.2007.01589.x出版狀態已發佈-六月2008ASJCScopussubjectareasInternalMedicine存取文件10.1111/j.1445-5994.2007.01589.x其它文件與鏈接LinktopublicationinScopusLinktocitationlistinScopusMyeloproliferativeDisordersMedicine&LifeSciencesMutationMedi

YouAreHere:Home→Genetics→Genes→JAK2geneURLofthispage:https://medlineplus.gov/genetics/gene/jak2/JAK2geneJanuskinase2FromGeneticsHomeReference.LearnmoreNormalFunctionTheJAK2geneprovidesinstructionsformakingaproteinthatpromotesthegrowthanddivision(proliferation)ofcells.ThisproteinispartofasignalingpathwaycalledtheJAK/STATpathway,whichtransmitschemicalsignalsfromoutsidethecelltothecell'snucleus.TheJAK2proteinisespeciallyimportantforcontrollingtheproductionofbloodcellsfromhematopoieticstemcells.Thesestemcellsarelocatedwithinthebonemarrowandhavethepotentialtodevelopintoredbloodcells,whitebloodcells,andplatelets.HealthConditionsRelatedtoGeneticChangesCrohndiseaseMedlinePlusGeneticsprovidesinformationaboutCrohndiseaseMoreAboutThisHealthConditionEssentialthrombocythemiaSomegenemutationsareacquiredduringaperson'slifetimeandarepresentonlyincertaincells.Thesechanges,whicharecalledsomaticmutations,arenotinherited.SomaticmutationsintheJAK2geneareassociatedwithessentialthrombocythemia,adisordercharacterizedbyanincreasednumberofplatelets,thebloodcellsinvolvedinnormalbloodclotting.Themostcommonmutation(writtenasVal617PheorV617F)replacestheproteinbuildingblock(aminoacid)valinewiththeaminoacidphenylalanineatposition617intheprotein.Thisparticularmutationisfoundinapproximatelyhalfofpeoplewithessentialthrombocythemia.AsmallnumberofaffectedindividualshaveasomaticmutationinanotherpartoftheJAK2geneknownasexon12.TheV617FJAK2genemutationresultsintheproductionofaJAK2proteinthatisconstantlyturnedon(constitutivelyactivated),which,inessentialthrombocythemia,leadstotheoverproductionofabnormalbloodcellscalledmegakaryocytes.Becauseplateletsareformedfrommegakaryocytes,theoverproductionofmegakaryocytesresultsinanincreasednumberofplatelets.Excessplateletscancauseabnormalbloodclotting(thrombosis),whichleadstomanysignsandsymptomsofessentialthrombocythemia.MoreAboutThisHealthConditionPolycythemiaveraSomaticmutationsintheJAK2geneareassociatedwithpolycythemiavera,adisordercharacterizedbyuncontrolledbloodce

JAK2 V617F mutation is acquired as opposed to inherited and results in the change of a single DNA nucleotide base pair. In JAK2, this kind of ...SkiptomaincontentJAK2MutationSendUsYourFeedbackChooseTopicAskaLaboratoryScientistAlsoKnownAsJanusKinase2FormalNameJAK2V617FJAK2Exon12MutationThisarticlewaslastreviewedonMarch6,2017.ThisarticlewaslastmodifiedonNovember15,2019.AtaGlanceWhyGetTested?Tohelpdiagnosebonemarrowdisordersknownasmyeloproliferativeneoplasms(MPNs)inwhichthebonemarrowproducestoomanyofoneormoretypesofbloodcellsWhenToGetTested?Whenyourhealthcarepractitionersuspectsthatyoumayhaveabonemarrowdisorder,includingpolycythemiavera,essentialthrombocythemia,orprimarymyelofibrosisSampleRequired?AbloodsampledrawnfromaveininyourarmorsometimesasampleofbonemarrowTestPreparationNeeded?NoneLookingforTestResults?Youmaybeabletofindyourtestresultsonyourlaboratory'swebsiteorpatientportal.However,youarecurrentlyatLabTestsOnline.Youmayhavebeendirectedherebyyourlab'swebsiteinordertoprovideyouwithbackgroundinformationaboutthetest(s)youhadperformed. Youwillneedtoreturntoyourlab'swebsiteorportal,orcontactyourhealthcarepractitioner inordertoobtain yourtestresults.LabTestsOnlineisanaward-winningpatienteducationwebsiteofferinginformationonlaboratorytests.Thecontentonthesite,whichhasbeenreviewedbylaboratoryscientistsandothermedicalprofessionals, providesgeneralexplanationsofwhatresultsmightmeanforeachtestlistedonthesite,suchaswhatahighorlowvaluemightsuggesttoyourhealthcarepractitioner aboutyourhealthormedicalcondition.LookingforReferenceRanges?Thereferencerangesforyourtestscanbefoundonyourlaboratoryreport.Theyaretypicallyfoundtotherightofyourresults.Ifyoudonothaveyourlabreport,consultyourhealthcareproviderorthelaboratorythatperformedthetest(s)toobtainthereferencerange.Laboratorytestresultsarenotmeaningfulbythemselves.Theirmeaningcomesfromcomparisontoreferenceranges.Referencerangesarethevaluesexpectedforahealthyperson.Theyaresometimescalled"normal"values.Bycomparingyourtestresultswithre

The JAK2V617F tyrosine kinase mutation identifies clinically latent myeloproliferative disorders in patients presenting with hepatic or portal vein thrombosis. Int J ...SkiptoMainContentAdvertisementCloseBloodBloodAdvancesHematologyASH-SAPASHClinicalNewsTheHematologistInternationalBloodChineseEditionBloodJapaneseEditionBloodItalianEditionBloodLatinAmericaEditionBloodSpanishEditionASHASHHomeResearchEducationAdvocacyMeetingsPublicationsASHStoreCartUserToolsCartSignInSearchsearchinputSearchinputautosuggestsearchfilterAllContentAllJournalsBloodSearchToggleMenuMenuIssuesCurrentIssueAllIssuesFirsteditionAbstracts2020AnnualMeeting2020LateBreaking2019AnnualMeeting2019LateBreaking2018AnnualMeetingAllMeetingAbstractsCollectionsCollectionsSpecialCollectionsMultimediaAlertsAuthorCenterSubmitAuthorGuideStyleGuideWhySubmittoBlood?AboutAboutBloodEditorialBoardandStaffSubscriptionsPublicAccessCopyrightAlertsBloodClassifiedsSkipNavDestinationContentMenuCloseMethodsResultsDiscussionAuthorshipAppendix:MedlinesearchstrategyReferencesArticleNavigationTHROMBOSISANDHEMOSTASIS|May28,2009JAK2V617FmutationfortheearlydiagnosisofPh−myeloproliferativeneoplasmsinpatientswithvenousthromboembolism:ameta-analysisFrancescoDentali,FrancescoDentali1DepartmentofClinicalMedicine,UniversityofInsubria,Varese,Italy;andSearchforotherworksbythisauthoron:ThisSitePubMedGoogleScholarAlessandroSquizzato,AlessandroSquizzato1DepartmentofClinicalMedicine,UniversityofInsubria,Varese,Italy;andSearchforotherworksbythisauthoron:ThisSitePubMedGoogleScholarLorenzaBrivio,LorenzaBrivio1DepartmentofClinicalMedicine,UniversityofInsubria,Varese,Italy;andSearchforotherworksbythisauthoron:ThisSitePubMedGoogleScholarLorenaAppio,LorenaAppio1DepartmentofClinicalMedicine,UniversityofInsubria,Varese,Italy;andSearchforotherworksbythisauthoron:ThisSitePubMedGoogleScholarLeonardoCampiotti,LeonardoCampiotti1DepartmentofClinicalMedicine,UniversityofInsubria,Varese,Italy;andSearchforotherworksbythisauthoron:ThisSitePubMedGoogleScholarMark

It has been demonstrated that the JAK2 V617F point mutation, a common molecular genetic abnormality, occurs in polycythemia vera (PV), essential thrombocythemia histiocytosis (ET) and primary myelofibrosis (PMF); therefore, the JAK2 mutation may be an important diagnostic tool for the detection of myeloproliferative ...HomeSubmitManuscriptMyAccountOncologyLettersJournalHomeCurrentIssueForthcomingIssueMostReadMostCited(Dimensions)PastTwoYearsTotalMostCited(CrossRef)PastYear0TotalSocialMediaPastMonthPastYearTotalArchiveInformationOnlineSubmissionInformationforAuthorsLanguageEditingInformationforReviewersEditorialPoliciesEditorialBoardAimsandScopeAbstractingandIndexingBibliographicInformationInformationforLibrariansInformationforAdvertisersReprintsandpermissionsContacttheEditorGeneralInformationAboutSpandidosConferencesJobOpportunitiesContactTermsandConditionsDetectionofJAK2V617FmutationincreasesthediagnosisofmyeloproliferativeneoplasmsAuthors:Shu‑PengZhangHuiLiRen‑ShengLaiViewAffiliationsAffiliations:DepartmentofPathology,TheAffiliatedHospitalofNanjingUniversityofTraditionalChineseMedicine,Nanjing,Jiangsu210029,P.R.ChinaPublishedonlineon:December12,2014   https://doi.org/10.3892/ol.2014.2801Pages:735-738Metrics:TotalViews:0(SpandidosPublications:|PMCStatistics:)Metrics:TotalPDFDownloads:0(SpandidosPublications:|PMCStatistics:)CitedBy(CrossRef):0citationsLoadingArticles...Thisarticleismentionedin:AbstractTheJanuskinase(JAK)2gene,whichislocatedonchromosome9p24,isinvolvedinthesignalingtransductionpathwaysofthehematopoieticandimmunesystem.MutationsintheJAK2genehaveservedasdiseasemarkersformyeloproliferativeneoplasms(MPNs).TheaimofthepresentstudywastoinvestigatetheoccurrenceoftheJAK2genemutationin140 clinicalsamples,andtoevaluateitsclinicalsignificanceinMPNsandotherhematologicaldiseases.GenomicDNAwasextractedfromtheperipheralbloodleukocytesorbonemarrowkaryocytesof140 clinicalsamples,whichincluded130 patientswithvarioustypesofhematologicaldiseaseand10 controlpatients.Inaddi

NCBISkiptomaincontentSkiptonavigationResourcesHowToAboutNCBIAccesskeysMyNCBISignintoNCBISignOutJournalListBloodPMC1895065Blood.2005Nov15;106(10):3370–3373.Prepublishedonline2005Jul21.doi: 10.1182/blood-2005-05-1800PMCID:PMC1895065PMID:16037387JAK2mutation1849G>TisrareinacuteleukemiasbutcanbefoundinCMML,Philadelphiachromosome–negativeCML,andmegakaryocyticleukemiaJaroslavJelinek,YasuhiroOki,VazganushGharibyan,CarlosBueso-Ramos,JosefT.Prchal,SrdanVerstovsek,MiloslavBeran,ElihuEstey,HagopM.Kantarjian,andJean-PierreJ.IssaAuthorinformationArticlenotesCopyrightandLicenseinformationDisclaimerFromtheDepartmentsofLeukemiaandHematopathology,TheUniversityofTexasM.D.AndersonCancerCenter,Houston,TX;BaylorCollegeofMedicineandMichaelDeBakeyVeteransAdministrationHospital,Houston,TX;andtheDepartmentofPathophysiology,FirstFacultyofMedicine,CharlesUniversity,Prague,CzechRepublic.Reprints:JaroslavJelinek,DepartmentofLeukemia,TheUniversityofTexasM.D.AndersonCancerCenter,Unit428,1515HolcombeBlvd,Houston,TX77030;e-mail:[email protected];Accepted2005Jul9.Copyright©2005,TheAmericanSocietyofHematologyThisarticlehasbeencitedbyotherarticlesinPMC.Anactivating1849G>TmutationofJAK2(Januskinase2)tyrosinekinasewasrecentlydescribedinchronicmyeloproliferativedisorders(MPDs).Itsroleinotherhematologicneoplasmsisunclear.Wedevelopedaquantitativepyrosequencingassayandanalyzed374samplesofhematologicneoplasms.Themutationwasfrequentinpolycythemiavera(PV)(86%)andmyelofibrosis(95%)butlessprevalentinacutemyeloidleukemia(AML)withanantecedentPVormyelofibrosis(5[36%]of14patients).JAK2mutationwasalsodetectedin3(19%)of16patientswithPhiladelphia-chromosome(Ph)–negativechronicmyelogenousleukemia(CML),2(18%)of11patientswithmegakaryocyticAML,7(13%)of52patientswithchronicmyelomonocyticleukemia,and1(1%)of68patientswithmyelodysplasticsyndromes.NomutationwasfoundinPh+CML(99patients),AMLM0-M6(28patients),oracutelymphoblasticleukemia(20patients).WeconcludethattheJAK21849G>TmutationiscommoninPh–MPDbutnotc

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NCBISkiptomaincontentSkiptonavigationResourcesHowToAboutNCBIAccesskeysMyNCBISignintoNCBISignOutJournalListHaematologicav.96(3);2011MarPMC3046277Haematologica.2011Mar;96(3):450–453.Publishedonline2010Dec15.doi: 10.3324/haematol.2010.033191PMCID:PMC3046277PMID:21160067TheJAK2V617Fsomaticmutation,mortalityandcancerriskinthegeneralpopulationCamillaNielsen,1HenrikS.Birgens,2BørgeG.Nordestgaard,1,3LasseKjær,2andStigE.Bojesen1,3CamillaNielsen1DepartmentofClinicalBiochemistryandFindarticlesbyCamillaNielsenHenrikS.Birgens2DepartmentofHematology,HerlevHospital,CopenhagenUniversityHospitalFindarticlesbyHenrikS.BirgensBørgeG.Nordestgaard1DepartmentofClinicalBiochemistryand3TheCopenhagenCityHeartStudy,BispebjergHospital,CopenhagenUniversityHospitalandFindarticlesbyBørgeG.NordestgaardLasseKjær2DepartmentofHematology,HerlevHospital,CopenhagenUniversityHospitalFindarticlesbyLasseKjærStigE.Bojesen1DepartmentofClinicalBiochemistryand3TheCopenhagenCityHeartStudy,BispebjergHospital,CopenhagenUniversityHospitalandFindarticlesbyStigE.BojesenAuthorinformationArticlenotesCopyrightandLicenseinformationDisclaimer1–3FacultyofHealthSciences,UniversityofCopenhagen,Denmark1DepartmentofClinicalBiochemistryand2DepartmentofHematology,HerlevHospital,CopenhagenUniversityHospital3TheCopenhagenCityHeartStudy,BispebjergHospital,CopenhagenUniversityHospitalandCorrespondence:StigE.Bojesen,DepartmentofClinicalBiochemistry,54M1,HerlevHospital,CopenhagenUniversityHospital,HerlevRingvej75,2730Herlev,Denmark.Phone:international+45.44883843.Fax:international+45.44883311.E-mail:kd.hnoiger.heh@obetsCNandHSBcontributedequallytothismanuscript.Received2010Sep17;Revised2010Nov24;Accepted2010Dec13.Copyright©FerrataStortiFoundationThisarticlehasbeencitedbyotherarticlesinPMC.JAK2V617Fispresentinthemajorityofpatientswithmyeloproliferativecancer;however,itsprevalenceandclinicalsignificanceinthegeneralpopulationisunknown.Wescreenedforpresenceofthemutationin10,507participantsfromtheCopenhagenCityHeartStudywithupto17.6yearso