Search results for "MESH: Heterozygote"

showing 2 items of 2 documents

Presence of calreticulin mutations in JAK2-negative polycythemia vera

2014

Abstract Calreticulin (CALR) mutations have recently been reported in JAK2- and MPL-negative Myeloproliferative Neoplasms (MPN), particularly essential thrombocythemia (ET) and primary myelofibrosis (PMF).The clinical course of sporadic CALR-mutated patients seems to be more indolent than that of JAK2-mutated patients. In contrast, no CALR mutation has been found in the 647 published cases of Polycythemia Vera (PV) patients tested. Consequently, CALR mutations were considered exclusive to JAK2 and MPL mutations. Since 98% of PV patients harbor a JAK2 mutation (mostly the V617F mutation in exon 14 and more rarely, in exon 12), the absence of CALR mutations in PV seemed logical. Here, we desc…

MaleErythrocytesMESH: Thrombocytosismedicine.disease_causeMESH: Polycythemia VeraBiochemistryMESH: Janus Kinase 2MESH: GenotypeHemoglobinsMESH: Aged 80 and overPolycythemia verahemic and lymphatic diseasesPolycythemia VeraMESH: HeterozygoteAged 80 and overThrombocytosisMESH: AgedMutation[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyJanus kinase 2biologyMESH: ErythrocytesExonsHematologyLeukemiaMESH: HemoglobinsMESH: Primary MyelofibrosisThrombocythemia EssentialHeterozygoteMESH: MutationGenotypeMESH: CalreticulinImmunologyContext (language use)medicineHumansMyelofibrosisAllelesAgedMESH: HumansEssential thrombocythemiabusiness.industryMESH: AllelesCell BiologyJanus Kinase 2medicine.diseaseMESH: MalePrimary MyelofibrosisMESH: Gene DeletionMutationImmunologybiology.proteinCancer researchMESH: Thrombocythemia EssentialCalreticulinMESH: ExonsbusinessCalreticulinGene Deletion[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyBlood
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Increased Activity of Coagulation Factor XII (Hageman Factor) Causes Hereditary Angioedema Type III

2006

International audience; Hereditary angioedema (HAE) is characterized clinically by recurrent acute skin swelling, abdominal pain, and potentially life-threatening laryngeal edema. Three forms of HAE have been described. The classic forms, HAE types I and II, occur as a consequence of mutations in the C1-inhibitor gene. In contrast to HAE types I and II, HAE type III has been observed exclusively in women, where it appears to be correlated with conditions of high estrogen levels--for example, pregnancy or the use of oral contraceptives. A recent report proposed two missense mutations (c.1032C-->A and c.1032C-->G) in F12, the gene encoding human coagulation factor XII (FXII, or Hageman factor…

MaleTime FactorsKinins030204 cardiovascular system & hematologyMESH: Founder Effect[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityLinkage Disequilibrium0302 clinical medicineMissense mutationHereditary Angioedema Type IIIGenetics(clinical)MESH: Models GeneticGenetics (clinical)MESH: Heterozygote0303 health sciencesFactor XII[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyFounder EffectMarkov ChainsPedigree3. Good healthMESH: Linkage DisequilibriumFactor XIIHereditary angioedemaFemalemedicine.symptomMESH: Factor XIIHeterozygotemedicine.medical_specialtyMESH: MutationMESH: PedigreeMESH: Bayes TheoremCoagulation Factor XIIBiology03 medical and health sciencesMESH: Markov ChainsReportInternal medicinemedicineGeneticsHumansMESH: AngioedemaAngioedema030304 developmental biologyMESH: HumansModels GeneticAngioedemaHaplotypeMESH: Time FactorsBayes TheoremHeterozygote advantageMESH: Haplotypesmedicine.diseaseMESH: KininsMESH: MaleEndocrinologyHaplotypesMutationImmunologyMESH: Microsatellite RepeatsMESH: FemaleMicrosatellite RepeatsThe American Journal of Human Genetics
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