Search results for "Heterozygote advantage"

showing 10 items of 56 documents

germline mutations in women with familial breast cancer and a relative with haematological malignancy

2009

Biallelic inactivation of the ATM gene causes ataxia-telangiectasia (A-T), a complex neurological disease associated with a high risk of leukaemias and lymphomas. Mothers of A-T children, obligate ATM heterozygote mutation carriers, have a breast cancer (BC) relative risk of about 3. The frequency of ATM carriers in BC women with a BC family history has been estimated to be 2.70%. To further our clinical understanding of familial BC and examine whether haematological malignancies are predictive of ATM germline mutation, we estimated the frequency of heterozygote mutation carriers in a series of 122 BC women with a family history of both BC and haematological malignancy and without BRCA1/2 m…

OncologyCancer ResearchLymphomaDNA Mutational AnalysisCell Cycle ProteinsAtaxia Telangiectasia Mutated Proteins0302 clinical medicineBreast cancerGene FrequencyRisk FactorsMissense mutationGenetics0303 health scienceseducation.field_of_studyLeukemiafamilial breast cancerAtaxia–telangiectasiaPedigreeDNA-Binding ProteinsOncology030220 oncology & carcinogenesisMutation (genetic algorithm)EMMAFemaleAdultHeterozygotemedicine.medical_specialtyMolecular Sequence DataPopulationBreast NeoplasmsProtein Serine-Threonine KinasesBiologyRisk Assessment03 medical and health sciencesGermline mutationBreast cancerPredictive Value of TestsInternal medicinemedicineHumansGenetic Predisposition to DiseaseGenetic TestingeducationAllele frequencyGerm-Line Mutation030304 developmental biologyBase SequenceTumor Suppressor ProteinsHeterozygote advantagemedicine.diseaseAtaxia-telangiectasia
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Familial hypercholesterolaemia: A global call to arms

2015

Familial Hypercholesterolaemia (FH) is the commonest autosomal co-dominantly inherited condition affecting man. It is caused by mutation in one of three genes, encoding the low-density lipoprotein (LDL) receptor, or the gene for apolipoprotein B (which is the major protein component of the LDL particle), or in the gene coding for PCSK9 (which is involved in the degradation of the LDL-receptor during its cellular recycling). These mutations result in impaired LDL metabolism, leading to life-long elevations in LDL-cholesterol (LDL-C) and development of premature atherosclerotic cardiovascular disease (ASCVD) [1], [2] and [3]. If left untreated, the relative risk of premature coronary artery d…

PathologyApolipoprotein BDisease030204 cardiovascular system & hematologymedicine.disease_causeGlobal HealthDISEASEDoenças Cardio e Cérebro-vasculares0302 clinical medicineHyperlipoproteinemia Type IISocieties MedicalRISK0303 health sciencesMutationbiology3. Good healthPREVALENCEEuropelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFamilial hypercholesterolaemiaLife Sciences & Biomedicinemedicine.medical_specialtyHeterozygote1102 Cardiovascular Medicine And HaematologyHyperlipoproteinemia Type II03 medical and health sciencesInternal medicinemedicineHumans030304 developmental biologyScience & Technologybusiness.industryGUIDANCEPCSK9Heterozygote advantage1103 Clinical SciencesEndocrinologyPeripheral Vascular DiseaseCardiovascular System & HematologyReceptors LDLRECEPTORES DE LIPOPROTEÍNASRelative riskMutationbiology.proteinCardiovascular System & CardiologyFamilial HypercholesterolaemiabusinessCLINICIANLipoprotein
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Lecithin-cholesterol-acyltransferase deficiency: autosomal recessive transmission in a large kindred.

2008

Thirty-four members of a single Sardinian kindred with lecithin-cholesterol-acyltransferase deficiency have been studied. The kindred spans four generations and the parents of the two affected siblings are blood relatives. Segregation of the acyltransferase deficiency gene in the family clearly demonstrated an autosomal recessive mode of inheritance. Thirteen family members, including all obligate heterozygotes, had roughly half-normal acyltransferase activities (mean +/- S.D. = 0.39 +/- 0.06 mU/ml) when compared to 17 intrafamilial controls and spouses (mean +/- S.D. = 0.72 +/- 0.09 mU/ml) and 40 blood donors from Marburg/Lahn (mean +/- S.D. =0.76 +/- 0.1 mU/ml). Characterization of the he…

Plasma lipoproteinMaleHeterozygoteThalassemiaLipoproteinsGenes RecessiveConsanguinityConsanguinityLecithin Cholesterol Acyltransferase DeficiencyGeneticsmedicineHumansGenetics (clinical)GeneticsLecithin cholesterol acyltransferase deficiencybiologyHeterozygote advantagemedicine.diseaseHypolipoproteinemiasPedigreeAcyltransferaseLecithin—cholesterol acyltransferasebiology.proteinThalassemiaFemaleHypolipoproteinemiaClinical genetics
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A family with various symptomatology suggestive of Anderson-Fabry disease and a genetic polymorphism of alpha galactosidase A gene.

2014

Background: Anderson/Fabry disease expresses a wide range of clinical variability in patients that it is possible to explain referring to a genetic variability with numerous mutations described in the literature (more than 600). Methods: We report some clinical cases of some members of a Sicilian family to express phenotypical variability of this disease in subjects with the same genetic mutation. Results: The first case was a 59-year-old female. Brain MRI revealed right frontal periventricular white matter of likely vascular-degenerative origin. The proband's alpha galactosidase A activity was 3.7. nmol/mL/h. Molecular genetics revealed a polymorphism: - 10 C. >. T; IVS 2-76_80del5; IVS…

ProbandAdultMalemedicine.medical_specialtyPathologySettore MED/09 - Medicina InternaAdolescentClinical BiochemistryMolecular Sequence DataBiologyAnderson-Fabry diseaseNucleic Acid DenaturationGastroenterologyPolymorphism (computer science)Internal medicineMolecular geneticsmedicineHaplotypeHumansFamilyGenetic Predisposition to DiseaseGenetic variabilitySymptomatologyChildPolymorphism GeneticBase SequenceHaplotypeHeterozygote advantageGeneral MedicineMiddle Agedmedicine.diseaseFabry diseaseMagnetic Resonance ImagingPedigreealpha-GalactosidaseFabry DiseaseMicroalbuminuriaFemaleHumanClinical biochemistry
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Additive effect of mutations in LDLR and PCSK9 genes on the phenotype of familial hypercholesterolemia.

2006

Patients homozygous or Compound heterozygous for LDLR mutations or double heterozygous for LDLR and apo B R3500Q mutation have higher LDL-C levels. more extensive xanthomatosis and more severe premature coronary disease (pCAD) than simple heterozygotes for mutations in either these genes or for missense mutations in PCSK9 gene. It is not known whether combined mutations in LDLR and PKCS9 are associated with such a severe phenotype. We sequenced Apo B and PCSK9 genes in two patients with the clinical diagnosis of homozygous FH who were heterozygous for LDLR gene mutations. Proband Z.P. (LDL-C 13.39 mmol/L and pCAD) was heterozygous for an LDLR mutation (p.E228K) inherited from her father (LD…

ProbandLDLR geneAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemia (FH); Autosomal dominant hypercholesterolemia 3 (ADH3); LDLR gene; PCSK9 gene; Premature coronary artery diseasePremature coronary artery diseaseLDLR PCSK9Mutation MissenseFamilial hypercholesterolemiaCompound heterozygositymedicine.disease_causeHyperlipoproteinemia Type IIFamilial hypercholesterolemia (FH) Autosomal dominant hypercholesterolemia 3 (ADH3) LDLR gene PCSK9 gene Premature coronary artery diseaseFamilial hypercholesterolemia (FH)medicineMissense mutationHumansCells CulturedGeneticsMutationbiologybusiness.industrySerine EndopeptidasesHeterozygote advantageMiddle Agedmedicine.diseaseAutosomal dominant hypercholesterolemia 3 (ADH3)PedigreePhenotypeSettore MED/03 - Genetica MedicaAmino Acid SubstitutionReceptors LDLPCSK9 geneLDL receptorbiology.proteinlipids (amino acids peptides and proteins)FemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessAtherosclerosis
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Lack of phenotypic additive effect of familial defective apolipoprotein B3531 in familial hypercholesterolaemia.

2020

Familial defective apolipoprotein (apo) B (FDB) and familial hypercholesterolaemia (FH) are the two common genetic conditions that cause hypercholesterolaemia. R3531C mutation of the APOB gene is a rare cause of FDB. Individuals with both FDB and FH are rare. A 51-year-old man with hypercholesterolaemia (11.4 mmol/L) and his family were studied. Low-density lipoprotein (LDL) receptor (LDLR) and APOB genes were analysed by direct sequencing. LDL of four subjects were studied in a fibroblast LDL receptor-binding displacement assay. We found a mutation of the LDLR gene (p.Y398X) in the proband and in four other family members: the p.R3531C APOB gene mutation was also found in the proband, his …

ProbandMalemedicine.medical_specialtyApolipoprotein B030204 cardiovascular system & hematologyCompound heterozygosityHyperlipoproteinemia Type II03 medical and health scienceschemistry.chemical_compoundFDB35310302 clinical medicineInternal medicineInternal MedicinemedicineHumans030212 general & internal medicineApolipoproteins Bdouble heterozygotebiologybusiness.industryCholesterolLDL receptornutritional and metabolic diseasesHeterozygote advantageMiddle AgedEndocrinologychemistryItalyReceptors LDLLDL receptorMutation (genetic algorithm)Mutationfamilial hypercholesterolaemiabiology.proteinlipids (amino acids peptides and proteins)businessLipoproteinInternal medicine journalReferences
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CC chemokine receptor 5Δ32 polymorphism-a risk factor for ischemic-type biliary lesions following orthotopic liver transplantation

2004

Ischemic-type biliary lesions are a major complication following orthotopic liver transplantation. They occur in up to 26% of liver transplant recipients. Among other factors, unknown immunologic factors have always been assumed to be partly responsible for these lesions. CC-chemokines and their receptors play a key role in postoperative immunomodulation after liver transplantation. The non-function CC-chemokine receptor 5Δ32 polymorphism (CCR5Δ32) has been shown to lead to a lower rate of acute rejection after kidney transplantation; in liver transplantation the role of CCR5Δ32 is unclear. We investigated the influence of the CCR5Δ32 after liver transplantation with special regard to ische…

TransplantationPathologymedicine.medical_specialtyHepatologyOrthotopic liver transplantationImmunologic Factorsbusiness.industrymedicine.medical_treatmentHeterozygote advantageLiver transplantationmedicine.diseaseGastroenterologyInternal medicinemedicineSurgeryMajor complicationReceptorbusinessCC chemokine receptorsKidney transplantationLiver Transplantation
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PGal4 excision reveals the pleiotropic effects of Voila, a Drosophila locus that affects development and courtship behaviour

2001

0016-6723 (Print) Journal Article Research Support, Non-U.S. Gov't; In Drosophila melanogaster, the PGal4 transposon inserted at the chromosomal site 86E1-2 is associated with the Voila1 allele that causes multiple phenotypes. Homozygous Voila1/1 flies rarely reach adulthood and heterozygous Voila1/+ adult males display strong homosexual courtship behaviour. Both normal behavioural and developmental phenotypes were rescued by remobilizing the PGal4 element. Yet, the rescue of heterosexual courtship and of adult viability did not occur in the same strains, indicating that these defects have different genetic origins. Furthermore, many strains showed a partial rescue of both characters. Molec…

Transposable elementMaleHeterozygoteEmbryo Nonmammalianmedia_common.quotation_subjectSexual BehaviorLocus (genetics)Nerve Tissue ProteinsLethalCourtshipSexual Behavior AnimalGeneticsAnimal/*physiologyAnimalsDrosophila ProteinsNerve Tissue Proteins/geneticsAlleleDrosophila melanogaster/*physiologyLarva/*growth & developmentmedia_commonGeneticsNonmammalianbiologyCourtship displayReproductionHomozygoteNuclear ProteinsHeterozygote advantageGeneral MedicineHomosexualitybiology.organism_classificationReproduction/geneticsNuclear Proteins/geneticsSurvival RateDrosophila melanogasterGenesEmbryoLarvaDNA Transposable ElementsGenes LethalFemaleDrosophila melanogaster5' Untranslated RegionsDrosophila ProteinTranscription Factors
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Signals of major histocompatibility complex overdominance in a wild salmonid population

2009

The major histocompatibility complex (MHC) contains the most variable genes in vertebrates, but despite extensive research, the mechanisms maintaining this polymorphism are still unresolved. One hypothesis is that MHC polymorphism is a result of balancing selection operating by overdominance, but convincing evidence for overdominant selection in natural populations has been lacking. We present strong evidence consistent with MHC-specific overdominance in a free-living population of Arctic charr (Salvelinus alpinus) in northernmost Europe. In this population, where just two MHC alleles were observed, MHC heterozygous fish had a lower parasite load, were in better condition (as estimated by a…

TroutPopulationOverdominanceBalancing selectionMajor histocompatibility complexGeneral Biochemistry Genetics and Molecular BiologyMajor Histocompatibility ComplexResearch articlesDiphyllobothriumPolymorphism (computer science)AnimalsAlleleeducationAllelesGeneral Environmental ScienceSalvelinusGeneticseducation.field_of_studyGenomePolymorphism GeneticGeneral Immunology and MicrobiologybiologyHeterozygote advantageGeneral Medicinebiology.organism_classificationBiological EvolutionEvolutionary biologybiology.proteinGeneral Agricultural and Biological SciencesMicrosatellite RepeatsProceedings of the Royal Society B: Biological Sciences
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Thymidylate synthase polymorphism and microsatellite instability: association in colorectal cancer.

2005

5-Fluorouracil (5FU) is the main drug used for the treatment of colorectal cancer (CRC) and Thymidilate Synthase (TS) is its target enzyme. TS gene has regulatory tandemly repeated sequences in its 5'' and 3''untraslated region (5''-3'' UTR). CRC often shows a kind of genomic instability called Microsatellite Instability (MSI) that is associated with TS levels and survival. Our data show that the genotype 2R/2R (homozygosity for 2 tandem repeat sequences in the 5''UTR) is more frequently associated with MSI+ and lower TS levels. More over we did not find any significant association between the 2R/3R (heterozygosity for 2 and 3 tandem repeat sequences in the 5''UTR) and 3R/3R (homozygosity f…

Untranslated regionGenome instabilityHeterozygoteGenotypeTranscription GeneticColorectal cancerBiologyBiochemistryThymidylate synthaseLoss of heterozygosityCell Line TumorGenotypeGeneticsmedicineHumansRNA MessengerneoplasmsGeneGeneticsPolymorphism GeneticChemistryMicrosatellite instabilityHeterozygote advantageGeneral MedicineThymidylate Synthasemedicine.diseaseMolecular biologydigestive system diseasesPhenotypeDrug Resistance NeoplasmProtein Biosynthesisbiology.proteinMolecular MedicineColorectal NeoplasmsMicrosatellite RepeatsNucleosides, nucleotidesnucleic acids
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