Search results for "Fanconi anemia"

showing 9 items of 19 documents

Fanconi's anaemia cells have normal steady-state levels and repair of oxidative DNA base modifications sensitive to Fpg protein

1998

Abstract Cells from Fanconi's anaemia (FA) patients are abnormally sensitive to oxygen. However, a distinct genetic defect in either the cellular defence against reactive oxygen species (ROS) or in their metabolic generation has not been identified to date. Recently, the gene for the human 8-hydroxyguanine (8-oxoG) glycosylase, which removes this oxidative base modification from the genome, has been localized on chromosome 3p25, i.e., in the same region as the FA complementation group D (FAD) gene. We therefore studied the removal of photosensitization-induced 8-oxoG residues from the DNA of FA cells, using Fpg protein, the bacterial 8-oxoG glycosylase, to quantify the lesions by alkaline e…

GuanineDNA RepairLightDNA repairBiologyToxicologymedicine.disease_causechemistry.chemical_compoundFanconi anemiaGeneticsmedicineHumansN-Glycosyl HydrolasesMolecular BiologyGeneCells CulturedPhotosensitizing AgentsDNAmedicine.diseaseMolecular biologyNuclear DNAComplementationOxidative StressFanconi AnemiaDNA-Formamidopyrimidine GlycosylaseBiochemistrychemistryDNA glycosylaseCell DivisionOxidative stressDNAMutation Research/DNA Repair
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Whole-exome sequencing and targeted gene sequencing provide insights into the role of PALB2 as a male breast cancer susceptibility gene

2016

Male breast cancer (MBC) is a rare disease whose etiology appears to be largely associated with genetic factors. BRCA1 and BRCA2 mutations account for about 10% of all MBC cases. Thus, a fraction of MBC cases are expected to be due to genetic factors not yet identified. To further explain the genetic susceptibility for MBC, whole-exome sequencing (WES) and targeted gene sequencing were applied to high-risk, BRCA1/2 mutation-negative MBC cases.Germ-line DNA of 1 male and 2 female BRCA1/2 mutation-negative breast cancer (BC) cases from a pedigree showing a first-degree family history of MBC was analyzed with WES. Targeted gene sequencing for the validation of WES results was performed for 48 …

MaleCancer ResearchDNA Mutational AnalysisBreast NeoplasmsBreast Neoplasms MaleDNA Mutational AnalysiGenetic susceptibility; Male breast cancer; N-acetyltransferase 1 (NAT1); Partner and localizer of BRCA2 (PALB2); Whole-exome sequencing; Oncology; Cancer ResearchGenetic susceptibilityHumansExomeGenetic Predisposition to DiseaseN-acetyltransferase 1 (NAT1)genetic susceptibility; male breast cancer; N-acetyltransferase 1 (NAT1); partner and localizer of BRCA2 (PALB2); whole-exome sequencing; BRCA1 Protein; BRCA2 Protein; Breast Neoplasms; Breast Neoplasms Male; Case-Control Studies; DNA Mutational Analysis; Exome; Fanconi Anemia Complementation Group N Protein; Female; Genetic Predisposition to Disease; Humans; Italy; Male; Mutation; Nuclear Proteins; Pedigree; Tumor Suppressor Proteins; Oncology; Cancer ResearchNuclear ProteinBRCA2 ProteinTumor Suppressor ProteinBRCA1 ProteinTumor Suppressor ProteinsPartner and localizer of BRCA2 (PALB2)Nuclear ProteinsPedigreeMale breast cancerItalyOncologyCase-Control StudiesWhole-exome sequencingMutationFemaleCase-Control StudieFanconi Anemia Complementation Group N ProteinBreast NeoplasmHuman
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Contribution of germline mutations in the BRCA and PALB2 genes to pancreatic cancer in Italy

2012

Pancreatic adenocarcinoma (PC) is the third most common cancer associated with BRCA mutations. Most notice has been given to BRCA2, while the association between BRCA1 and PC is less widely reported. Recently, PALB2 has been implicated in both PC and breast cancer (BC) susceptibility. We selected 29 Italian PC patients from a case-control study of PC according to their personal and family history of both PC and breast/ovarian cancer (BC/OC) and tested them for presence of germline mutations in BRCA1, BRCA2 and PALB2. We identified no germline mutations or deletions in PALB2, but detected 7 BRCA mutations (4 in BRCA1 and 3 in BRCA2). These findings suggest that PALB2 does not play a major ro…

MaleCancer Researchendocrine system diseasesSettore MED/06 - Oncologia MedicaBRCAGermlineGermline mutationHereditary breast ovarian cancer syndrome (HBOC)skin and connective tissue diseasesGenetics (clinical)Nuclear ProteinOvarian NeoplasmsAged 80 and overGeneticseducation.field_of_studyBRCA1 ProteinPancreatic NeoplasmNuclear ProteinsMiddle Agedfemale genital diseases and pregnancy complicationsPedigreeItalyOncologyAdenocarcinomaFemaleCase-Control StudieFanconi Anemia Complementation Group N ProteinPancreatic cancer susceptibility; BRCA; PALB2; Hereditary breast ovarian cancer syndrome (HBOC); Germline mutationBreast NeoplasmHumanAdultPALB2PopulationBreast NeoplasmsAdenocarcinomaGermline mutationBreast cancerGeneticPancreatic cancerGeneticsmedicineHumansGenetic Predisposition to DiseaseeducationGerm-Line MutationAgedBRCA2 ProteinTumor Suppressor Proteinbusiness.industryTumor Suppressor ProteinsOvarian NeoplasmCancermedicine.diseasePancreatic cancer susceptibilityPancreatic NeoplasmsCase-Control StudiesPALB2businessGene DeletionFamilial Cancer
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Gender- and age-related distinctions for the in vivo prooxidant state in Fanconi anaemia patients.

2004

Abstract Some selected oxidative stress parameters were measured in 56 Fanconi anaemia (FA) patients (42 untransplanted and 14 transplanted), 54 FA heterozygotes (parents) and 173 controls. Untransplanted FA patients showed a highly significant increase in leukocyte 8-hydroxy-2’-deoxyguanosine (8-OHdG) (p = 0.00003) and a borderline increase (p = 0.076) in urinary levels of 8-OHdG vs. child controls. These increases were more pronounced in female FA patients (p = 0.00005 for leukocyte 8-OHdG, and p = 0.021 for urinary 8-OHdG). Female FA patients also displayed a highly significant excess of spontaneous chromosomal breaks vs. male patients (p = 0.00026), in the same female:male ratio (≅ 1.4)…

MaleCancer Researchmedicine.medical_treatmentTransplantsUrineAscorbic Acidmedicine.disease_causechemistry.chemical_compoundLeukocytesChromosomes HumanVitamin EChildRespiratory BurstGlutathione DisulfideAge FactorsChromosome BreakageGeneral MedicinePyruvaldehydeGlutathioneBiochemistry8-Hydroxy-2'-DeoxyguanosineChild PreschoolFemaleOxidation-ReductionAdultmedicine.medical_specialtyHeterozygoteAdolescentUrinary systemBiologySex FactorsInternal medicinemedicineHumansVitamin CVitamin EDeoxyguanosineInfantGlutathioneDNAAscorbic acidUric AcidOxidative StressEndocrinologyFanconi AnemiachemistryCase-Control StudiesUric acidReactive Oxygen SpeciesOxidative stressCarcinogenesis
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Bone marrow cell transcripts from Fanconi anaemia patients revealin vivoalterations in mitochondrial, redox and DNA repair pathways

2013

Fanconi anaemia (FA) is a genetic cancer predisposition disorder associated with cytogenetic instability, bone marrow failure and a pleiotropic cellular phenotype, including low thresholds of responses to oxidative stress, cross-linking agents and selected cytokines. This study was aimed at defining the scope of abnormalities in gene expression using the publicly available FA Transcriptome Consortium (FTC) database (Gene Expression Omnibus, 2009 and publicly available as GSE16334). We evaluated the data set that included transcriptomal analyses on RNA obtained from low-density bone marrow cells (BMC) from 20 patients with FA and 11 healthy volunteers, by seeking to identify changes in expre…

MaleDNA Repairiron-chelating proteinsTranscriptome0302 clinical medicineFanconi anemiaGene expressioncytokineoxidative stressChildbioenergetic pathwayRegulation of gene expression0303 health sciencesHematologyGeneral Medicineheat-shock proteinMitochondria3. Good health030220 oncology & carcinogenesisFemaleFanconi anaemiaOxidation-ReductionSignal TransductionAdultiron-chelating proteinDNA repairDNA repairBone Marrow CellsBiologyProinflammatory cytokine03 medical and health sciencesmedicineHumanstranscriptsGene030304 developmental biologyoxidative streGene Expression Profilingheat-shock proteinsMolecular Sequence Annotationmedicine.diseaseMolecular biologycytokinesDNA repair Fanconi anaemia bioenergetic pathways cytokines heat-shock proteins iron-chelating proteins oxidative stress transcriptsGene expression profilingOxidative StressFanconi AnemiaCase-Control Studiesbioenergetic pathwaysTranscriptomeEuropean Journal of Haematology
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Cancer in Children With Fanconi Anemia and Ataxia-Telangiectasia—A Nationwide Register-Based Cohort Study in Germany

2021

PURPOSE Fanconi anemia (FA) and ataxia-telangiectasia (AT) are rare inherited syndromes characterized by abnormal DNA damage response and caused by pathogenic variants in key DNA repair proteins that are also relevant in the pathogenesis of breast cancer and other cancer types. The risk of cancer in children with these diseases is poorly understood and has never been assessed in a population-based cohort before. METHODS We identified 421 patients with FA and 160 patients with AT diagnosed between 1973 and 2020 through German DNA repair disorder reference laboratories. We linked patients' laboratory data with childhood cancer data from the German Childhood Cancer Registry. RESULTS Among 421 …

MaleOncologyRegister basedCancer Researchmedicine.medical_specialtyTime FactorsAdolescentDNA damageAnemiaDNA repairRisk AssessmentAtaxia TelangiectasiaRisk FactorsFanconi anemiaGermanyNeoplasmsInternal medicinemedicineHumansRegistriesChildbusiness.industryIncidenceAge FactorsInfantCancerPrognosismedicine.diseaseFanconi AnemiaOncologyChild PreschoolAtaxia-telangiectasiaFemalebusinessCohort studyJournal of Clinical Oncology
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Insight into genetic susceptibility to male breast cancer by multigene panel testing: results from a multicenter study in Italy

2019

Breast cancer (BC) in men is rare and genetic predisposition is likely to play a relevant role in its etiology. Inherited mutations in BRCA1/2 account for about 13% of all cases and additional genes that may contribute to the missing heritability need to be investigated. In our study, a well-characterized series of 523 male BC (MBC) patients from the Italian multicenter study on MBC, enriched for non-BRCA1/2 MBC cases, was screened by a multigene custom panel of 50 cancer-associated genes. The main clinical-pathologic characteristics of MBC in pathogenic variant carriers and non-carriers were also compared. BRCA1/2 pathogenic variants were detected in twenty patients, thus, a total of 503 n…

OncologyAdultMaleCancer Researchmedicine.medical_specialtyPALB2Adenomatous Polyposis Coli Proteinmale breast cancerGene mutationBreast Neoplasms MaleDNA GlycosylasesBRCA1/2; cancer susceptibility genes; germline mutations; male breast cancer; multigene panel testing03 medical and health sciencesYoung Adult0302 clinical medicinemultigene panel testingMUTYHMissing heritability problemBRCA1/2Internal medicinemedicineGenetic predispositionHumansGenetic Predisposition to Diseasecancer susceptibility genecancer susceptibility genesskin and connective tissue diseasesCHEK2Genetic Association StudiesAgedAged 80 and overbusiness.industryCase-control studySequence Analysis DNAMiddle Agedmedicine.diseaseCheckpoint Kinase 2germline mutationOncologyItaly030220 oncology & carcinogenesisMale breast cancerCase-Control StudiesMutationgermline mutationsbusinessFanconi Anemia Complementation Group N Protein
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From clinical description, to in vitro and animal studies, and backward to patients: Oxidative stress and mitochondrial dysfunction in Fanconi anemia

2013

Fanconi anemia (FA) is a rare genetic disease associated with deficiencies in DNA repair pathways. A body of literature points to a pro-oxidant state in FA patients, along with evidence for oxidative stress (OS) in the FA phenotype reported by in vitro, molecular, and animal studies. A highlight arises from the detection of mitochondrial dysfunction (MDF) in FA cell lines of complementation groups A, C, D2, and G. As yet lacking, in vivo studies should focus on FA-associated MDF, which may help in the understanding of the mitochondrial basis of OS detected in cells and body fluids from FA patients. Beyond the in vitro and animal databases, the available analytical devices may prompt the dir…

Pathologymedicine.medical_specialtyDNA RepairFree RadicalsDNA repairmitochondrial nutrientsCell Cycle ProteinsFree radicalsDiseaseBiologymedicine.disease_causeBioinformaticsBiochemistryChemopreventionPathogenesis03 medical and health sciencesMice0302 clinical medicineIn vivoFanconi anemiaPhysiology (medical)medicineAnimalsHumans030304 developmental biology0303 health sciencesMitochondrial nutrientNuclear ProteinsFanconi anemia Mitochondrial dysfunction Mitochondrial nutrients Chemoprevention Free radicalsmedicine.diseasePhenotype3. Good healthMitochondriaOxidative StressFanconi Anemia030220 oncology & carcinogenesisFanconi anemiaAnimal studiesReactive Oxygen SpeciesMitochondrial dysfunctionOxidative stress
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Understanding disease mechanisms with models of signaling pathway activities

2014

Background Understanding the aspects of the cell functionality that account for disease or drug action mechanisms is one of the main challenges in the analysis of genomic data and is on the basis of the future implementation of precision medicine. Results Here we propose a simple probabilistic model in which signaling pathways are separated into elementary sub-pathways or signal transmission circuits (which ultimately trigger cell functions) and then transforms gene expression measurements into probabilities of activation of such signal transmission circuits. Using this model, differential activation of such circuits between biological conditions can be estimated. Thus, circuit activation s…

Signaling pathwaysComputer scienceSystems biologyStem cellsDiseaseDrug actionComputational biologyModels BiologicalMiceSpecies SpecificityStructural BiologyModelling and SimulationAnimalsHumansComputer SimulationDiseaseObesityMolecular BiologyCancerRegulation of gene expressionInternetMechanism (biology)Methodology ArticleApplied MathematicsProbabilistic modelPrecision medicineStatistical modelPrecision medicineComputer Science ApplicationsGene Expression RegulationFanconi anemiaModeling and SimulationDisease mechanismSignal transductionAlgorithmBiomarkersSoftwareSignal TransductionBMC Systems Biology
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