Search results for "Disposition"

showing 10 items of 832 documents

Impact of deleterious variants in other genes beyond BRCA1/2 detected in breast/ovarian and pancreatic cancer patients by NGS-based multi-gene panel …

2021

Background Hereditary breast cancer (BC), ovarian cancer (OC), and pancreatic cancer (PC) are the major BRCA-associated tumours. However, some BRCA1/2-wild-type (wt) patients with a strong personal and/or family history of cancer need a further genetic testing through a multi-gene panel containing other high- and moderate-risk susceptibility genes. Patients and methods Our study was aimed to assess if some BC, OC, or PC patients should be offered multi-gene panel testing, based on well-defined criteria concerning their personal and/or family history of cancer, such as earliness of cancer onset, occurrence of multiple tumours, or presence of at least two or more affected first-degree relativ…

OncologyCancer Researchmedicine.medical_specialtySettore MED/06 - Oncologia MedicaPALB2pancreatic cancerBreast NeoplasmsBreast cancerbreast cancerMUTYHInternal medicinePancreatic cancerMedicineHumansGenetic Predisposition to DiseaseGenetic TestingFamily historyCHEK2Original ResearchGenetic testingOvarian Neoplasmsmedicine.diagnostic_testbusiness.industryBRCA1 ProteinCancermedicine.diseasePancreatic Neoplasmsovarian cancerOncologymulti-gene panel testingFemalegermline pathogenic variantsbusiness
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Genetic determinants of ototoxicity during and after childhood cancer treatment: Protocol for the pancarelife study

2019

BACKGROUND: Survival rates after childhood cancer now reach nearly 80% in developed countries. However, treatments that lead to survival and cure can cause serious adverse effects with lifelong negative impacts on survivor quality of life. Hearing impairment is a common adverse effect in children treated with cisplatin-based chemotherapy or cranial radiotherapy. Ototoxicity can extend from high-tone hearing impairment to involvement of speech frequencies. Hearing impairment can impede speech and language and neurocognitive development. Although treatment-related risk factors for hearing loss following childhood cancer treatment have been identified, the individual variability in toxicity of…

OncologyCandidate gene020205 medical informaticscisplatinCHILDREN02 engineering and technologyVARIANTSPLATINUM-INDUCED OTOTOXICITYChildhood cancer survivors0302 clinical medicineTPMT0202 electrical engineering electronic engineering information engineeringProtocolGWASgenetics030212 general & internal medicineSURVIVORSGeneral MedicineCHEMOTHERAPY3. Good healthototoxicityCohortmedicine.symptomcandidate genes020 Library & information sciencesmedicine.medical_specialtyINDUCED HEARING-LOSSHearing losschildhood cancer survivors610 Medicine & healthINTERNATIONAL SOCIETYCandidate genes03 medical and health sciencesACYP2OtotoxicitySDG 3 - Good Health and Well-being360 Social problems & social servicesInternal medicinemedicineGenetic predispositionGeneticsCISPLATIN-INDUCED OTOTOXICITYAdverse effecthearing lossbusiness.industryCancerHearing lossmedicine.diseaseOtotoxicityClinical trialCisplatinbusinessPolymorphismspolymorphisms
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Association of candidate pharmacogenetic markers with platinum-induced ototoxicity

2020

Genetic association studies suggest a genetic predisposition for cisplatin-induced ototoxicity. Among other candidate genes, thiopurine methyltransferase (TPMT) is considered a critical gene for susceptibility to cisplatin-induced hearing loss in a pharmacogenetic guideline. The PanCareLIFE cross-sectional cohort study evaluated the genetic associations in a large pan-European population and assessed the diagnostic accuracy of the genetic markers. 1,112 pediatric cancer survivors who had provided biomaterial for genotyping were screened for participation in the pharmacogenetic association study. 900 participants qualified for inclusion. Based on the assessment of original audiograms, patien…

OncologyDrug-induced ototoxicitymedicine.medical_specialtyCandidate geneHearing lossMulticenter cohort studyCancer survivorsPopulationAdverse drug reaction610 Medicine & healthlcsh:Computer applications to medicine. Medical informatics03 medical and health sciences0302 clinical medicine360 Social problems & social servicesInternal medicinemedicineGenetic predisposition610 Medicine & healtheducationlcsh:Science (General)030304 developmental biologyGenetic association0303 health scienceseducation.field_of_studyMultidisciplinaryThiopurine methyltransferasebiologycarboplatin [Cisplatin]business.industryMedicine and DentistryPediatric cancerCisplatin: carboplatinPharmacogeneticsbiology.proteinlcsh:R858-859.7Genetic markersmedicine.symptombusinessChildhood cancer360 Social problems & social services030217 neurology & neurosurgeryPharmacogeneticslcsh:Q1-390Data in brief
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Associations between aromatase CYP19 rs10046 polymorphism and breast cancer risk: from a case-control to a meta-analysis of 20,098 subjects.

2012

Lifetime exposure to estrogen is a factor that plays an important role in the pathogenesis and progression of breast cancer. Genetic variants in genes of the biosynthesis and metabolism of estrogen have been associated with breast cancer risk. Among them, the CYP19 gene encodes for aromatase, the enzyme that catalyzes the conversion of androgens to estrogens. The rs10046 polymorphism on the CYP19 gene has been related to levels of circulating estradiol and to the estradiol/testosterone ratio. To date, epidemiological studies of rs10046 have been performed in different populations with contradictory results. In the present study, we have conducted a case-control analysis (522 cases and 1221 …

OncologyEpidemiologylcsh:MedicineBreast TumorsAromataselcsh:ScienceAged 80 and overMultidisciplinarybiologyObstetrics and GynecologyMiddle AgedOncologyMeta-analysisMedicineFemaleCancer EpidemiologyResearch ArticleAdultmedicine.medical_specialtyAdolescentmedicine.drug_classBreast NeoplasmsPolymorphism Single NucleotideYoung AdultBreast cancerAromataseInternal medicineGenetic modelBreast CancermedicineGeneticsHumansGenetic Predisposition to DiseaseAlleleBiologyAgedPopulation Biologylcsh:RCase-control studyReproducibility of ResultsCancers and NeoplasmsOdds ratiomedicine.diseaseEndocrinologyEstrogenCase-Control Studiesbiology.proteinGenetic PolymorphismWomen's Healthlcsh:QPopulation GeneticsPLoS ONE
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Germline loss-of-function variants in the BARD1 gene are associated with early-onset familial breast cancer but not ovarian cancer

2019

Background The role of the BARD1 gene in breast cancer (BC) and ovarian cancer (OC) predisposition remains elusive, as published case-control investigations have revealed controversial results. We aimed to assess the role of deleterious BARD1 germline variants in BC/OC predisposition in a sample of 4920 BRCA1/2-negative female BC/OC index patients of the German Consortium for Hereditary Breast and Ovarian Cancer (GC-HBOC). Methods A total of 4469 female index patients with BC, 451 index patients with OC, and 2767 geographically matched female control individuals were screened for loss-of-function (LoF) mutations and potentially damaging rare missense variants in BARD1. All patients met the …

OncologyGermline0302 clinical medicineLoss of Function MutationSurgical oncologyOdds RatioPrevalenceMissense mutation030212 general & internal medicineAge of Onset10. No inequalityExomeEarly onset breast cancerAged 80 and overOvarian NeoplasmsBARD1 GeneHigh-Throughput Nucleotide SequencingMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good health030220 oncology & carcinogenesisFemaleTechnology PlatformsResearch ArticleAdultmedicine.medical_specialtyAdolescentUbiquitin-Protein Ligases610Breast Neoplasmslcsh:RC254-282Young Adult03 medical and health sciencesGermline mutationBreast cancerOvarian cancerInternal medicinemedicineBARD1HumansGenetic Predisposition to DiseaseGermline mutationsGenetic Association StudiesGerm-Line MutationAgedbusiness.industryTumor Suppressor ProteinsOdds ratiomedicine.diseaseConfidence intervalBARD1; Early onset breast cancer; Germline mutations; Ovarian cancerOvarian cancerbusiness
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Analysis of Germline Gene Copy Number Variants of Patients with Sporadic Pancreatic Adenocarcinoma Reveals Specific Variations

2013

<b><i>Objectives:</i></b> The rapid fatality of pancreatic cancer is, in large part, the result of diagnosis at an advanced stage in the majority of patients. Identification of individuals at risk of developing pancreatic adenocarcinoma would be useful to improve the prognosis of this disease. There is presently no biological or genetic indicator allowing the detection of patients at risk. Our main goal was to identify copy number variants (CNVs) common to all patients with sporadic pancreatic cancer. <b><i>Methods:</i></b> We analyzed gene CNVs in leukocyte DNA from 31 patients with sporadic pancreatic adenocarcinoma and from 93 matched contr…

OncologyMaleCancer Researchmedicine.medical_specialtySettore MED/06 - Oncologia MedicaGene DosageCancer-associated genesBiologyAdenocarcinomaGene dosagePolymorphism Single NucleotideSensitivity and SpecificityGermlineGermline mutationGermline alterationsPolymorphism (computer science)Internal medicinePancreatic cancermedicinepancreatic adenocarcinomaHumansGenetic Predisposition to DiseaseCopy number variationsCopy-number variationGerm-Line MutationGermline alterationAgedCancer-associated geneCopy number variations; Cancer-associated genes; Germline alterations; Sporadic pancreatic cancerCopy number variationCase-control studyGeneral MedicineDNA NeoplasmMiddle Agedmedicine.diseasePancreatic NeoplasmsSporadic pancreatic cancerOncologyTissue Array AnalysisCase-Control StudiesAdenocarcinomaFemale
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Correction:Cancer risks by gene, age, and gender in 6350 carriers of pathogenic mismatch repair variants: findings from the Prospective Lynch Syndrom…

2020

Lynch syndrome (LS) results from pathogenic variants in the mismatch repair (MMR) genes and is the most common hereditary cancer syndrome, affecting an estimated 1 in 300 individuals. Pathogenic variants in each of the MMR genes path_MLH1, path_MSH2, path_MSH6, and path_PMS2 result in different risks for cancers in organs including the colorectum, endometrium, ovaries, stomach, small bowel, bile duct, pancreas, and upper urinary tract. Accurate estimates of these risks are essential for planning appropriate approaches to the prevention or early diagnosis of cancers but the robustness of previous studies has been limited by factors including retrospective design,1,2 lack of validation in ind…

OncologyMaleColorectal cancer*Lynch syndromePenetranceDNA Mismatch Repair0302 clinical medicineDatabases GeneticMalalties hereditàriesProspective StudiesCàncer*PMS2Genetics (clinical)Mismatch Repair Endonuclease PMS2Cancer0303 health sciencesSex CharacteristicsFactors de risc en les malalties1184 Genetics developmental biology physiologyMLH1Middle Aged16. Peace & justiceLynch syndrome3. Good healthDNA-Binding ProteinsMutS Homolog 2 Proteinsyöpägeenit*MSH2030220 oncology & carcinogenesis*MSH6030211 gastroenterology & hepatologyDNA mismatch repairFemalegeneettiset tekijätMutL Protein Homolog 1Genetic diseasesAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesRisk factors in diseasessuolistosyövätMUTATION CARRIERSMLH1Risk AssessmentArticlesukupuoliAge and gender03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLynchin oireyhtymäGene030304 developmental biologyAgedbusiness.industryEndometrial cancerCorrectionnutritional and metabolic diseasesCancer*MLH1MSH6medicine.diseaseColorectal Neoplasms Hereditary NonpolyposisSurvival Analysisdigestive system diseasesMSH2MSH6Lynch syndromePMS2MSH2Mutation3111 BiomedicineikäbusinessOvarian cancer
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Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes.

2019

International audience; Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional g…

OncologyMaleMultifactorial InheritanceLymphomaEpidemiologyChronic lymphocytic leukemiaFollicular lymphomaGenome-wide association studyDiseaseNeurodegenerativemeta-analysiimmune system diseasesHLA AntigensRisk Factorshemic and lymphatic diseases2.1 Biological and endogenous factorsHLA AntigenAetiologyGenetics (clinical)CancerAllele0303 health sciences[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyLymphoma Non-Hodgkinnon-Hodgkin lymphoma030305 genetics & hereditySingle NucleotideHematologyMiddle Aged3. Good healthnon-Hodgkin lymphoma.Public Health and Health ServicesFemaleHumanmedicine.medical_specialtyautoimmune disease; genome-wide association study; meta-analysis; non-Hodgkin lymphoma; Alleles; Autoimmune Diseases; Female; HLA Antigens; Humans; Lymphoma Non-Hodgkin; Male; Middle Aged; Multifactorial Inheritance; Polymorphism Single Nucleotide; Risk Factors; Genetic Predisposition to DiseaseNon-Hodgkinautoimmune diseasePolymorphism Single NucleotideArticleAutoimmune Diseases03 medical and health sciencesRare DiseasesInternal medicineGenetic variationmedicineGeneticsHumansGenetic Predisposition to DiseasePolymorphismAlleles030304 developmental biologyAutoimmune diseasegenome-wide association studybusiness.industryMultiple sclerosisRisk FactorArthritisInflammatory and immune systemHuman Genomemedicine.diseaseLymphomaBrain Disordersmeta-analysisbusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Acquired BRAF inhibitor resistance: A multicenter meta-analysis of the spectrum and frequencies, clinical behaviour, and phenotypic associations of r…

2015

BackgroundAcquired resistance to BRAF inhibitors (BRAFi) is a near-universal phenomenon caused by numerous genetic and non-genetic alterations. In this study, we evaluated the spectrum, onset, pattern of progression, and subsequent clinical outcomes associated with specific mechanisms of resistance.MethodsWe compiled clinical and genetic data from 100 patients with 132 tissue samples obtained at progression on BRAFi therapy from 3 large, previously published studies of BRAFi resistance. These samples were subjected to whole-exome sequencing and/or polymerase chain reaction-based genetic testing.ResultsAmong 132 samples, putative resistance mechanisms were identified in 58%, including NRAS o…

OncologyNeuroblastoma RAS viral oncogene homologMaleCancer ResearchSkin NeoplasmsTime FactorsResistanceDNA Mutational AnalysisDrug ResistanceMedizinKaplan-Meier EstimateBioinformaticsmedicine.disease_causeRisk Factors2.1 Biological and endogenous factorsAetiologyVemurafenibMelanomaCancerMutationTumorDabrafenibMelanomaAcquiredMiddle AgedPhenotypeEuropePhenotypeTreatment OutcomeSpliceOncologyMeta-analysisPublic Health and Health ServicesDisease ProgressionFemalemedicine.drugSignal TransductionProto-Oncogene Proteins B-rafmedicine.medical_specialtyOncology and CarcinogenesisNRASAntineoplastic AgentsBiologyDisease-Free SurvivalArticleBRAFMEK1Clinical ResearchInternal medicineGeneticsmedicineBiomarkers TumorHumansGenetic Predisposition to DiseaseOncology & CarcinogenesisProtein Kinase InhibitorsProportional Hazards ModelsProportional hazards modelAustraliaDabrafenibmedicine.diseaseMAPKUnited StatesMeta-analysisVemurafenibDrug Resistance NeoplasmMutationNeoplasmBiomarkersEuropean journal of cancer (Oxford, England : 1990)
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Impact of NPM1/FLT3-ITD genotypes defined by the 2017 European LeukemiaNet in patients with acute myeloid leukemia

2020

Contains fulltext : 218279.pdf (Publisher’s version ) (Open Access) Patients with acute myeloid leukemia (AML) harboring FLT3 internal tandem duplications (ITDs) have poor outcomes, in particular AML with a high (>/=0.5) mutant/wild-type allelic ratio (AR). The 2017 European LeukemiaNet (ELN) recommendations defined 4 distinct FLT3-ITD genotypes based on the ITD AR and the NPM1 mutational status. In this retrospective exploratory study, we investigated the prognostic and predictive impact of the NPM1/FLT3-ITD genotypes categorized according to the 2017 ELN risk groups in patients randomized within the RATIFY trial, which evaluated the addition of midostaurin to standard chemotherapy. The 4 …

OncologyPROBABILITIESMalePROGNOSISCancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2]NPM1 MUTATIONBiochemistryEuropean LeukemiaNetchemistry.chemical_compoundALLELIC RATIOAMLRisk FactorsGene Duplicationhemic and lymphatic diseasesMidostaurinFLT3Myeloid NeoplasiaHematopoietic Stem Cell TransplantationMyeloid leukemiaNuclear ProteinsHematologyCHEMOTHERAPYMiddle AgedPrognosisChemotherapy regimenEuropeLeukemia Myeloid Acutemedicine.anatomical_structureTreatment OutcomeTandem Repeat SequencesFemaleNucleophosminmedicine.medical_specialtyNPM1GenotypeImmunologyYOUNGER ADULTSInternal medicineWhite blood cellmedicineNORMAL CYTOGENETICSHumansGenetic Predisposition to DiseaseProportional Hazards ModelsProportional hazards modelbusiness.industryCell BiologyINTERNAL TANDEM DUPLICATIONTransplantationchemistryfms-Like Tyrosine Kinase 3Multivariate AnalysisbusinessSettore MED/15 - Malattie del Sangue
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