Search results for "Germ-Line Mutation"

showing 8 items of 48 documents

Patterns of Prior and Subsequent Neoplasms in Children and Adolescents With Soft Tissue Sarcomas.

2020

Background The occurrence of prior, concurrent and subsequent neoplasms (SN) represents a serious problem in children and adolescents with soft tissue sarcomas. Pathogenic germline variants contribute to the diagnosis of multiple neoplasms in sarcoma survivors. Materials and methods The records of 748 children and adolescents, diagnosed with soft tissue sarcomas and registered in trials/registries by the cooperative soft tissue sarcoma (Cooperative Weichteilsarkom Studie) group, were reviewed for the occurrence of SNs. Reference histology review was available for all cases; the presence of oncogenic fusions known at the time of diagnosis was confirmed for fusion-positive (F+) entities. Resu…

OncologyMalemedicine.medical_specialtyAdolescentOncogene Proteins FusionGermline03 medical and health sciences0302 clinical medicineCancer SurvivorsRisk FactorsInternal medicineGermanyBiomarkers TumorMedicineHumansRegistriesNeurofibromatosisChildGerm-Line MutationClinical Trials as Topicbusiness.industryIncidence (epidemiology)Soft tissue sarcomaIncidenceSoft tissueInfantHistologyNeoplasms Second PrimarySarcomaHematologymedicine.diseasePrognosisCombined Modality TherapySurvival RateOncology030220 oncology & carcinogenesisChild PreschoolPediatrics Perinatology and Child HealthFemaleSarcomabusiness030215 immunologyFollow-Up StudiesJournal of pediatric hematology/oncology
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Pathology of Breast and Ovarian Cancers among BRCA1 and BRCA2 Mutation Carriers: Results from the Consortium of Investigators of Modifiers of BRCA1/2…

2012

Abstract Background: Previously, small studies have found that BRCA1 and BRCA2 breast tumors differ in their pathology. Analysis of larger datasets of mutation carriers should allow further tumor characterization. Methods: We used data from 4,325 BRCA1 and 2,568 BRCA2 mutation carriers to analyze the pathology of invasive breast, ovarian, and contralateral breast cancers. Results: There was strong evidence that the proportion of estrogen receptor (ER)-negative breast tumors decreased with age at diagnosis among BRCA1 (P-trend = 1.2 × 10−5), but increased with age at diagnosis among BRCA2, carriers (P-trend = 6.8 × 10−6). The proportion of triple-negative tumors decreased with age at diagnos…

OncologyPathologyendocrine system diseasesEpidemiologyGenes BRCA2Genes BRCA1Estrogen receptorGene mutation0302 clinical medicineCancer screeningMedicineskin and connective tissue diseasesEstrogen Receptor StatusOvarian Neoplasms0303 health sciencesMiddle Agedfemale genital diseases and pregnancy complications3. Good healthSerous fluidtriple-negative tumorsOncology030220 oncology & carcinogenesisFemaleestrogen receptorAdultmedicine.medical_specialtyBRCA1; BRCA2; breast cancer; estrogen receptor; triple-negative tumorsHereditary cancer and cancer-related syndromes Genetics and epigenetic pathways of disease [ONCOL 1]Breast NeoplasmsArticle03 medical and health sciencesbreast cancerBreast cancerSDG 3 - Good Health and Well-beingTranslational research [ONCOL 3]Internal medicineHumansGenetic Predisposition to DiseaseGenetics and epigenetic pathways of disease Translational research [NCMLS 6]Germ-Line MutationAged030304 developmental biologyHereditary cancer and cancer-related syndromes [ONCOL 1]business.industryCancerBRCA1medicine.diseaseBRCA2Neoplasm GradingbusinessOvarian cancer
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Time-point and dosage of gene inactivation determine the tumor spectrum in conditional Ptch knockouts

2009

Mutations in Patched (PTCH) have been associated with tumors characteristic both for children [medulloblastoma (MB) and rhabdomyosarcoma (RMS)] and for elderly [basal cell carcinoma (BCC)]. The determinants of the variability in tumor onset and histology are unknown. We investigated the effects of the time-point and dosage of Ptch inactivation on tumor spectrum using conditional Ptch-knockout mice. Ptch heterozygosity induced prenatally resulted in the formation of RMS, which was accompanied by the silencing of the remaining wild-type Ptch allele. In contrast, RMS was observed neither after mono- nor biallelic postnatal deletion of Ptch. Postnatal biallelic deletion of Ptch led to BCC preca…

PatchedPatched ReceptorsCancer ResearchPathologymedicine.medical_specialtyAgingSkin NeoplasmsGene DosageReceptors Cell SurfaceBiologymedicine.disease_causeGene dosageGastrointestinal epitheliumLoss of heterozygosity03 medical and health sciencesMice0302 clinical medicineRhabdomyosarcomamedicineAnimalsGene SilencingRhabdomyosarcomaMuscle SkeletalGerm-Line MutationPeritoneal Neoplasms030304 developmental biologyGastrointestinal NeoplasmsMedulloblastomaMice Knockout0303 health sciencesMutationMuscle NeoplasmsCystsGeneral MedicinePTCH1 Genemedicine.disease3. Good healthPatched-1 Receptorstomatognathic diseasesCarcinoma Basal Cell030220 oncology & carcinogenesisMutationCancer researchPrecancerous ConditionsCarcinogenesis
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Y179C, F486L and N550H are BRCA1 variants that may be associated with breast cancer in a Sicilian family: results of a 5-year GOIM (Gruppo Oncologico…

2006

Background Over 600 different pathogenic mutations have been identified in the BRCA1 gene. Nevertheless, numerous missense mutations of unknown biological function still exist. Understanding of biological significance of these mutations should help in genetic counselling to carriers and their families. Patients and methods A total of 104 patients with breast and/or ovarian cancer whose genetic counselling answered the criteria of the American Society of Clinical Oncology (ASCO 2003), were prospectively screened for mutations in all coding exons of the BRCA1 gene by automatic direct sequencing. Results During these mutational screening procedures one case presented three mutations classified…

ProbandAdultmedicine.medical_specialtyProtein ConformationGenetic counselingGenes BRCA1Mutation MissenseBreast NeoplasmsGenetic CounselingExonBreast cancermedicineMissense mutationHumansProspective StudiesGeneSicilyScreening proceduresGerm-Line MutationGynecologyGeneticsFamily HealthOvarian Neoplasmsbusiness.industryBRCA1 ProteinGenetic VariationHematologyDNA NeoplasmExonsmedicine.diseasePedigreeOncologyFemalebusinessOvarian cancerAnnals of oncology : official journal of the European Society for Medical Oncology
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Updated Field Synopsis and Systematic Meta-Analyses of Genetic Association Studies in Cutaneous Melanoma: The MelGene Database

2015

We updated a field synopsis of genetic associations of cutaneous melanoma (CM) by systematically retrieving and combining data from all studies in the field published as of August 31, 2013. Data were available from 197 studies, which included 83,343 CM cases and 187,809 controls and reported on 1,126 polymorphisms in 289 different genes. Random-effects meta-analyses of 81 eligible polymorphisms evaluated in4 data sets confirmed 20 single-nucleotide polymorphisms across 10 loci (TYR, AFG3L1P, CDK10, MYH7B, SLC45A2, MTAP, ATM, CLPTM1L, FTO, and CASP8) that have previously been published with genome-wide significant evidence for association (P5 × 10(-8)) with CM risk, with certain variants pos…

SLC45A2Skin NeoplasmsLocus (genetics)DermatologyPolymorphism Single NucleotideBiochemistryLinkage DisequilibriumGermlineStatistical significanceDatabases GeneticOdds RatioHumansGenetic Predisposition to DiseaseMelanomaGeneMolecular BiologyGerm-Line MutationGenetic associationGeneticsbiologyChromosome MappingGenetic VariationCell BiologyGene Expression Regulation NeoplasticCutaneous melanomabiology.proteinGenome-Wide Association StudyJournal of Investigative Dermatology
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The Suppressor of fused Gene Encodes a Novel PEST Protein Involved in Drosophila Segment Polarity Establishment

1995

Abstract Suppressor of fused, Su(fu), was identified as a semi-dominant suppressor of the putative serine/threonine kinase encoded by the segment polarity gene fused in Drosophila melanogaster. The amorphic Su(fu) mutation is viable, shows a maternal effect and displays no phenotype by itself. Su(fu) mutations are often found associated to karmoisin (kar) mutations but two complementation groups can be clearly identified. By using a differential hybridization screening method, we have cloned the Su(fu) region and identified chromosomal rearrangements associated with Su(fu) mutations. Two classes of cDNAs with similar developmental patterns, including a maternal contribution, are detectable …

Untranslated regionDNA Complementary[SDV]Life Sciences [q-bio]Recombinant Fusion ProteinsMolecular Sequence DataRestriction MappingInvestigations03 medical and health sciencesPEST sequence0302 clinical medicineTranscription (biology)GeneticsAnimalsDrosophila ProteinsAmino Acid SequenceCloning MolecularGenes SuppressorPeptide sequenceGeneGerm-Line MutationIn Situ Hybridization030304 developmental biologyGenetics0303 health sciencesBase SequencebiologyBlotting Northernbiology.organism_classificationMolecular biology[SDV] Life Sciences [q-bio]Repressor ProteinsComplementationDrosophila melanogasterPhenotypeSegment polarity geneDrosophila melanogaster030217 neurology & neurosurgery
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A SUMOylation-defective MITF germline mutation predisposes to melanoma and renal carcinoma

2011

International audience; So far, no common environmental and/or phenotypic factor has been associated with melanoma and renal cell carcinoma (RCC). The known risk factors for melanoma include sun exposure, pigmentation and nevus phenotypes; risk factors associated with RCC include smoking, obesity and hypertension. A recent study of coexisting melanoma and RCC in the same patients supports a genetic predisposition underlying the association between these two cancers. The microphthalmia-associated transcription factor (MITF) has been proposed to act as a melanoma oncogene; it also stimulates the transcription of hypoxia inducible factor (HIF1A), the pathway of which is targeted by kidney canc…

multidisciplinary sciencesMESH : Germ-Line MutationSUMO proteinurologic and male genital diseasesmedicine.disease_causeMESH : Neoplasm Invasiveness[ SDV.CAN ] Life Sciences [q-bio]/CancerMESH : Carcinoma Renal Cell0302 clinical medicineGene FrequencyCell MovementMESH: Germ-Line MutationMESH : Cell MovementMESH : Gene FrequencyMESH: Cell MovementComputingMilieux_MISCELLANEOUSGenetics0303 health sciencesMultidisciplinaryMESH: SumoylationMelanomaMESH : SumoylationMESH: Genetic Predisposition to Diseaserenal carcinomaMESH: Carcinoma Renal CellMicrophthalmia-associated transcription factorMESH : Microphthalmia-Associated Transcription Factor3. Good healthgermline mutation030220 oncology & carcinogenesisMESH: Microphthalmia-Associated Transcription Factorscience and technologyMESH: MelanomasumoMESH : Melanoma[SDV.CAN]Life Sciences [q-bio]/CancerBiology03 medical and health sciencesGermline mutationmelanomaMESH: Gene FrequencyGenetic predispositionmedicineHumansGenetic Predisposition to DiseaseNeoplasm InvasivenessCarcinoma Renal CellneoplasmsTranscription factorGerm-Line Mutation030304 developmental biologyMicrophthalmia-Associated Transcription FactorMESH: HumansMESH : HumansSumoylationMESH: Neoplasm Invasivenessmedicine.diseaseHIF1Acancer cellsCancer researchMESH : Genetic Predisposition to DiseaseCarcinogenesis
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Intron variants of the p53 gene are associated with increased risk for ovarian cancer but not in carriers of BRCA1 or BRCA2 germline mutations

1999

Two biallelic polymorphisms in introns 3 and 6 of the p53 gene were analysed for a possible risk-modifying effect for ovarian cancer. Germline DNA was genotyped from 310 German Caucasian ovarian cancer patients and 364 healthy controls. We also typed 124 affected and 276 unaffected female carriers with known deleterious BRCA1 or BRCA2 germline mutation from high-risk breast-ovarian cancer families. Genotyping was based on PCR and high-resolution gel electrophoresis. German ovarian cancer patients who carried the rare allele of the MspI restriction fragment length polymorphism (RELP) in intron 6 were found to have an overall 1.93-fold increased risk (95% confidence internal (CI) 1.27–2.91) w…

p53AdultCancer Researchendocrine system diseasesAdolescentGenotypeGenes BRCA1BiologypolymorphismGermline mutationRisk FactorsGenotypemedicineTumor Cells CulturedHumansAlleleAllele frequencyGerm-Line MutationAgedGeneticsAged 80 and overBRCA2 ProteinOvarian NeoplasmsGenetic Carrier ScreeningCancerGenetic VariationRegular ArticleMiddle Agedmedicine.diseaseBRCA2 ProteinBRCA1Genes p53BRCA2IntronsNeoplasm Proteinsovarian cancerOncologyCase-Control StudiesCancer researchFemaleRestriction fragment length polymorphismOvarian cancergenetic susceptibilityTranscription FactorsBritish Journal of Cancer
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