Search results for "germline"

showing 10 items of 154 documents

Phenotypic analysis of individuals with Costello syndrome due to HRAS p.G13C.

2011

Costello syndrome is characterized by severe failure-to-thrive, short stature, cardiac abnormalities (heart defects, tachyarrhythmia, and hypertrophic cardiomyopathy (HCM)), distinctive facial features, a predisposition to papillomata and malignant tumors, postnatal cerebellar overgrowth resulting in Chiari 1 malformation, and cognitive disabilities. De novo germline mutations in the proto-oncogene HRAS cause Costello syndrome. Most mutations affect the glycine residues in position 12 or 13, and more than 80% of patients share p.G12S. To test the hypothesis that subtle genotype-phenotype differences exist, we report the first cohort comparison between 12 Costello syndrome individuals with p…

AdultHeart Defects CongenitalMalemedicine.medical_specialtyAdolescentrasopathy.RASopathyShort statureProto-Oncogene MasArticleProto-Oncogene Proteins p21(ras)Young AdultGermline mutationSettore MED/38 - Pediatria Generale E SpecialisticaCostello syndromePregnancyInternal medicineNeoplasmsGeneticsMedicineHumansHRASChildGenetics (clinical)business.industryloose anagen hairCostello SyndromeMacrocephalyHypertrophic cardiomyopathyBrainInfantgenotype–phenotype correlationmedicine.diseaseDermatologyMagnetic Resonance ImagingMusculoskeletal AbnormalitiesEndocrinologyPhenotypeChild PreschoolFaceMutationFemalemedicine.symptombusinessMultifocal atrial tachycardiaAmerican journal of medical genetics. Part A
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BRAF-V600E expression in precursor versus differentiated dendritic cells defines clinically distinct LCH risk groups.

2014

BRAF-V600E expression is identified in hematopoietic progenitor and precursor myeloid dendritic cells in patients with high-risk LCH, and enforced expression of BRAF-V600E in CD11c+ cells recapitulates a high-risk LCH-like phenotype in mice.

MalePathologyendocrine system diseasesCellular differentiationCD34Antigens CD34Mice0302 clinical medicineLangerhans cell histiocytosisBone MarrowRisk FactorsImmunology and Allergyskin and connective tissue diseasesChild0303 health sciencesCell Differentiation3. Good healthHistiocytosismedicine.anatomical_structurePhenotypeTreatment Outcome030220 oncology & carcinogenesisChild PreschoolAntigens Surface2723 Immunology and AllergyFemaleProto-Oncogene Proteins B-rafmedicine.medical_specialtyImmunologyCD11c610 Medicine & healthBiologyArticle03 medical and health sciencesGermline mutationmedicineAnimalsHumansCell LineageGenetic Predisposition to DiseaseLectins C-TypeProgenitor cellneoplasms030304 developmental biology2403 ImmunologyHistocompatibility Antigens Class II302InfantCorrectionDendritic Cellsmedicine.diseaseHematopoietic Stem Cellsdigestive system diseasesCD11c Antigenenzymes and coenzymes (carbohydrates)Histiocytosis Langerhans-CellMannose-Binding Lectins10032 Clinic for Oncology and HematologyMutationBone marrowThe Journal of experimental medicine
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Distinctive Patterns of Intraclonal Diversification In IGHV1-2*04 Immunoglobulin Receptors of Patients with Splenic Marginal Zone Lymphoma: A of Ongo…

2011

Abstract Abstract 2638 We recently demonstrated that over 30% of cases with splenic marginal-zone lymphoma (SMZL) express distinctive immunoglobulin (IG) receptors that utilize a single polymorphic variant of the IGHV1-2 gene (IGHV1-2*04) and also exhibit restricted antigen-binding site motifs and precise targeting of somatic hypermutation (SHM). On these grounds, we proposed the existence of molecular subtypes of SMZL defined by immunogenetic analysis of the IG receptors with implications for selection by specific (super) antigenic element(s) in the development of at least a major subset of SMZL. In order to gain insight as to whether antigen involvement is relevant only prior to the malig…

GeneticsImmunologySomatic hypermutationCell BiologyHematologyComplementarity determining regionBiologymedicine.diseaseBiochemistryGermlineSubcloningmedicinebiology.proteinSplenic marginal zone lymphomaAntibodyIGHV@GeneBlood
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Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma

2018

Recurrent mutations in chromatin modifiers are specifically prevalent in adolescent or adult patients with Sonic hedgehog-associated medulloblastoma (SHH MB). Here, we report that mutations in the acetyltransferase CREBBP have opposing effects during the development of the cerebellum, the primary site of origin of SHH MB. Our data reveal that loss of Crebbp in cerebellar granule neuron progenitors (GNPs) during embryonic development of mice compromises GNP development, in part by downregulation of brain-derived neurotrophic factor (Bdnf). Interestingly, concomitant cerebellar hypoplasia was also observed in patients with Rubinstein-Taybi syndrome, a congenital disorder caused by germline mu…

0301 basic medicineCerebellumCrebbp protein mousemetabolism [Cerebellar Neoplasms]acetyltransferase; cerebellum; CREBBP; development; Rubinstein-Taybi syndrome; SHH medulloblastomagenetics [Hedgehog Proteins]MiceNeurotrophic factorsmetabolism [CREB-Binding Protein]Mice KnockoutNeuronsRubinstein-Taybi Syndromepathology [Rubinstein-Taybi Syndrome]CREBBPCREB-Binding ProteinPhenotypegenetics [CREB-Binding Protein]3. Good healthpathology [Cerebellar Neoplasms]acetyltransferasePhenotypemedicine.anatomical_structuregenetics [Rubinstein-Taybi Syndrome]Femalemetabolism [Hedgehog Proteins]Signal TransductionSHH medulloblastomaAdultcerebellumBiologyGeneral Biochemistry Genetics and Molecular BiologyCREBBP; Rubinstein-Taybi syndrome; SHH medulloblastoma; acetyltransferase; cerebellum; development.03 medical and health sciencesGermline mutationAcetyltransferasesmetabolism [Medulloblastoma]medicineAnimalsHumansgenetics [Cerebellar Neoplasms]Hedgehog Proteinsddc:610Cerebellar NeoplasmsdevelopmentMolecular BiologyMedulloblastomaRubinstein–Taybi syndromegenetics [Medulloblastoma]metabolism [Rubinstein-Taybi Syndrome]pathology [Medulloblastoma]Cell Biologymedicine.disease030104 developmental biologyMutationphysiology [CREB-Binding Protein]Cancer researchSHH protein humanCerebellar hypoplasia (non-human)metabolism [Acetyltransferases]CREBBP protein humanMedulloblastomaDevelopmental BiologyCongenital disorderDevelopmental Cell
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Somatic loss of an EXT2 gene mutation during malignant progression in a patient with hereditary multiple osteochondromas

2015

Multiple osteochondromas (MO) is an autosomal-dominant skeletal disorder caused by mutations in the exostosin-1 ( EXT1 ) or exostosin-2 ( EXT2 ) genes. In this study, we report the analysis of the mutational status of the EXT2 gene in tumor samples derived from a patient affected by hereditary MO, documenting the somatic loss of the germline mutation in a giant chondrosarcoma and in a rapidly growing osteochondroma. The sequencing of all exons and exon–intron junctions of the EXT1 and EXT2 genes from blood DNA of the proband did not reveal any mutation in the EXT1 gene but did demonstrate the presence of the transition point mutation c.67C > T in the EXT2 gene, determining the introduction …

AdultMaleOsteochondromaCancer ResearchMultiple osteochondromaSettore MED/06 - Oncologia MedicaChondrosarcomaLoss of HeterozygositySettore BIO/11 - Biologia MolecolareBone NeoplasmsGene mutationBiologyN-Acetylglucosaminyltransferasesmedicine.disease_causeGermlineLoss of heterozygosityGermline mutationGeneticChondrosarcoma; Hereditary cancer; Hereditary multiple osteochondromas; Tumor suppressor gene; Molecular Biology; Genetics; Cancer ResearchSkeletal disorderGeneticsmedicineHumansTumor suppressor geneHereditary multiple osteochondromaMolecular BiologyGeneticsMutationChromosomes Human Pair 11DNA Neoplasmmedicine.diseaseHereditary cancerSettore MED/18 - Chirurgia GeneraleSettore MED/03 - Genetica MedicaMutationDisease ProgressionCancer Genetics
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The severe phenotype of Diamond-Blackfan anemia is modulated by heat shock protein 70.

2017

International audience; Diamond-Blackfan anemia (DBA) is a rare congenital bone marrow failure syndrome that exhibits an erythroid-specific phenotype. In at least 70% of cases, DBA is related to a haploinsufficient germ line mutation in a ribosomal protein (RP) gene. Additional cases have been associated with mutations in GATA1. We have previously established that the RPL11+/Mut phenotype is more severe than RPS19+/Mut phenotype because of delayed erythroid differentiation and increased apoptosis of RPL11+/Mut erythroid progenitors. The HSP70 protein is known to protect GATA1, the major erythroid transcription factor, from caspase-3 mediated cleavage during normal erythroid differentiation.…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesIdentificationApoptosis-Inducing FactorGata1 MutationsInhibits ApoptosisBiologyHsp7003 medical and health sciencesGermline mutationRed Cells Iron and Erythropoiesishemic and lymphatic diseasesmedicine[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyNuclear ImportErythropoiesisDiamond–Blackfan anemiaHuman ErythroblastsBone marrow failure[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyGATA1Hematologymedicine.diseasePhenotypeMolecular biology3. Good healthHsp70030104 developmental biologyRibosomal-ProteinsProtein Gene DeletionsErythropoiesisHaploinsufficiencyBlood advances
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Multicenter Phase II Study of Lurbinectedin in BRCA-Mutated and Unselected Metastatic Advanced Breast Cancer and Biomarker Assessment Substudy

2018

Purpose This multicenter phase II trial evaluated lurbinectedin (PM01183), a selective inhibitor of active transcription of protein-coding genes, in patients with metastatic breast cancer. A unicenter translational substudy assessed potential mechanisms of lurbinectedin resistance. Patients and Methods Two arms were evaluated according to germline BRCA1/2 status: BRCA1/2 mutated (arm A; n = 54) and unselected ( BRCA1/2 wild-type or unknown status; arm B; n = 35). Lurbinectedin starting dose was a 7-mg flat dose and later, 3.5 mg/m2 in arm A. The primary end point was objective response rate (ORR) per Response Evaluation Criteria in Solid Tumors (RECIST). The translational substudy of resist…

Adult0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyGenes BRCA2Genes BRCA1Phases of clinical researchAntineoplastic AgentsBreast NeoplasmsHeterocyclic Compounds 4 or More RingsMice03 medical and health sciences0302 clinical medicineGermline mutationInternal medicineBiomarkers TumorClinical endpointAnimalsHumansMedicineProgression-free survivalGerm-Line MutationAgedDose-Response Relationship DrugErratabusiness.industryMiddle Agedmedicine.diseaseXenograft Model Antitumor AssaysMetastatic breast cancerProgression-Free SurvivalClinical trial030104 developmental biologyOncologyResponse Evaluation Criteria in Solid Tumors030220 oncology & carcinogenesisBiomarker (medicine)FemalebusinessCarbolinesJournal of Clinical Oncology
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Somatic mutation profiles as molecular classifiers of ulcerative colitis-associated colorectal cancer.

2021

Ulcerative colitis increases colorectal cancer risk by mechanisms that remain incompletely understood. We approached this question by determining the genetic and epigenetic profiles of colitis-associated colorectal carcinomas (CA-CRC). The findings were compared to Lynch syndrome (LS), a different form of cancer predisposition that shares the importance of immunological factors in tumorigenesis. CA-CRCs (n=27) were investigated for microsatellite instability, CpG island methylator phenotype, and somatic mutations of 999 cancer-relevant genes ("Pan-cancer" panel). A subpanel of "Pan-cancer" design (578 genes) was used for LS colorectal tumors (n=28). Mutational loads and signatures stratifie…

MaleCancer ResearchColorectal cancermedicine.disease_cause0302 clinical medicinesomatic mutationPromoter Regions Genetictulehdukselliset suolistosairaudetMiddle AgedLynch syndrome3. Good healthOncology030220 oncology & carcinogenesissyöpätauditDNA mismatch repairFemaleMicrosatellite InstabilityMutL Protein Homolog 1Adult3122 Cancerscolorectal cancersuolistosyövätBiologymikrosatelliititMLH103 medical and health sciencesGermline mutationmedicineHumansLynchin oireyhtymäulcerative colitisDNA-analyysiCpG Island Methylator PhenotypeMicrosatellite instabilitySequence Analysis DNADNA Methylationmedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisLynch syndromeUlcerative colitisMutationCancer researchmicrosatellite instabilityColitis UlcerativeCpG IslandsmutaatiotColitis-Associated NeoplasmsTumor Suppressor Protein p53CarcinogenesisInternational journal of cancerREFERENCES
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"Omics" of HER2-positive breast cancer.

2013

HER2/neu amplification/overexpression is the only somatic mutation widely considered to be a marker of disease outcome and response to treatment in breast cancer. Pathologists have made large efforts to achieve accuracy in characterizing HER2/neu status. The introduction of transtuzumab contributed to development of additional measures to identify sensitive and resistant subclasses of HER2/neu-positive tumors. In this article, we describe the latest advances in HER2/neu status diagnostic assessment and the most relevant research emerging from ‘‘Omics’’ (genomics, epigenetics, transcriptomics, and proteomics) studies on HER2/neu-positive breast cancer. A large quantity of biomarkers from dif…

ProteomicsReceptor ErbB-2Breast NeoplasmsBiologyBioinformaticsProteomicsAntibodies Monoclonal HumanizedBiochemistryEpigenesis GeneticHER2/Neu PositiveGermline mutationBreast cancerbreast cancerTrastuzumabGeneticsmedicineBiomarkers TumorHumansOMICSEpigeneticsskin and connective tissue diseasesneoplasmsMolecular BiologyGenomicsGenes erbB-2TrastuzumabOmicsmedicine.diseaseTumor progressionMolecular MedicineHER2/neu-positiveFemaleTranscriptomeBiotechnologymedicine.drugOmics : a journal of integrative biology
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

2014

The Ewing sarcoma family of tumors (EFT) is a group of highly malignant small round blue cell tumors occurring in children and young adults. We report here the largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines). Using a combination of whole genome sequencing and targeted sequencing approaches, we discover that EFT has a very low mutational burden (0.15 mutations/Mb) but frequent deleterious mutations in the cohesin complex subunit STAG2 (21.5% tumors, 44.4% cell lines), homozygous deletion of CDKN2A (13.8% and 50%) and mutations of TP53 (6.2% and 71.9%). We additionally note an increased prevalence of the BRCA2 K3326X polymorphism in EFT patient samples (7.3%) compared …

MaleCancer ResearchCell Cycle Proteinsmedicine.disease_causeFusion geneCDKN2AMedicine and Health Sciences2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)CancerPediatricMutationTissue microarrayTumorGenomeSarcomasHigh-Throughput Nucleotide SequencingAntigens NuclearSarcomaNeoplasm ProteinsOncologyChild PreschoolFemaleSarcomaResearch ArticleBiotechnologyHumanAdultPediatric Research Initiativelcsh:QH426-470Cohesin complexAdolescentPediatric CancerEwing SarcomaSarcoma EwingBiologyDisease-Free SurvivalFrameshift mutationCell LineGermline mutationRare DiseasesCell Line TumorEwingCancer GeneticsmedicineGeneticsHumansNuclearGenetic TestingAntigensPreschoolMolecular BiologyEcology Evolution Behavior and SystematicsGenome HumanHuman GenomeBiology and Life SciencesCancers and NeoplasmsInfantmedicine.diseaselcsh:GeneticsOrphan DrugMutationCancer researchGene DeletionDevelopmental Biology
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