Search results for "Breakpoint"

showing 10 items of 70 documents

Loss of heterozygosity at the short arm of chromosome 3 in renal‐cell cancer correlates with the cytological tumour type

1993

A majority of renal-cell tumours retain heterozygosity at the short arm of chromosome 3. To investigate possible histopathological differences between tumours with and without such losses, we compared loss of heterozygosity data from 51 tumours with 1 histological and 2 different cytological classifications of renal-cell tumour. Using the cytological classification of Thoenes et al., we only found tumours with loss of heterozygosity in these authors' clear-cell category. Possibly, only these tumours arise by a mechanism of double loss of a tumour-suppressor gene on 3p, non-clear-cell renal tumours having a different genetic background. Alternatively, deletions may occur in all subtypes, in …

HeterozygoteCancer Researchmedicine.medical_specialtyPathologyMitotic crossoverCARCINOMAChromosome DisordersBiologyMOLECULAR ANALYSISLoss of heterozygosityGene duplicationmedicineHumansCarcinoma Renal CellSequence DeletionChromosome AberrationsDELETIONBreakpointCytogeneticsChromosomeCYTOGENETICSKidney NeoplasmsOncologyChromosome 3Clear cell carcinomaChromosomes Human Pair 3Polymorphism Restriction Fragment LengthInternational Journal of Cancer
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Mapping candidate genes for Drosophila melanogaster resistance to the parasitoid wasp Leptopilina boulardi.

2006

Drosophila melanogaster resistance against the parasitoid wasp Leptopilina boulardi is under the control of a single gene (Rlb), with two alleles, the resistant one being dominant. Using strains bearing deletions, we previously demonstrated that the 55E2–E6; 55F3 region on chromosome 2R is involved in the resistance phenomenon. In this paper, we first restricted the Rlb containing region by mapping at the molecular level the breakpoints of the Df(2R)Pc66, Df(2R)P34 and Df(2R)Pc4 deficiencies, using both chromosomal in situ hybridization and Southern analyses. The resistance gene was localized in a 100 kb fragment, predicted to contain about 10 different genes. Male recombination genetic exp…

Male0106 biological sciencesCandidate geneWaspsGenes Insect010603 evolutionary biology01 natural sciencesParasitoid wasp03 medical and health sciencesGenes RegulatorGeneticsAnimalsDrosophila Proteins[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyAlleleGeneIn Situ Hybridization030304 developmental biologyRecombination GeneticGenetics0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsModels GeneticbiologyBreakpointIntracellular Signaling Peptides and ProteinsChromosome MappingMembrane ProteinsChromosomeGeneral MedicineCosmidsbiology.organism_classificationDrosophila melanogasterLarvaDrosophila melanogasterRecombination
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A de novo microdeletion of SEMA5A in a boy with autism spectrum disorder and intellectual disability.

2016

AbstractSemaphorins are a large family of secreted and membrane-associated proteins necessary for wiring of the brain. Semaphorin 5A (SEMA5A) acts as a bifunctional guidance cue, exerting both attractive and inhibitory effects on developing axons. Previous studies have suggested that SEMA5A could be a susceptibility gene for autism spectrum disorders (ASDs). We first identified a de novo translocation t(5;22)(p15.3;q11.21) in a patient with ASD and intellectual disability (ID). At the translocation breakpoint on chromosome 5, we observed a 861-kb deletion encompassing the end of the SEMA5A gene. We delineated the breakpoint by NGS and observed that no gene was disrupted on chromosome 22. We…

Male0301 basic medicinemedicine.medical_specialtyAutism Spectrum DisorderChromosomes Human Pair 22Translocation BreakpointNerve Tissue ProteinsSemaphorinsBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBioinformaticsArticleTranslocation GeneticautismeChromosome Breakpoints03 medical and health sciencesSemaphorin[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual Disabilitymental disordersIntellectual disabilityGeneticsmedicineHumans[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsChildGenetics (clinical)Genetics[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyNeurosciencesMembrane Proteinsmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderNeurons and CognitionPaternal InheritancecerveauChromosomes Human Pair 5AutismMedical geneticsChromosome DeletionmicrodélétionhumainChromosome 22[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenetic screen
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Metronomic cyclophosphamide induces regulatory T cells depletion and PSA‐specific T cells reactivation in patients with biochemical recurrent prostat…

2019

Biochemical recurrence (BCR) occurs in up to 40% of prostate cancer patients after prostatectomy. In our study, we performed an immune monitoring study in 20 prostate cancer patients with BCR previously treated with metronomic cyclophosphamide (mCTX). We observed a decrease of regulatory T cells (Tregs) from 2 months and this was more pronounced after 6 months of mCTX treatment. This drop of Tregs was associated with increased level of activated HLADR+ CD45R0+ T cells in peripheral blood. Furthermore, a reactivation of Th1 polarized anti-PSA T-cell response was detected in BCR patients treated with mCTX. However, dendritic cell subsets counts and activation were not influenced by the treatm…

MaleBiochemical recurrenceCancer ResearchT-Lymphocytesmedicine.medical_treatmentLymphocyte ActivationT-Lymphocytes RegulatoryLymphocyte DepletionAndrogen deprivation therapy03 medical and health sciencesProstate cancer0302 clinical medicinemedicineHumansAntineoplastic Agents AlkylatingCyclophosphamideMetronomic cyclophosphamideDiminutionProstatectomybusiness.industrybreakpoint cluster regionProstatic NeoplasmsDendritic cellProstate-Specific Antigenmedicine.diseaseOncology030220 oncology & carcinogenesisAdministration MetronomicCancer researchNeoplasm Recurrence LocalbusinessInternational Journal of Cancer
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Analysis of t(15;17) chromosomal breakpoint sequences in therapy-related versus de novo acute promyelocytic leukemia: Association of DNA breaks with …

2010

We compared genomic breakpoints at the PML and RARA loci in 23 patients with therapy-related acute promyelocytic leukemia (t-APL) and 25 de novo APL cases.Eighteen of 23 t-APL cases received the topoisomerase II poison mitoxantrone for their primary disorder. DNA breaks were clustered in a previously reported 8 bp "hot spot" region of PML corresponding to a preferred site of mitoxantrone-induced DNA topoisomerase II-mediated cleavage in 39% of t-APL occurring in patients exposed to this agent and in none of the cases arising de novo (P = 0.007). As to RARA breakpoints, clustering in a 3' region of intron 2 (region B) was found in 65% of t-APL and 28% of de novo APL patients, respectively. S…

MaleCancer ResearchReceptors Retinoic AcidRetinoic AcidMessengerPromyelocytic Leukemia ProteinTranslocation GeneticChromosome BreakpointsLeukemia Promyelocytic Acuteimmune system diseasesReceptorsPromyelocyticGeneticsLeukemiabiologyReverse Transcriptase Polymerase Chain ReactionRetinoic Acid Receptor alphaNuclear ProteinsDNA NeoplasmMiddle AgedFemaleHumanAdultAcute promyelocytic leukemiaChromosome BreakpointsTranslocationAntineoplastic AgentsAcuteChromosomesYoung AdultPromyelocytic leukemia proteinGeneticGeneticsmedicineConsensus sequenceHumansRNA MessengerReceptors Retinoic Acid; Male; Young Adult; Middle Aged; Chromosome Breakpoints; Female; Chromosomes Human Pair 17; Tumor Suppressor Proteins; Humans; DNA Neoplasm; Translocation Genetic; Leukemia Promyelocytic Acute; Antineoplastic Agents; Nuclear Proteins; RNA Messenger; Mitoxantrone; Reverse Transcriptase Polymerase Chain Reaction; Chromosomes Human Pair 15; Transcription Factors; Aged; AdultneoplasmsAgedChromosomes Human Pair 15Pair 17Tumor Suppressor ProteinsTopoisomeraseBreakpointPair 15DNAmedicine.diseaseRetinoic acid receptor alphabiology.proteinNeoplasmRNAHuman genomeMitoxantroneSettore MED/15 - Malattie del SangueChromosomes Human Pair 17Transcription FactorsGenes, Chromosomes and Cancer
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Detection and clinical implications of a novel BCR-ABL1 E12A2 insertion/deletion in a CML patient expressing the E13A2 isoform

2019

Background/Aim: The Philadelphia chromosome is the most frequent cytogenetic abnormality in chronic myelogenous (CML). More than 95% of CML patients are diagnosed with the e13a2 or e14a2 BCR-ABL1 fusion transcripts while, in about 1% of these individuals, the break generates the e1a2 rearrangement. Furthermore, about 5% of CML patients are diagnosed with rare BCR-ABL1 fusion transcripts, such as e19a2, e8a2, e13a3, e14a3, e1a3 and e6a2. However, there is limited evidence concerning the clinical and prognostic implications of these infrequent oncogenic variants for CML patients receiving tyrosine kinase inhibitors (TKIs). Case Report: We describe a novel atypical e12a2 insertion/deletion (In…

MaleCancer Researchbcr-ablFusion Proteins bcr-ablBCR-ABL1; CML; E12a2; E13a2; Nilotinib; Ponatinib; TKIs; Antineoplastic Combined Chemotherapy Protocols; Fusion Proteins bcr-abl; Humans; INDEL Mutation; Imidazoles; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Protein Isoforms; Pyridazines; Pyrimidines; Treatment Outcomechemistry.chemical_compoundExon0302 clinical medicineINDEL Mutationhemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsProtein IsoformsChronicCMLLeukemiaPonatinibImidazolesGeneral MedicineMiddle AgedTKIPyridazinesTreatment OutcomeOncology030220 oncology & carcinogenesisPonatinibPyridazineTyrosine kinaseINDEL MutationE13a2Humanmedicine.drugPhiladelphia chromosome03 medical and health sciencesMyelogenousLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansImidazoleAntineoplastic Combined Chemotherapy Protocolbusiness.industryBreakpointProtein IsoformFusion Proteinsmedicine.diseaseNilotinibBCR-ABL1PyrimidinesPyrimidinechemistryNilotinibTKIsCancer researchBCR-ABL PositivebusinessE12a2Myelogenous
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Detection of translocations affecting the BCL6 locus in B cell non-Hodgkin's lymphoma by interphase fluorescence in situ hybridization

2001

Structural alterations in 3q27 affecting the BCL6 locus are among the most frequent changes in B-NHL. The aim of the present study was to establish an interphase-FISH assay for the detection of all diverse BCL6 translocations in B-NHL. Two different approaches were tested, one using a PAC-clone spanning the major breakpoint region (MBR) of BCL6 (span-assay), and another using two BAC clones flanking the MBR (flank-assay). Interphase FISH with the span-assay detected the various BCL6 translocations in seven B-NHL cell lines. The dual-color flank-assay was evaluated in two laboratories independently: in normal controls, the cutoff level for false-positive signals was 2.6%, whereas the cutoff …

MaleCancer Researchmedicine.medical_specialtyLymphoma B-CellLymphomaMolecular Sequence DataTranslocationChromosomal translocationLocus (genetics)BiologyTranslocation GeneticFluorescenceChromosomesGeneticimmune system diseaseshemic and lymphatic diseasesmedicineHumansIn Situ Hybridization FluorescenceIn Situ HybridizationGeneticsGene Rearrangementmedicine.diagnostic_testBase SequenceBreakpointCytogeneticsB-CellBase Sequence; Chromosome Banding; Female; Gene Rearrangement; Humans; In Situ Hybridization Fluorescence; Karyotyping; Lymphoma B-Cell; Male; Molecular Sequence Data; Chromosomes Human Pair 3; Translocation GeneticHematologyGene rearrangementmedicine.diseaseMolecular biologyChromosome BandingOncologyChromosome 3KaryotypingPair 3FemaleChromosomes Human Pair 3TrisomyFluorescence in situ hybridizationHuman
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Distinct Xp11.2 breakpoints in two renal cell carcinomas exhibiting X;autosome translocations

1995

Several human renal cell carcinomas with X;autosome translocations have been reported in recent years. The t(X; I)(p11.2;q21) appears to be a specific primary anomaly, suggesting that tumors with this translocation form a distinct subgroup of RCC. Here we report two new cases, one with a t(X;10)(p11.2;q23), the other with a t(X;1)(p11.2;p34). The common breakpoint in Xp11.2 suggests that they belong to the above-mentioned subset of RCC. Using FISH in conjunction with X-specific YAC clones, we demonstrate that the two new cases exhibited distinct breakpoints within Xp11.2. (C) 1995 Wiley-Liss, Inc.

MaleCancer Researchmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesX ChromosomeChromosomal translocationBiologyTranslocation GeneticCLASSIFICATIONCHILDGeneticsmedicineCarcinomaHumansDe rol van chromosoomafwijkingen en (anti-)oncogenen in humane tumorenCarcinoma Renal CellGeneralLiterature_REFERENCE(e.g.dictionariesencyclopediasglossaries)In Situ Hybridization FluorescenceX chromosomeAgedGeneticsAutosomeBreakpointCytogeneticsKaryotypeADENOCARCINOMAMiddle Agedmedicine.diseaseMolecular biologyTUMORSCYTOGENETICSKidney NeoplasmsChromosome BandingAdenocarcinomaThe role of chromosomal aberrations and (anti-)oncogenes in human tumoursGenes, chromosomes & cancer
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Homozygous disruption of PDZD7 by reciprocal translocation in a consanguineous family: a new member of the Usher syndrome protein interactome causing…

2008

A homozygous reciprocal translocation, 46,XY,t(10;11),t(10;11), was detected in a boy with non-syndromic congenital sensorineural hearing impairment. Both parents and their four other children were heterozygous translocation carriers, 46,XX,t(10;11) and 46,XY,t(10;11), respectively. Fluorescence in situ hybridization of region-specific clones to patient chromosomes was used to localize the breakpoints within bacterial artificial chromosome (BAC) RP11-108L7 on chromosome 10q24.3 and within BAC CTD-2527F12 on chromosome 11q23.3. Junction fragments were cloned by vector ligation and sequenced. The chromosome 10 breakpoint was identified within the PDZ domain containing 7 (PDZD7) gene, disrupti…

MaleCandidate geneHeterozygoteUsher syndromePDZ domainMolecular Sequence DataChromosomal translocationBiologyTranslocation GeneticConsanguinityotorhinolaryngologic diseasesGeneticsmedicineHumansAmino Acid SequenceHearing LossMolecular BiologyGenetics (clinical)GeneticsGene RearrangementBacterial artificial chromosomemedicine.diagnostic_testBase SequenceChromosomes Human Pair 10Chromosomes Human Pair 11BreakpointHomozygoteChromosomeGeneral Medicinemedicine.diseaseMolecular biologyPedigreeChild PreschoolEar InnerFemaleUsher SyndromesFluorescence in situ hybridizationHuman molecular genetics
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The Aromatase Gene CYP19A1: Several Genetic and Functional Lines of Evidence Supporting a Role in Reading, Speech and Language

2012

Inspired by the localization, on 15q21.2 of the CYP19A1 gene in the linkage region of speech and language disorders, and a rare translocation in a dyslexic individual that was brought to our attention, we conducted a series of studies on the properties of CYP19A1 as a candidate gene for dyslexia and related conditions. The aromatase enzyme is a member of the cytochrome P450 super family, and it serves several key functions: it catalyzes the conversion of androgens into estrogens; during early mammalian development it controls the differentiation of specific brain areas (e.g. local estrogen synthesis in the hippocampus regulates synaptic plasticity and axonal growth); it is involved in sexua…

MaleCandidate geneSLIEstrogen synthesisTranslocation GeneticDyslexiaCohort StudiesMice0302 clinical medicineGenetics(clinical)Receptors ImmunologicAromatasePromoter Regions GeneticGenetics (clinical)Original ResearchQuantitative trait analysisMice KnockoutGeneticsRegulation of gene expression0303 health sciencesbiologyBrainNuclear ProteinsHuman brainmedicine.anatomical_structureTranslocation breakpointFemaleendocrine systemmedicine.drug_classQuantitative Trait LociNerve Tissue ProteinsPolymorphism Single NucleotideSpeech Disorders03 medical and health sciencesAromataseROBO1GeneticsmedicineAnimalsHumansGenetic Predisposition to DiseaseRNA MessengerEcology Evolution Behavior and SystematicsSSD030304 developmental biologyLanguage DisordersAromatase inhibitorCategorical trait associationDyslexiamedicine.diseaseCytoskeletal ProteinsGene Expression RegulationSynaptic plasticitybiology.protein030217 neurology & neurosurgeryBehavior Genetics
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