Search results for "chromosome"

showing 10 items of 1175 documents

Efficacy and safety of bosutinib (BOS) for Philadelphia chromosome–positive (Ph+) leukemia in older versus younger patients (pts).

2012

6511 Background: BOS is an oral dual Src/Abl kinase inhibitor with potent activity in Ph+ leukemia. Methods: Efficacy and safety of BOS 500 mg/d was evaluated in older (≥65 y; n = 119) and younger (<65 y; n = 451) pts in 3 cohorts: chronic phase chronic myeloid leukemia (CP CML) after imatinib (IM; CP2L cohort; n = 287); CP CML after IM + dasatinib (DAS) and/or nilotinib (NIL; CP3L cohort; n = 119); and accelerated/blast phase (AP/BP) CML or acute lymphoblastic leukemia after IM ± DAS and/or NIL (ADV cohort; n = 164). Results: Baseline events (≥65 y vs <65 y) included respiratory disorders (35% vs 13%), cardiac disorders (29% vs 9%), and diabetes (4% vs 4%). Median baseline medicatio…

Cancer Researchmedicine.medical_specialtyPediatricsPhiladelphia Chromosome Positivebusiness.industryImatinibmedicine.diseaseGastroenterologyDasatinibLeukemiaOncologyNilotinibhemic and lymphatic diseasesInternal medicineCohortmedicineAdverse effectbusinessBosutinibmedicine.drugJournal of Clinical Oncology
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Abstract 753: Genomic alterations of autophagy genes disrupts autophagic flux in human lung adenocarcinomas

2015

Abstract Targeted therapy using EGFR tyrosine kinase inhibitor (TKI) is a standard therapy for a subset of non-small cell lung cancer (NSCLC) patients with lung adenocarcinomas (LADs) harboring EGFR kinase domain mutations; however, EGFR TKI therapy shows limited efficacy due to de novo and acquired resistance. Consequently, formulating strategies to potentiate the efficacy of EGFR TKI is of great interest. In EGFR TKI sensitive cells harboring EGFR mutation, it has been shown that EGFR inhibition induces autophagy to protect the cells from metabolic stress. Hydroxychloroquine (HQ), an inhibitor of autophagy, has been shown to potentiate EGFR TKIs in preclinical models, however, preliminary…

Cancer Researchmedicine.medical_treatmentATG5AutophagyBiologyBioinformaticsmedicine.diseaseTargeted therapyOncologyProtein kinase domainChromosome 3Cancer researchmedicineErlotinibLung cancerGenemedicine.drugCancer Research
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Divergently Transcribed Overlapping Genes Expressed in Liver and Kidney and Located in the 11p15.5 Imprinted Domain

1998

Human chromosomal band 11p15.5 has been shown to contain genes involved in the development of several pediatric and adult tumors and in Beckwith-Wiedemann syndrome (BWS). Overlapping P1 artificial chromosome clones from this region have been used as templates for genomic sequencing in an effort to identify candidate genes for these disorders. PowerBLAST identified several matches with expressed sequence tags (ESTs) from fetal brain and liver cDNA libraries. Northern blot analysis indicated that two of the genes identified by these ESTs encode transcripts of 1-1.5 kb with predominant expression in fetal and adult liver and kidney. With RT-PCR and RACE, full-length transcripts were isolated f…

Candidate geneBeckwith-Wiedemann SyndromeDNA ComplementaryTranscription GeneticDNA Mutational AnalysisMolecular Sequence DataBiologyKidneyWilms TumorGenomic ImprintingMiceExonGene mappingGene expressionGenes OverlappingGeneticsAnimalsHumansAmino Acid SequenceGeneGeneticsExpressed sequence tagBase SequencecDNA libraryChromosomes Human Pair 11Membrane ProteinsMolecular biologyLiverCarrier ProteinsGenomic imprintingGenomics
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Long-range DNA looping and gene expression analyses identify DEXI as an autoimmune disease candidate gene

2011

The chromosome 16p13 region has been associated with several autoimmune diseases, including type 1 diabetes (T1D) and multiple sclerosis (MS). CLEC16A has been reported as the most likely candidate gene in the region, since it contains the most disease-associated single-nucleotide polymorphisms (SNPs), as well as an imunoreceptor tyrosine-based activation motif. However, here we report that intron 19 of CLEC16A, containing the most autoimmune disease-associated SNPs, appears to behave as a regulatory sequence, affecting the expression of a neighbouring gene, DEXI. The CLEC16A alleles that are protective from T1D and MS are associated with increased expression of DEXI, and no other genes in …

Candidate geneQuantitative Trait LociSingle-nucleotide polymorphismBiologyPolymerase Chain ReactionPolymorphism Single NucleotideMonocytesAutoimmune Diseases03 medical and health sciences0302 clinical medicineGeneticsHumansEnhancerMolecular BiologyGeneGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesIntronMembrane ProteinsPromoterGeneral MedicineArticlesDNADNA-Binding ProteinsRegulatory sequenceCandidate Disease Gene030217 neurology & neurosurgeryChromosomes Human Pair 16Human Molecular Genetics
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FISH and CHIPs: Colorful Clues to Radiation-Induced Chromosomal Instability

2004

Radiation produces a variety of clonal and non-clonal chromosome aberrations that can be characterized by fluorescence in situ hybridization (FISH). Epigenetic changes affecting the expression of an essential DNA repair gene(s) may be an importantant mechanism for radiation-induced chromosomal instability. Expression profiling with specialized cDNA chips promises to identify candidate genes for the delayed effects of radiation and to provide new insights into the manifold and complex cellular responses to DNA damage. Much progress can be made by using FISH and CHIPs to study the mechanisms and biological consequences of ionizing radiation.

Candidate genemedicine.diagnostic_testDNA repairbusiness.industryDNA damageChromosomeBiologyBiotechnologyCell biologyGene expression profilingChromosome instabilitymedicineEpigeneticsbusinessFluorescence in situ hybridization
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Fulminant hepatic failure requiring liver transplantation in 22q13.3 deletion syndrome.

2010

We report on a 4-year-old girl with severe developmental delay, absent speech, and chromosome 22q13.3 deletion (Phelan-McDermid syndrome), karyotype 46,XX.ish del(22)(q13.31qter)(ARSA-,N85A-,SHANK3-). At the age of 3 years, she needed an emergency liver transplantation because of fulminant hepatic failure, most likely caused by hyperacute autoimmune hepatitis triggered by a viral infection. This is the second report of a patient with 22q13.3 deletion and fulminant liver failure. By array-CGH we identified in this patient a 5.675 Mb terminal deletion (22q13.31 --> qter; including approximately 55 genes; from NUP50 to RABL2B) and in the previous patient a 1.535 Mb deletion (22q13.32 --> qter;…

Candidate genemedicine.medical_specialtyFulminantmedicine.medical_treatmentChromosomes Human Pair 22Chromosome DisordersAutoimmune hepatitisDiseaseLiver transplantationGastroenterologyFulminant hepatic failureInternal medicineGeneticsmedicineHumansGenetics (clinical)In Situ Hybridization FluorescenceOligonucleotide Array Sequence AnalysisComparative Genomic Hybridizationmedicine.diagnostic_testbusiness.industryKaryotypeSyndromeLiver Failure Acutemedicine.diseaseLiver TransplantationChild PreschoolFemaleChromosome DeletionLiver function testsbusinessAmerican journal of medical genetics. Part A
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Genome-wide association analysis in dilated cardiomyopathy reveals two new players in systolic heart failure on chromosomes 3p25.1 and 22q11.23

2021

Abstract Aims  Our objective was to better understand the genetic bases of dilated cardiomyopathy (DCM), a leading cause of systolic heart failure. Methods and results  We conducted the largest genome-wide association study performed so far in DCM, with 2719 cases and 4440 controls in the discovery population. We identified and replicated two new DCM-associated loci on chromosome 3p25.1 [lead single-nucleotide polymorphism (SNP) rs62232870, P = 8.7 × 10−11 and 7.7 × 10−4 in the discovery and replication steps, respectively] and chromosome 22q11.23 (lead SNP rs7284877, P = 3.3 × 10−8 and 1.4 × 10−3 in the discovery and replication steps, respectively), while confirming two previously identif…

Cardiac & Cardiovascular SystemsCardiomyopathy Dilated/genetics[SDV]Life Sciences [q-bio]Signal Transducing/geneticsDilated cardiomyopathyGenome-wide association studyAdaptor Proteins Signal Transducing/genetics030204 cardiovascular system & hematologyTAURINE0302 clinical medicineGWASMedicinePOSITION STATEMENT1102 Cardiorespiratory Medicine and HaematologyGenetics0303 health scienceseducation.field_of_studyGenetic Predisposition to Disease/geneticsAdaptor ProteinsDilated cardiomyopathy4C-sequencingPolymorphism Single Nucleotide/geneticsGenetic risk scoreCardiology and Cardiovascular MedicineLife Sciences & BiomedicineSingle Nucleotide/geneticsCardiomyopathy DilatedCardiomyopathyPopulationLocus (genetics)Single-nucleotide polymorphismPolymorphism Single NucleotideChromosomes03 medical and health sciencesSystolic/geneticsHeart Failure Systolic/geneticsSNPAnimalsHumansGenetic Predisposition to DiseaseAllelePolymorphismeducationImputationAdaptor Proteins Signal Transducing030304 developmental biologyHeart FailureScience & Technologybusiness.industryWORKING GROUP1103 Clinical Sciencesmedicine.diseaseGenetic architectureCardiovascular System & Hematology Dilated cardiomyopathyDilated/geneticsCardiovascular System & Cardiology[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologiebusinessApoptosis Regulatory ProteinsHeart Failure SystolicGenome-Wide Association Study
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Termination of transcription in an ‘in vitro’ system is dependent on a polyadenylation sequence

1991

Using HeLa cell nuclear extract as a source of the different transcription and polyadenylation factors and reverse transcription to analyze the levels of RNA 5' and 3' to the cleavage-polyadenylation site, an in vitro assay has been established to study polyadenylation coupled to transcription directed by different adenovirus promoters. The levels of transcription 5' and 3' to the cleavage site in the L3 polyadenylation region are practically the same as described previously, however, the level of transcription 3' to the cleavage site in the SV40 early polyadenylation region decreases immediately after the cleavage site indicating a termination of the transcription.

Cell ExtractsTranscription GeneticPolyadenylationMolecular Sequence DataRNA polymerase IISimian virus 40BiologyCleavage (embryo)AdenoviridaeTranscription (biology)GeneticsRNA MessengerPromoter Regions GeneticBase SequenceRNARNA-Directed DNA PolymerasePromoterMolecular biologyReverse transcriptasebiology.proteinRNA Polymerase IIChromosome DeletionPoly ACytokinesisHeLa CellsPlasmidsNucleic Acids Research
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Cisplatin sensitivity is related to late DNA damage processing and checkpoint control rather than to the early DNA damage response

2008

The present study aimed at elucidating mechanisms dictating cell death triggered by cisplatin-induced DNA damage. We show that CL-V5B hamster mutant cells, a derivative of V79B, are hypersensitive to cisplatin-induced apoptotic death. CL-V5B cells are characterized by attenuated cisplatin-induced early (2-6 h) stress response, such as phosphorylation of stress-activated protein kinases (SAPK/JNK), ATM and Rad3-related (ATR) protein kinase, histone H2AX and checkpoint kinase-1 (Chk-1). Human FANCC cells also showed a reduced phosphorylation of H2AX and SAPK/JNK at early time point after cisplatin treatment. This was not the case for BRCA2-defective VC-8 hamster cells, indicating that the FA …

Cell cycle checkpointCisplatin-DNA adducts ; DNA repair ; Interstrand cross links ; DNA damage response ; Cell cycle checkpoint ; Cell deathDNA damageDNA repairHealth Toxicology and MutagenesisApoptosisCell LineHistonesDNA AdductsCricetinaeGeneticsmedicineAnimalsHumansCHEK1PhosphorylationMolecular BiologyChromosome AberrationsCisplatinbiologyJNK Mitogen-Activated Protein KinasesDNA replicationG2-M DNA damage checkpointMolecular biologyCell biologyHistonebiology.proteinCisplatinDNA DamageMutagensmedicine.drug
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Simultaneous reduction of MAD2 and BUBR1 expression induces mitotic spindle alterations associated with p53 dependent cell cycle arrest and death

2014

Most human tumors are characterized by aneuploidy that is believed to be the consequence of chromosomal instability (CIN). The mechanism(s) leading to aneuploidy and the pathways that allow its tolerance are not completely understood. The Spindle Assembly Checkpoint (SAC) is a cellular surveillance mechanism working during mitosis, and alterations of genes that encode components of the SAC weakening the mitotic checkpoint, induce aneuploidy by chromosome mis-segregation. We induced aneuploidy in near-diploid tumor cells by simultaneous depletion of the SAC proteins MAD2 and BUBR1 by RNA interference in the attempt to gain further insight on the cellular responses to aneuploidy. Individual r…

Cell cycle checkpointMad2AneuploidyCell BiologyGeneral MedicineCell cycleBiologymedicine.diseaseSpindle apparatusCell biologySpindle checkpointChromosome instabilitymedicineMitosisCell Biology International
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