Search results for "Chromosomal Alterations"

showing 5 items of 5 documents

Frequency and prognostic impact of ALK amplifications and mutations in the European Neuroblastoma Study Group (SIOPEN) high-risk neuroblastoma trial …

2021

Purpose: In neuroblastoma (NB), the ALK receptor tyrosine kinase can be constitutively activated through activating point mutations or genomic amplification. We studied ALK genetic alterations in high-risk (HR) patients on the HR-NBL1/SIOPEN trial to determine their frequency, correlation with clinical parameters, and prognostic impact. Materials and methods: Diagnostic tumor samples were available from 1,092 HR-NBL1/SIOPEN patients to determine ALK amplification status (n = 330), ALK mutational profile (n = 191), or both (n = 571). Results: Genomic ALK amplification (ALKa) was detected in 4.5% of cases (41 out of 901), all except one with MYCN amplification (MNA). ALKa was associated with …

0301 basic medicineCancer ResearchPrognostic ImpactAnaplastic Lymphoma Kinase/genetics; Child Preschool; Clinical Trials Phase III as Topic; Europe; Female; Follow-Up Studies; Gene Amplification; Humans; Infant; Male; Mutation Rate; N-Myc Proto-Oncogene Protein/genetics; Neuroblastoma/genetics; Prognosis; Randomized Controlled Trials as Topic; Risk Factors; Survival RateEuropean Neuroblastoma Study GroupSIOPENRELAPSE03 medical and health sciencesNeuroblastoma0302 clinical medicineText miningNeuroblastomahemic and lymphatic diseasesREVEALSMedicine and Health SciencesKINASEMedicineHigh risk neuroblastomaHETEROGENEITYCRIZOTINIBSEGMENTAL CHROMOSOMAL ALTERATIONSACTIVATING MUTATIONSPEDIATRIC-PATIENTSbusiness.industryALK receptor tyrosine kinasePoint mutationREARRANGEMENTSCHEMOTHERAPYmedicine.diseaseDoenças Genéticas030104 developmental biologyALKOncology030220 oncology & carcinogenesisCancer researchbusiness
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Recombinations of chromosomal bands 10q24, 12q14-q15, and 14q24 in two cases of pulmonary chondroid hamartoma studied by fluorescence in situ hybridi…

2003

Abstract Pulmonary chondroid hamartomas (PCH) are benign mesenchymal tumors consisting of at least two cytogenetic subgroups. These subgroups are defined by chromosomal alterations at either 12q14∼q15 or 6p21. Cytogenetic analysis of short-term cultures from two PCHs revealed two different rearrangements with 12q14∼q15. One of these had a unique translocation t(12;14)(q14∼15;q24) with presence of two normal chromosomes 12 and a der(14), but missing the der(12). The other showed a complex rearrangement between chromosomes 10 and 12 with two different derivatives. Our data have been confirmed with fluorescence in situ hybridization analysis. These cases represent variant forms of the standard…

AdultLung DiseasesMaleCancer ResearchChromosomal Bandsmedicine.medical_specialtyChromosomal AlterationsHamartomaChromosomal translocationBiologyTranslocation GeneticGeneticsmedicineHamartomaHumansMolecular BiologyChromosome 12In Situ Hybridization FluorescenceGeneticsChromosomes Human Pair 14Chromosomes Human Pair 12medicine.diagnostic_testChromosomes Human Pair 10CytogeneticsMiddle Agedmedicine.diseaseMolecular biologyKaryotypingChondroid HamartomaFluorescence in situ hybridizationCancer genetics and cytogenetics
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Segmental chromosomal alterations lead to a higher risk of relapse in infants with MYCN-non-amplified localised unresectable/disseminated neuroblasto…

2011

BACKGROUND: In neuroblastoma (NB), the presence of segmental chromosome alterations (SCAs) is associated with a higher risk of relapse. METHODS: In order to analyse the role of SCAs in infants with localised unresectable/disseminated NB without MYCN amplification, we have performed an array CGH analysis of tumours from infants enrolled in the prospective European INES trials. RESULTS: Tumour samples from 218 out of 300 enroled patients could be analysed. Segmental chromosome alterations were observed in 11%, 20% and 59% of infants enroled in trials INES99.1 (localised unresectable NB), INES99.2 (stage 4s) and INES99.3 (stage 4) (P<0.0001). Progression-free survival was poorer in patients wh…

OncologyCancer Researchmedicine.medical_specialtyPathologyChromosomal AlterationsN-Myc Proto-Oncogene Proteinsegmental chromosome alterationsneuroblastomaNeuroblastomaRecurrenceInternal medicineNeuroblastomamedicineHumansProspective StudiesStage (cooking)Relapse riskProspective cohort studygenomic profileSurvival analysisChromosome AberrationsOncogene ProteinsN-Myc Proto-Oncogene Proteininfantsbusiness.industryInfantNuclear ProteinsGenetics and GenomicsPrognosismedicine.diseaseSurvival AnalysisDoenças GenéticasOncologySegmental Chromosome AlterationsHigh RiskGenomic ProfilebusinessBritish Journal of Cancer
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RB, epigenetic changes and chromosomal alterations in human primary fibroblasts in culture

2008

The regulation of chromatin structure is a dynamic and complex process modulated by epigenetic mechanisms. Epigenetic changes as malfunctioning of histone modifications and DNA methylation could affect several different cellular processes like regulation of gene transcription and could compromise the correct chromosome condensation and segregation. Is important to note that these alterations have been correlated with cancer initiation/progression. In particular hypomethylation of pericentromeric regions, usually methylated, has been associated to chromosomal instability, as well as hypermethylation of promoter CpG islands of tumor suppressor genes (p16, CHFR, BRCA1) is considered a cause of…

Settore BIO/18 - GeneticaRB epigenetics chromosomal alterations
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CHARACTERIZATION OF TRANSFORMED CELL LINES OBTAINED FROM PRIMARY RAT CORTICAL ASTROCYTES

2021

Brain cancers are complex and heterogeneous; most of them derive from glial cells[1], and are called gliomas, further subdivided into astrocytomas, oligodendrogliomas, ependymomas and glioastrocytomas[2]. The malignant cells undergo modifications of their metabolism and behaviour, and acquire the ability to migrate along the blood vessels in small groups (model of the guerrilla war)[3], thus invading the surrounding brain parenchyma. Most important, they have the capacity to affect the surrounding microenvironment, by altering both the extracellular matrix and the properties of the normal cells present in the brain, including glial-, endothelial-, and immune-cells, further promoting cancer …

Settore BIO/18 - Geneticaastrocyteepigenetic and chromosomal alterations.Settore BIO/10 - Biochimicaextracellular vesicleSettore BIO/06 - Anatomia Comparata E CitologiaBrain cancer
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