Search results for "Blastoma"

showing 10 items of 603 documents

Gastroblastoma in Adulthood—A Rarity among Rare Cancers—A Case Report and Review of the Literature

2019

Gastroblastoma (GB) is a rare gastric epithelial-mesenchymal neoplasm, first described by Miettinen et al. So far, all reported cases described the tumor in children or young adults, and similarities with other childhood blastomas have been postulated. We report a case of GB in a 43-year-old patient with long follow up and no recurrence up to 100 months after surgery. So far, this is the second case of GB occurring in the adult age >40-year-old. Hence, GB should be considered in the differential diagnosis of microscopically comparable conditions in adults carrying a worse prognosis and different clinical approach.

0301 basic medicineepithelial-mesenchymal neoplasmPediatricsmedicine.medical_specialtyPathologyGastroblastomabusiness.industryrare biphasic neoplasmMEDLINECase ReportGeneral MedicinegastroblastomaSettore MED/08 - Anatomia PatologicaAdult age03 medical and health sciences030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesislcsh:PathologyMedicineDifferential diagnosisYoung adultbusinesslcsh:RB1-214Case Reports in Pathology
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Integrated CGH/WES Analyses Advance Understanding of Aggressive Neuroblastoma Evolution: A Case Study

2021

Neuroblastoma (NB) is the most common extra-cranial malignancy in preschool children. To portray the genetic landscape of an overly aggressive NB leading to a rapid clinical progression of the disease, tumor DNA collected pre- and post-treatment has been analyzed. Array comparative genomic hybridization (aCGH), whole-exome sequencing (WES), and pharmacogenetics approaches, respectively, have identified relevant copy number alterations (CNAs), single nucleotide variants (SNVs), and polymorphisms (SNPs) that were then combined into an integrated analysis. Spontaneously formed 3D tumoroids obtained from the recurrent mass have also been characterized. The results prove the power of combining C…

3D tumoroids; Array CGH; Clonal evolution; Neuroblastoma; Pharmacogenetics; Recurrent tumor; Single nucleotide variants; Whole exome sequencing; Child Preschool; Disease Progression; Drug Resistance Neoplasm; Fatal Outcome; Humans; Immunophenotyping; Neuroblastoma; Polymorphism Single Nucleotide; Comparative Genomic Hybridization; Whole Exome SequencingQH301-705.5Drug Resistanceclonal evolutionCase Report3D tumoroidsSingle-nucleotide polymorphismDiseaseComputational biologyBiologyMalignancyPolymorphism Single NucleotideSomatic evolution in cancerImmunophenotypingwhole exome sequencingNeuroblastomaFatal OutcomeNeuroblastomaExome SequencingmedicineHumansarray CGHrecurrent tumorPolymorphismBiology (General)ChildPreschoolExome sequencingTumorsComparative Genomic HybridizationSingle NucleotideGeneral Medicinemedicine.diseaseSingle nucleotide variantsDrug Resistance NeoplasmPharmacogeneticsChild PreschoolDisease ProgressionFarmacogenèticaNeoplasmPharmacogeneticsComparative genomic hybridization
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Retinoic-Acid-Induced Downregulation of the 67 KDa Laminin Receptor Correlates with Reduced Biological Aggressiveness of Human Neuroblastoma Cells

2012

Neuroblastoma is a common tumor of the childhood arising from embryonal sympathetic neural cell precursors. Despite of the improved therapeutic strategies, the survival rate of high-risk neuroblastoma patients is poor. Although complete clinical remissions can be achieved, relapse is relatively frequent, indicating a role for the persistence of the minimal residual disease (for review, Maris, 2010). Treatments with derivatives of retinoic acid (RA), the biologically active form of vitamin A, produce significant improvements on the therapy of high-risk neuroblastoma patients, when used together with intensive multimodal therapies (Reynolds et al., 2003, for review). Despite some controversy …

67 kDa Laminin Receptorchemistry.chemical_compoundDifferential displayDownregulation and upregulationChemistryApoptosisNeuroblastomaRetinoic acidmedicinemedicine.diseaseReceptorMolecular biologyMinimal residual disease
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A subset of flavaglines inhibits KRAS nanoclustering and activation.

2020

The RAS oncogenes are frequently mutated in human cancers and among the three isoforms (KRAS, HRAS and NRAS), KRAS is the most frequently mutated oncogene. Here, we demonstrate that a subset of flavaglines, a class of natural anti-tumour drugs and chemical ligands of prohibitins, inhibit RAS GTP loading and oncogene activation in cells at nanomolar concentrations. Treatment with rocaglamide, the first discovered flavagline, inhibited the nanoclustering of KRAS, but not HRAS and NRAS, at specific phospholipid-enriched plasma membrane domains. We further demonstrate that plasma membrane-associated prohibitins directly interact with KRAS, phosphatidylserine and phosphatidic acid, and these int…

:Bioengineering [Engineering]Neuroblastoma RAS viral oncogene homologGene isoformLung NeoplasmsGTP'[SDV]Life Sciences [q-bio]AucunBiology: Biochemistry biophysics & molecular biology [F05] [Life sciences]medicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRocaglamideCarcinoma Non-Small-Cell LungmedicineKRASHumansdrug therapy;geneticsgeneticsHRASProhibitin: Biochimie biophysique & biologie moléculaire [F05] [Sciences du vivant]neoplasmsComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesOncogeneLipid nanoclusterOncogenesCell Biologydigestive system diseases3. Good healthrespiratory tract diseasesPhospholipidchemistry030220 oncology & carcinogenesisMutationCancer researchKRASFlavaglineRocaglamideProhibitinSignal Transduction
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Análisis digital del infiltrado inmune en neuroblastoma. Impacto pronóstico.

2018

El neuroblastoma es el tumor sólido extracraneal más común en la niñez con un índice de supervivencia a los cinco años del 40% en pacientes de riesgo elevado a pesar de terapias intensivas. Recientemente, aunque la inmunoterapia, incluida la terapia de células T con receptor de antígeno quimérico, representa un tratamiento revolucionario para las neoplasias hematológicas, sigue habiendo grandes desafíos para aplicar esta estrategia terapéutica con los tumores sólidos, incluido el neuroblastoma, como resultado de la naturaleza inmunosupresiva del microambiente tumoral. Se ha descrito que las células cancerosas desarrollan múltiples mecanismos para escapar del reconocimiento inmune o para mod…

:CIENCIAS MÉDICAS ::Patología::Neuropatología [UNESCO]digital:CIENCIAS MÉDICAS ::Patología::Inmunopatología [UNESCO]:CIENCIAS MÉDICAS ::Ciencias clínicas::Oncología [UNESCO]UNESCO::CIENCIAS MÉDICAS ::Patología::Neuropatologíasistema inmuneneuroblastomaUNESCO::CIENCIAS MÉDICAS ::Ciencias clínicas::OncologíapediátricoUNESCO::CIENCIAS MÉDICAS ::Ciencias clínicas::Pediatríacáncer:CIENCIAS MÉDICAS ::Ciencias clínicas::Pediatría [UNESCO]UNESCO::CIENCIAS MÉDICAS ::Patología::Inmunopatologíapatología
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Slit-Robo Pathway Is Clinically Relevant and May Represent a Potential Target in Acute Promyelocytic Leukemia

2018

Abstract Background: The Slit-Robo pathway has been shown to participate in the pathogenesis of several malignant diseases in addition to its physiologic role during the development of the central nervous system (CNS). However, the relevance of the Slit-Robo pathway in acute promyelocytic leukemia (APL) is presently unknown. We investigated the status of the Slit-Robo pathway in APL following the recent demonstration by Amodeo et al (CellRep. 2017) that the PML protein induces neural stem/progenitor cells migration by inhibiting the SLIT2 gene, which was associated with an increased presence of H3K27me3 in the SLIT2 promotor region. Moreover, sensitivity towards the PML-targeting drug arsen…

Acute promyelocytic leukemiaPrimary Glioblastomamedicine.medical_specialtyAcute leukemiaProliferation indexbusiness.industryImmunologyHealthy subjectsCell BiologyHematologymedicine.diseaseSlit2 proteinBiochemistryColony formationFamily medicinemedicinebusinessCell survivalBlood
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Comparative genetic study of intratumoral heterogenous MYCN amplified neuroblastoma versus aggressive genetic profile neuroblastic tumors.

2016

Intratumoral heterogeneous MYCN amplification (hetMNA) is an unusual event in neuroblastoma with unascertained biological and clinical implications. Diagnosis is based on the detection of MYCN amplification surrounded by non-amplified tumor cells by fluorescence in situ hybridization (FISH). To better define the genetic features of hetMNA tumors, we studied the Spanish cohort of neuroblastic tumors by FISH and single nucleotide polymorphism arrays. We compared hetMNA tumors with homogeneous MNA (homMNA) and nonMNA tumors with 11q deletion (nonMNA w11q-). Of 1091 primary tumors, 28 were hetMNA by FISH. Intratumoral heterogeneity of 1p, 2p, 11q and 17q was closely associated with hetMNA tumor…

Adult0301 basic medicineCancer ResearchCandidate geneAdolescentGene DosageSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideGene dosageGenetic profileCohort StudiesNeuroblastomaYoung Adult03 medical and health sciences0302 clinical medicineNeuroblastomaGeneticsmedicineHumansChildMolecular BiologyIn Situ Hybridization FluorescenceAgedAged 80 and overOncogene ProteinsGeneticsN-Myc Proto-Oncogene Proteinmedicine.diagnostic_testChromosomes Human Pair 11Nuclear ProteinsChromosomeMiddle Agedmedicine.diseaseNeuroblastic Tumor030104 developmental biologyChromosomes Human Pair 1Child PreschoolChromosomes Human Pair 2030220 oncology & carcinogenesisCancer researchChromosome DeletionChromosomes Human Pair 17Fluorescence in situ hybridization
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Ameloblastomas mimicking apical periodontitis: a case series

2022

Ameloblastomas are benign odontogenic tumors that can eventually mimic the clinical and radiological features of apical periodontitis. The aim of the present study was to evaluate the clinical, radiological and histological characteristics from a series of ameloblastomas mimicking apical periodontitis diagnosed in a 14-year period. all cases histologically diagnosed as ameloblastomas from 2005 to 2018 presenting a clinical diagnosis of periapical lesion of endodontic origin were selected for the study. Clinical, radiological and histological characteristics from all cases were tabulated and descriptively and comparatively analyzed. Twenty cases composed the final sample, including 18 solid …

AdultAmeloblastomaMaleRadiographyOtorhinolaryngologyHumansOdontogenic TumorsSurgeryGeneral DentistryPeriapical PeriodontitisUNESCO:CIENCIAS MÉDICASMedicina Oral Patología Oral y Cirugia Bucal
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Retinoblastoma epidemiology: Does the evidence matter?

2007

It has been proposed that retinoblastoma is 'caused' by two sequential mutations affecting the RB1 gene, but this is a rather outdated view of cancer aetiology that does not take into account a large amount of new acquisitions such as chromosomal and epigenetic alterations. Retinoblastoma remains probably the only cancer in which the rather simplistic 'two hit' mutational model is still considered of value, although cancer is known to be associated with genomic and microsatellite instability, defects of the DNA mismatch repair system, alterations of DNA methylation and hystone acethylation/deacethylation, and aneuploidy. Moreover, as it is shown herein, the predictions made by the 'two hit'…

AdultCancer ResearchAdolescentRetinal NeoplasmsRetinoblastoma Aneuploidy Two hit theoryDiseaseBiologyAge DistributionChromosome instabilitymedicineHumansEpigeneticsAge of OnsetChildGerm-Line MutationGeneticsRetinoblastomaRetinoblastomaMicrosatellite instabilityCancerInfantMiddle Agedmedicine.diseasePedigreeSettore BIO/18 - GeneticaOncologyChild PreschoolDNA methylationDNA mismatch repair
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Expression of adhesion factors and degrading proteins in primary and secondary glioblastomas and their precursor tumors.

2000

In tumor tissue specimens of 27 primary and 17 secondary glioblastomas and the precursor lesions, the immunohistochemical expression patterns of the membrane protein CD44s, the basal lamina proteins laminin, collagen IV, and fibronectin, the lectin galectin-3 recognizing tenascin and N-CAM as well as of the matrix-degrading enzymes matrix metalloproteinase MMP-2 and MMP-9, and cathepsin D were studied. Besides expression of basal lamina proteins in vessels, all glioblastomas and the precursor lesions showed strong immunoreactivity of CD44s, tenascin, galectin-3, and N-CAM which were restricted to solid tumor masses. Present in solid tumor areas, MMP-2, MMP-9 and cathepsin D were also strong…

AdultCancer Researchanimal structuresGalectin 3TenascinCathepsin DBiologyAstrocytomaCathepsin DLamininGliomamedicineHumansCell adhesionNeural Cell Adhesion MoleculesBrain NeoplasmsMiddle Agedmedicine.diseaseMolecular biologyAntigens DifferentiationImmunohistochemistryMatrix MetalloproteinasesFibronectinsFibronectinmedicine.anatomical_structureHyaluronan ReceptorsMembrane proteinMatrix Metalloproteinase 9biology.proteinMatrix Metalloproteinase 2Basal laminaCollagenLamininNeoplasm Recurrence LocalGlioblastomaInvasionmetastasis
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