Search results for "10049 Institute of Pathology and Molecular Pathology"

showing 9 items of 9 documents

Cognate HLA absence in trans diminishes human NK cell education

2016

NK cells are innate lymphocytes with protective functions against viral infections and tumor formation. Human NK cells carry inhibitory killer cell Ig-like receptors (KIRs), which recognize distinct HLAs. NK cells with KIRs for self-HLA molecules acquire superior cytotoxicity against HLA– tumor cells during education for improved missing-self recognition. Here, we reconstituted mice with human hematopoietic cells from donors with homozygous KIR ligands or with a mix of hematopoietic cells from these homozygous donors, allowing assessment of the resulting KIR repertoire and NK cell education. We found that co-reconstitution with 2 KIR ligand–mismatched compartments did not alter the frequenc…

0301 basic medicine10028 Institute of Medical VirologyEpstein-Barr Virus InfectionsHerpesvirus 4 HumanCellchemical and pharmacologic phenomena610 Medicine & healthMice SCIDHuman leukocyte antigen2700 General MedicineAdaptive ImmunityBiology10263 Institute of Experimental Immunology03 medical and health sciencesMice Inbred NOD10049 Institute of Pathology and Molecular PathologymedicineAnimalsHumansCytotoxicityReceptorHistocompatibility Antigens Class IHEK 293 cellsGeneral MedicineAcquired immune systemKiller Cells NaturalHaematopoiesisHEK293 Cells030104 developmental biologymedicine.anatomical_structureNatural-Killer-Cells Cord Blood Transplantation Cytomegalovirus-Infection Class-I Inhibitory receptors Pediatric Patients TumorsImmunologyK562 CellsResearch ArticleK562 cells
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Mass Spectrometry Imaging Differentiates Chromophobe Renal Cell Carcinoma and Renal Oncocytoma with High Accuracy

2020

Background: While subtyping of the majority of malignant chromophobe renal cell carcinoma (cRCC) and benign renal oncocytoma (rO) is possible on morphology alone, additional histochemical, immunohistochemical or molecular investigations are required in a subset of cases. As currently used histochemical and immunohistological stains as well as genetic aberrations show considerable overlap in both tumors, additional techniques are required for differential diagnostics. Mass spectrometry imaging (MSI) combining the detection of multiple peptides with information about their localization in tissue may be a suitable technology to overcome this diagnostic challenge. Patients and Methods: Formalin…

0301 basic medicineChromophobe Renal Cell Carcinoma610610 Medicine & healthmass spectrometry imagingBiologyCross-validationMass spectrometry imagingOncocytic renal tumors03 medical and health sciences0302 clinical medicineproteomics10049 Institute of Pathology and Molecular PathologymedicineRenal oncocytomachromophobe renal cell carcinomabusiness.industrymedicine.diseaseLinear discriminant analysisRandom forestSupport vector machine030104 developmental biologyOncology030220 oncology & carcinogenesis2730 OncologyDifferential diagnosisNuclear medicinebusinessrenal oncocytomaResearch PaperJournal of Cancer
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Decreased Fibrogenesis After Treatment with Pirfenidone in a Newly Developed Mouse Model of Intestinal Fibrosis

2016

BACKGROUND Fibrosis as a common problem in patients with Crohn's disease is a result of an imbalance toward excessive tissue repair. At present, there is no specific treatment option. Pirfenidone is approved for the treatment of idiopathic pulmonary fibrosis with both antifibrotic and anti-inflammatory effects. We subsequently investigated the impact of pirfenidone treatment on development of fibrosis in a new mouse model of intestinal fibrosis. METHODS Small bowel resections from donor mice were transplanted subcutaneously into the neck of recipients. Animals received either pirfenidone (100 mg/kg, three times daily, orally) or vehicle. RESULTS After administration of pirfenidone, a signif…

0301 basic medicinemedicine.medical_specialtyPyridonesBlotting Western610 Medicine & healthGastroenterologyImmunoenzyme TechniquesMice03 medical and health sciencesIdiopathic pulmonary fibrosis0302 clinical medicineTransforming Growth Factor betaFibrosis10049 Institute of Pathology and Molecular PathologyInternal medicinemedicineAnimalsImmunology and Allergy2715 GastroenterologyCell ProliferationMice Inbred BALB CbiologyCell growthbusiness.industryAnti-Inflammatory Agents Non-SteroidalGastroenterologyPirfenidoneTransforming growth factor betamedicine.diseaseFibrosisMice Inbred C57BLTransplantationBlotDisease Models AnimalIntestinal Diseases10219 Clinic for Gastroenterology and Hepatology030104 developmental biology2723 Immunology and Allergybiology.proteinFemale030211 gastroenterology & hepatologyCollagen10069 Clinic of Cranio-Maxillofacial SurgerybusinessAfter treatmentmedicine.drugInflammatory Bowel Diseases
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Somatostatin-producing neuroendocrine tumors of the duodenum and pancreas: incidence, types, biological behavior, association with inherited syndrome…

2008

Somatostatin-producing neuroendocrine tumors (SOM-NETs) of the duodenum and pancreas appear to be heterogeneous. To determine their clinicopathological profiles, respective data were analyzed on a series of 82 duodenal and 541 pancreatic NETs. In addition, the clinical records of 821 patients with duodenal or pancreatic NETs were reviewed for evidence of a somatostatinoma syndrome. Predominant or exclusive expression of somatostatin was found in 21 (26%) duodenal and 21 (4%) pancreatic NETs. They were classified as sporadic (n=31) or neurofibromatosis type 1 (NF1)-associated duodenal NETs (n=3), gangliocytic paragangliomas (GCPGs; n=6), or poorly differentiated neuroendocrine carcinomas (pd…

AdultMaleCancer Researchmedicine.medical_specialtyEndocrinology Diabetes and Metabolism610 Medicine & healthNeuroendocrine tumorsGastroenterologyParagangliomaEndocrinologyDuodenal NeoplasmsInternal medicine10049 Institute of Pathology and Molecular PathologySomatostatinomaMultiple Endocrine Neoplasia Type 1MedicineHumansMEN11306 Cancer ResearchGenetic Predisposition to DiseaseNeurofibromatosisMultiple endocrine neoplasia610 Medicine & healthAgedAged 80 and overbusiness.industryIncidenceSyndromeSomatostatinomaMiddle Agedmedicine.diseasePrognosis1310 EndocrinologyPancreatic Neoplasms2712 Endocrinology Diabetes and MetabolismNeuroendocrine Tumorsmedicine.anatomical_structureSomatostatinOncologyDuodenum570 Life sciences; biology2730 OncologyFemalebusinessPancreasSomatostatinFollow-Up Studies
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Prevalence and Clinical Outcomes for Patients With ALK-Positive Resected Stage I to III Adenocarcinoma: Results From the European Thoracic Oncology P…

2014

Purpose The prevalence of anaplastic lymphoma kinase (ALK) gene fusion (ALK positivity) in early-stage non–small-cell lung cancer (NSCLC) varies by population examined and detection method used. The Lungscape ALK project was designed to address the prevalence and prognostic impact of ALK positivity in resected lung adenocarcinoma in a primarily European population. Methods Analysis of ALK status was performed by immunohistochemistry (IHC) and fluorescent in situ hybridization (FISH) in tissue sections of 1,281 patients with adenocarcinoma in the European Thoracic Oncology Platform Lungscape iBiobank. Positive patients were matched with negative patients in a 1:2 ratio, both for IHC and for …

AdultMaleCancer Researchmedicine.medical_specialtyPathologyLung NeoplasmsPopulation610 Medicine & healthAdenocarcinoma of LungAdenocarcinomaGastroenterologyCohort Studies10049 Institute of Pathology and Molecular Pathologyhemic and lymphatic diseasesThoracic OncologyInternal medicinePrevalencemedicineHumansAnaplastic lymphoma kinase1306 Cancer ResearchAnaplastic Lymphoma KinaseLung cancereducationIn Situ Hybridization FluorescenceAgedNeoplasm Stagingeducation.field_of_studyLungbusiness.industryALK-PositiveReceptor Protein-Tyrosine KinasesMiddle Agedmedicine.diseaseImmunohistochemistryEuropeTreatment Outcomemedicine.anatomical_structureOncology10032 Clinic for Oncology and HematologyImmunohistochemistryAdenocarcinoma2730 OncologyFemalebusiness
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Hepatitis E Virus Detection in Liver Tissue from Patients with Suspected Drug-Induced Liver Injury

2015

Hepatitis E virus (HEV) infection is increasingly recognized as a cause of acute hepatitis in the industrialized world. We aimed to determine the frequency of acute Hepatitis E virus (HEV) infection in cases of suspected drug-induced liver injury (DILI), mainly a diagnosis of exclusion. To this aim, formalin-fixed, paraffin-embedded (FFPE) liver tissues of all cases routinely processed in our institute during a 2 ½ years period in which DILI was amongst the differential diagnoses (157 liver biopsies, one liver explant) were subjected to semi-nested RT-PCR for the detection of hepatitis E virus (HEV) RNA. Histopathology was re-evaluated on all cases tested positive. HEV RNA was detectable in…

DrugPathologymedicine.medical_specialtymedia_common.quotation_subjectviruses610 Medicine & health2700 General Medicinemedicine.disease_causeliverHepatitis E virushepatitis E virus infection10049 Institute of Pathology and Molecular PathologyGenotypeHepatitis E virusmedicinehepatitismedia_commonLiver injuryHepatitislcsh:R5-920molecular testingbusiness.industryvirus diseasesGeneral Medicinemedicine.diseaseDiagnosis of exclusiondigestive system diseasesOriginal Research in MedicineEtiologyMedicineHistopathologylcsh:Medicine (General)businessdrug-induced liver injuryFrontiers in Medicine
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The inhibitor of differentiation-1 (Id1) enables lung cancer liver colonization through activation of an EMT program in tumor cells and establishment…

2017

Abstract: Id1 promotes carcinogenesis and metastasis, and predicts prognosis of non-small cell lung cancer (NSCLC)-adenocarcionoma patients. We hypothesized that Id1 may play a critical role in lung cancer colonization of the liver by affecting both tumor cells and the microenvironment. Depleted levels of Id1 in LLC (Lewis lung carcinoma cells, LLC shId1) significantly reduced cell proliferation and migration in vitro. Genetic loss of Id1 in the host tissue (Id1(-/-) mice) impaired liver colonization and increased survival of Id1 animals. Histologically, the presence of Idl in tumor cells of liver metastasis was responsible for liver colonization. Microarray analysis comparing liver tumor n…

Inhibitor of Differentiation Protein 10301 basic medicineCancer ResearchPathologyLung NeoplasmsTime Factors10255 Clinic for Thoracic SurgeryVimentinmedicine.disease_causeMetastasisCarcinoma Lewis Lung0302 clinical medicineCell MovementCarcinoma Non-Small-Cell LungTumor Microenvironment1306 Cancer ResearchMice KnockoutTissue microarrayIntegrin beta1Liver NeoplasmsTumor BurdenGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesis2730 OncologySignal Transductionmedicine.medical_specialtyEpithelial-Mesenchymal TransitionLiver tumor610 Medicine & healthBiologyTransforming Growth Factor beta103 medical and health sciencesCell Line Tumor10049 Institute of Pathology and Molecular PathologymedicineAnimalsHumansVimentinEpithelial–mesenchymal transitionLung cancerCell ProliferationLewis lung carcinomamedicine.diseaseMice Inbred C57BL030104 developmental biologyCancer researchbiology.proteinHuman medicineSnail Family Transcription FactorsCarcinogenesisCancer Letters
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Knockout of myeloid cell leukemia-1 induces liver damage and increases apoptosis susceptibility of murine hepatocytes

2008

Apoptosis, or programmed cell death, regulates tissue development and homeostasis in multi-cellular organisms. Extrinsic or intrinsic death signals activate pro-apoptotic pathways, resulting in the activation of caspases and finally in cell death. An important event during apoptosis process is the permeabilization of the outer mitochondrial membrane (OMM). Integrity of the OMM is regulated by the Bcl-2 protein family, which is divided into three groups: anti-apoptotic members Bcl-2, Bcl-xL and myeloid cell leukemia-1 (Mcl-1), pro-apoptotic multidomain members Bax and Bak, and pro-apoptotic BH3-only proteins. Mitochondrial activation is regulated by selective interactions of Bcl-2 proteins v…

Programmed cell deathGenotypeCellular differentiation610 Medicine & healthApoptosisBiologyPolymerase Chain ReactionArticleMiceimmune system diseases10049 Institute of Pathology and Molecular Pathologyhemic and lymphatic diseasesmedicineAnimalsAspartate AminotransferasesneoplasmsDNA PrimersHepatologyCaspase 3Alanine TransaminaseCell DifferentiationDNAFas receptorCell biologyMyeloid Cell Leukemia Sequence 1 ProteinHaematopoiesisGene Expression RegulationLiverProto-Oncogene Proteins c-bcl-2ApoptosisHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinRNA2721 HepatologyHepatocyte growth factorStem cellmedicine.drugHepatology
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Hepatocyte-specific deletion of the antiapoptotic protein myeloid cell leukemia-1 triggers proliferation and hepatocarcinogenesis in mice

2010

Regulation of hepatocellular apoptosis is crucial for liver homeostasis. Increased sensitivity of hepatocytes toward apoptosis results in chronic liver injury, whereas apoptosis resistance is linked to hepatocarcinogenesis and nonresponsiveness to therapy-induced cell death. Recently, we have demonstrated an essential role of the antiapoptotic Bcl-2 family member Myeloid cell leukemia-1 (Mcl-1) in hepatocyte survival. In mice lacking Mcl-1 specifically in hepatocytes (Mcl-1Δhep), spontaneous apoptosis caused severe liver damage. Here, we demonstrate that chronically increased apoptosis of hepatocytes coincides with strong hepatocyte proliferation resulting in hepatocellular carcinoma (HCC).…

Programmed cell deathPathologymedicine.medical_specialty10208 Institute of NeuropathologyApoptosis610 Medicine & health10071 Functional Genomics Center ZurichBiologyArticleMiceLiver Neoplasms Experimental10049 Institute of Pathology and Molecular PathologySurvivinmedicineAnimalsneoplasmsCell ProliferationChromosome AberrationsMice KnockoutHepatologyCell growthLiver cellmedicine.diseaseMyeloid Cell Leukemia Sequence 1 ProteinLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisHepatocyteHepatocytesCancer researchMyeloid Cell Leukemia Sequence 1 Protein570 Life sciences; biology2721 HepatologyU7 Systems Biology / Functional GenomicsHepatology
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