Search results for "malignant transformation"

showing 10 items of 108 documents

Zolbetuximab combined with EOX as first-line therapy in advanced CLDN18.2+ gastric (G) and gastroesophageal junction (GEJ) adenocarcinoma : Updated r…

2019

16 Background: Physiologically, the tight junction protein CLDN18.2 is present only in the gastric mucosa. Upon malignant transformation, CLDN18.2 epitopes are exposed on the cell surface and accessible to targeted therapy. Zolbetuximab (formerly IMAB362) is a chimeric mAb that mediates specific killing of CLDN18.2+ cancer cells through immune effector mechanisms; single-agent activity has been reported in G/GEJ cancer. Methods: Patients (pts) with advanced HER2-negative (HER–) G/GEJ cancer with CLDN18.2 expression of ≥ 2+ staining intensity with the anti-CLDN18 43-14A mAb in ≥ 40% tumor cells were eligible (NCT01630083). Patients were randomized 1:1 to receive first-line EOX ± zolbetuxima…

Cancer ResearchTight junctionbusiness.industryCellMedizinmedicine.diseaseGastroesophageal JunctionEpitopeMalignant transformation03 medical and health sciences0302 clinical medicineFirst line therapymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchGastric mucosaMedicineAdenocarcinomabusiness030215 immunology
researchProduct

Implication of Heat Shock Factors in Tumorigenesis: Therapeutical Potential

2011

International audience; Heat Shock Factors (HSF) form a family of transcription factors (four in mammals) which were named according to the discovery of their activation by a heat shock. HSFs trigger the expression of genes encoding Heat Shock Proteins (HSPs) that function as molecular chaperones, contributing to establish a cytoprotective state to various proteotoxic stresses and in pathological conditions. Increasing evidence indicates that this ancient transcriptional protective program acts genome-widely and performs unexpected functions in the absence of experimentally defined stress. Indeed, HSFs are able to re-shape cellular pathways controlling longevity, growth, metabolism and deve…

Cancer Research[SDV]Life Sciences [q-bio][SDV.CAN]Life Sciences [q-bio]/CancerReviewBiologymedicine.disease_causeBioinformaticslcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicineHeat shock proteinmedicinecancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEnhancerHSF1Transcription factorComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciences[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthCell biologytherapeutical approachesOncologyHeat Shock Factors030220 oncology & carcinogenesisCancer cellSignal transductionCarcinogenesis[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
researchProduct

Production of superoxide by human malignant melanoma cells.

1998

Metastasis is a complicated multi-step process involving interactions between tumour cells, the extracellular matrix and the vessel walls. Experimental observations suggest that leucocyte migration and function could be a suitable model in order to understand tumour cell dissemination. In the present report we show and quantify the production of free radicals by human malignant melanoma cells (St-ml12) by means of a spectrophotometrical method, using an enzyme immunoassay reader. Endothelial cells and activated polymorphonuclear leucocytes were used as controls. Melanoma cells without stimulants produced large amounts of superoxide anion at an increasing rate in relation to time, which coul…

Cancer ResearchbiologySuperoxideMelanomaRadicalCellDermatologyHydrogen Peroxidemedicine.diseaseMolecular biologyMalignant transformationExtracellular matrixSuperoxide dismutaseImmunoenzyme Techniqueschemistry.chemical_compoundmedicine.anatomical_structureOncologychemistrySuperoxidesmedicinebiology.proteinTumor Cells CulturedHumansHydrogen peroxideMelanomaMelanoma research
researchProduct

Cloning, structure, cellular localization, and possible function of the tumor suppressor gene lethal(3)malignant blood neoplasm-1 of Drosophila melan…

1994

The tumor suppressor gene, lethal(3)malignant blood neoplasm-1+, of Drosophila melanogaster is required for the differentiation of the phagocytic blood-cell type, the plasmatocyte. In the homozygously mutated state it causes the malignant transformation of these blood cells. We present here the cloning, sequencing, structure, and expression of the l(3)mbn-1+ gene during development. The cloned gene was identified by germ-line transformation, generation of revertants, and the detection of the corresponding mRNA in blood cells and other tissues. Homologies of the G-S-rich C-terminus of the putative MBN83 protein to human cytokeratins K1, K10, and mouse loricrin were found. The structure and p…

DNA ComplementaryTumor suppressor geneMolecular Sequence DataMalignant transformationGene expressionAnimalsGenes Tumor SuppressorAmino Acid SequenceRNA MessengerCloning MolecularMolecular BiologyGeneCellular localizationAllelesCloningBlood CellsbiologyBase SequenceChromosome MappingCell Biologybiology.organism_classificationMolecular biologyCell Transformation NeoplasticDrosophila melanogasterLoricrinDrosophila melanogasterDevelopmental BiologyDevelopmental biology
researchProduct

A temperature-sensitive brain tumor suppressor mutation of Drosophila melanogaster: Developmental studies and molecular localization of the gene

1993

The recessive-lethal, temperature-sensitive (ts) mutation of the tumor suppressor gene lethal(3)malignant brain tumor (l(3)mbt) causes in a single step the malignant transformation of the adult optic neuroblasts and ganglion mother cells in the larval brain at the restrictive temperature of 29 degrees C. The transformed cells are differentiation-incompetent and grow autonomously in a lethal and invasive fashion in situ in the brain as well as after transplantation in vivo into wild-type adult hosts. The imaginal discs show epithelial overgrowth. At the permissive temperature of 22 degrees C development is completely normal. The ts-period of gene activity responsible for 100% brain tumor sup…

EmbryologyHot TemperatureTumor suppressor geneBiologymedicine.disease_causeMalignant transformationmedicineAnimalsGenes Tumor SuppressorGeneSuppressor mutationGeneticsMutationBrain NeoplasmsStem CellsOptic Lobe NonmammalianChromosome Mappingbiology.organism_classificationCell biologyTransplantationImaginal discDrosophila melanogasterGangliaGenes LethalDrosophila melanogasterDevelopmental BiologyMechanisms of Development
researchProduct

Retraction: Oral leukoplakia, a clinical-histopathological study in 412 patients

2021

The authors detected some minor errors in the published manuscript (Rubert A, Bagan L, Bagan JV. Oral leukoplakia, a clinical-histopathological study in 412 patients. J Clin Exp Dent. 2020 Jun 1;12(6):e540-e546. doi: 10.4317/jced.57091. PMID: 32665812; PMCID: PMC7335600.) and have requested that the entire article be republished with these errors already rectified. Background A retrospective clinical-histopathological study was made of the evolution of oral leukoplakia over time, staging the disease according to the classification of van der Waal. Material and methods A study was made of 412 patients with oral leukoplakia, analyzing the corresponding clinical factors and histopathological f…

Epithelial dysplasiamedicine.medical_specialtyOral Medicine and Pathologybusiness.industryResearch030206 dentistryDiseaseDermatologyMalignant transformationLesionOral leukoplakia030207 dermatology & venereal diseases03 medical and health sciencesstomatognathic diseases0302 clinical medicinemedicine.anatomical_structureTongueHomogeneousmedicinemedicine.symptomStage (cooking)businessGeneral DentistryUNESCO:CIENCIAS MÉDICASJournal of Clinical and Experimental Dentistry
researchProduct

Oral leukoplakia, a clinical-histopathological study in 412 patients

2020

Background A retrospective clinical-histopathological study was made of the evolution of oral leukoplakia over time, staging the disease according to the classification of van der Waal. Material and Methods A study was made of 412 patients with oral leukoplakia, analyzing the corresponding clinical factors and histopathological findings; assessing associations between the different clinical presentations and epithelial dysplasia; and evaluating the factors influencing malignant transformation of the lesions. Results Clinically, homogeneous presentations were seen to predominate (n = 336, 81.6%), while histologically most of the lesions exhibited no dysplastic changes (n = 271; 65.7%). Stage…

Epithelial dysplasiamedicine.medical_specialtyTerapéuticaOdontologíaDiseaseMalignant transformationLesionTratamiento médico03 medical and health sciences0302 clinical medicineTonguemedicineStage (cooking)General DentistryOral Medicine and Pathologybusiness.industryResearch030206 dentistry:CIENCIAS MÉDICAS [UNESCO]DermatologyOral leukoplakiastomatognathic diseasesmedicine.anatomical_structureHomogeneous030220 oncology & carcinogenesisUNESCO::CIENCIAS MÉDICASmedicine.symptombusinessJournal of Clinical and Experimental Dentistry
researchProduct

The Co‐mutational Spectrum Determines the Therapeutic Response in Murine FGFR2 Fusion‐Driven Cholangiocarcinoma

2021

Background and aims Intrahepatic cholangiocarcinoma (ICC) is the second most common primary liver cancer and a highly lethal malignancy. Chemotherapeutic options are limited, but a considerable subset of patients harbors genetic lesions for which targeted agents exist. Fibroblast growth factor receptor 2 (FGFR2) fusions belong to the most frequent and therapeutically relevant alterations in ICC, and the first FGFR inhibitor was recently approved for the treatment of patients with progressed, fusion-positive ICC. Response rates of up to 35% indicate that FGFR-targeted therapies are beneficial in many but not all patients. Thus far, no established biomarkers exist that predict resistance or r…

Fetal Proteins0301 basic medicineAntimetabolites AntineoplasticCombination therapymedicine.medical_treatmentFGFR InhibitionVesicular Transport ProteinsCyclic AMP Response Element-Binding Protein Amedicine.disease_causeDeoxycytidineMalignant transformationTargeted therapyCholangiocarcinomaProto-Oncogene Proteins p21(ras)Mice03 medical and health sciencesLiver Neoplasms Experimental0302 clinical medicineAntigens NeoplasmmedicineAnimalsReceptor Fibroblast Growth Factor Type 2Protein Kinase InhibitorsCell ProliferationHepatologyOncogenebusiness.industryFibroblast growth factor receptor 2AdenosylhomocysteinasePhenylurea CompoundsGemcitabineBile Ducts IntrahepaticCell Transformation NeoplasticPyrimidines030104 developmental biologyBile Duct NeoplasmsFibroblast growth factor receptorMutationCancer research030211 gastroenterology & hepatologyKRASGene FusionbusinessCo-Repressor ProteinsMicrotubule-Associated ProteinsHepatology
researchProduct

RSPO2 gene rearrangement: a powerful driver of β-catenin activation in liver tumours

2019

ObjectiveWe aimed at the identification of genetic alterations that may functionally substitute for CTNNB1 mutation in ß-catenin-activated hepatocellular adenomas (HCAs) and hepatocellular carcinoma (HCC).DesignLarge cohorts of HCA (n=185) and HCC (n=468) were classified using immunohistochemistry. The mutational status of the CTNNB1 gene was determined in ß-catenin-activated HCA (b-HCA) and HCC with at least moderate nuclear CTNNB1 accumulation. Ultra-deep sequencing was used to characterise CTNNB1wild-type and ß-catenin-activated HCA and HCC. Expression profiling of HCA subtypes was performed.ResultsA roof plate-specific spondin 2 (RSPO2) gene rearrangement resulting from a 46.4 kb microd…

Gene expression profilingGastroenterologyCancer researchWnt signaling pathwayTelomerase reverse transcriptaseGene rearrangementHCCSBiologyRSPO2Malignant transformationRSPO2 GeneGut
researchProduct

Role of the insulin-like growth factor system in adrenocortical growth control and carcinogenesis.

2004

Clinically silent adrenocortical adenomas are the most frequent abnormalities in the adrenal gland. In contrast, adrenocortical carcinoma is a rare tumor with an extremely poor prognosis. The factors responsible for the frequent occurrence of benign adrenocortical tumors on one hand and the rare malignant transformation on the other are not known. Several genetic alterations such as loss of imprinting or loss of heterozygosity of the 11p15 gene locus causing a strong IGF-II overexpression have been demonstrated in the majority of adrenocortical carcinomas. In addition to IGF-II overexpression, increased levels of the IGF-I-receptor and IGFBP-2 have been found in advanced human adrenocortica…

Genetically modified mousemedicine.medical_specialtyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryAdrenal Gland NeoplasmsLoss of HeterozygosityBiologymedicine.disease_causeBiochemistryMalignant transformationReceptor IGF Type 1Loss of heterozygosityInsulin-like growth factorMiceEndocrinologyInsulin-Like Growth Factor IIInternal medicineCell Line TumormedicineAdrenocortical carcinomaAnimalsHumansNeoplastic transformationNeoplastic ProcessesAdrenal glandChromosomes Human Pair 11Biochemistry (medical)CarcinomaGeneral Medicinemedicine.diseaseGene Expression Regulation NeoplasticInsulin-Like Growth Factor Binding Protein 2medicine.anatomical_structureEndocrinologyCarcinogenesisSignal TransductionHormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme
researchProduct