Search results for "malignant transformation"

showing 10 items of 108 documents

Recurrent odontogenic ghost cell carcinoma (OGCC) at a reconstructed fibular flap : a case report with immunohistochemical findings

2010

Odontogenic ghost cell carcinoma (OGCC), a malignant counterpart of the odontogenic ghost cell tumor (OGCT), with aggressive growth characteristics, is exceedingly rare. A painful swelling in the jaw with local paresthesia is the most common symptom. We described a case of 47-year Korean woman who had a rare central epithelial odontogenic ghost cell carcinoma which recurred at reconstructed fibular flap. Immunohistochemical differences between OGCT and OGCC analyzed using primary and recurred surgical specimen. On the basis of this case, the tumor started as an OGCT and transformed into OGCC with highly aggressive, rapidly growing, infiltrative tumors. Our findings suggest that some of the …

Pathologymedicine.medical_specialtymedicine.medical_treatmentOdontogenic TumorsMalignancySurgical FlapsMalignant transformationMedicineHumansGeneral DentistryOdontogenic ghost cell tumorFibular flapbusiness.industryWide local excisionGhost cellMiddle Agedmedicine.disease:CIENCIAS MÉDICAS [UNESCO]ImmunohistochemistryMandibular NeoplasmsOdontogenic ghost cell carcinomaOtorhinolaryngologyFibulaUNESCO::CIENCIAS MÉDICASImmunohistochemistrySurgeryFemaleNeoplasm Recurrence Localbusiness
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Lactate in solid malignant tumors: potential basis of a metabolic classification in clinical oncology.

2004

A number of studies have demonstrated that malignant transformation is associated with an increase in glycolytic flux and in anaerobic and aerobic cellular lactate excretion. Using quantitative bioluminescence imaging in various primary carcinomas in patients (uterine cervix, head and neck, colorectal region) at first diagnosis of the disease, we showed that lactate concentrations in tumors in vivo could be relatively low or extremely high (up to 40 micromol/g) in different individual tumors or within the same lesion. In all tumor entities investigated, high molar concentrations of lactate were correlated with a high incidence of distant metastasis already in an early stage of the disease. …

PharmacologyPathologymedicine.medical_specialtyOrganic ChemistryBiologyMalignancymedicine.diseaseMedical OncologyBiochemistryMalignant transformationchemistry.chemical_compoundchemistryIn vivoTumor progressionLactate dehydrogenaseNeoplasmsDrug DiscoveryCancer cellmedicineMolecular MedicineBioluminescence imagingAnimalsHumansLactic AcidAnaerobic exerciseCurrent medicinal chemistry
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Manipulation of glycolysis in malignant tumors: fantasy or therapy?

2009

After Warburg stated his hypothesis on tumor cell metabolism about 80 years ago, the field of carbohydrate metabolism of cancer cells and solid tumors is experiencing a boom for the past few years. Numerous studies have been focused on the characteristics of cancer metabolism and its accessibility to novel therapeutic interventions. Malignant transformation is associated with an increase in glycolytic flux, mainly caused by an upregulation of numerous glycolysis-related genes in the majority of human cancers. As a consequence of these alterations, tumor cells are producing lactate at higher levels compared to non-malignant tissue, even in the presence of oxygen, a phenomenon termed “aerobic…

Pharmacologymedicine.medical_specialtymedicine.medical_treatmentOrganic ChemistryCancerFree Radical ScavengersBiologymedicine.diseaseBiochemistryWarburg effectMalignant transformationTargeted therapyGlycolysis InhibitionEndocrinologyAnaerobic glycolysisInternal medicineNeoplasmsDrug DiscoveryCancer cellmedicineCancer researchMolecular MedicineHumansGlycolysisGlycolysisCurrent medicinal chemistry
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Therapeutic targeting of apoptotic pathways in cancer.

2006

Programmed cell death (apoptosis) is a key tumor suppressor mechanism. Consequently, most if not all cancers develop mechanisms to abolish or circumvent this genetic program. Besides enabling malignant transformation and tumor progression, defects in apoptosis can result in resistance to cytotoxic cancer therapies. Much progress has been made in the delineation of the molecular pathways leading to apoptosis. This allows the identification of target molecules and lead compounds to develop novel therapies, which make use of this intrinsic death program for the treatment of cancer. Here, we review the current understanding of apoptotic signal transduction pathways, and strategies of their ther…

Programmed cell deathClinical BiochemistryAntineoplastic AgentsApoptosislaw.inventionMalignant transformationDrug Delivery SystemslawNeoplasmsDrug DiscoverymedicineAnimalsHumansPharmacologyMechanism (biology)business.industryCancermedicine.diseaseApoptosisTumor progressionGene TargetingCancer researchMolecular MedicineSuppressorSignal transductionbusinessSignal TransductionCurrent drug targets
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Iron Metabolism in the Tumor Microenvironment-Implications for Anti-Cancer Immune Response

2021

New insights into the field of iron metabolism within the tumor microenvironment have been uncovered in recent years. Iron promotes the production of reactive oxygen species, which may either trigger ferroptosis cell death or contribute to malignant transformation. Once transformed, cancer cells divert tumor-infiltrating immune cells to satisfy their iron demand, thus affecting the tumor immunosurveillance. In this review, we highlight how the bioavailability of this metal shapes complex metabolic pathways within the tumor microenvironment and how this affects both tumor-associated macrophages and tumor-infiltrating lymphocytes functions. Furthermore, we discuss the potentials as well as th…

Programmed cell deathIronReviewMalignant transformationImmune systemNeoplasmsTumor MicroenvironmentmedicineHumanscanceriron metabolismlcsh:QH301-705.5chemistry.chemical_classificationReactive oxygen speciesTumor microenvironmentInnate immune systemImmunityCancerGeneral Medicinemedicine.diseaseferroptosisferroptosiadaptive immune response tumor microenvironmentlcsh:Biology (General)chemistryCancer cellCancer researchinnate immune response
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Curcumin Affects HSP60 Folding Activity and Levels in Neuroblastoma Cells.

2020

The fundamental challenge in fighting cancer is the development of protective agents able to interfere with the classical pathways of malignant transformation, such as extracellular matrix remodeling, epithelial−mesenchymal transition and, alteration of protein homeostasis. In the tumors of the brain, proteotoxic stress represents one of the main triggering agents for cell transformation. Curcumin is a natural compound with anti-inflammatory and anti-cancer properties with promising potential for the development of therapeutic drugs for the treatment of cancer as well as neurodegenerative diseases. Among the mediators of cancer development, HSP60 is a key factor for the maintenance of…

Protein FoldingCurcuminCell SurvivalCellCatalysisMalignant transformationCell Linelcsh:ChemistryInorganic ChemistryMitochondrial Proteinschemistry.chemical_compoundNeuroblastomaDownregulation and upregulationHeat shock proteinmedicinepost-translational modificationsHumansSecretionPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyCell ProliferationHeat shock proteinDose-Response Relationship DrugCommunicationOrganic Chemistrymolecular chaperonesUbiquitinationGeneral MedicineChaperonin 60Computer Science ApplicationsCell biologyUp-RegulationBrain tumorGene Expression Regulation Neoplasticmedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999chemistryApoptosisheat shock proteinsMolecular chaperoneCurcuminbrain tumorsHSP60Post-translational modificationHSP60extracellular HSP60International journal of molecular sciences
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Cystic mucinous adenocarcinoma of the lung: a case report.

2011

Abstract Mucinous cystic tumors of the lung are uncommon, the preoperative pathologic diagnosis is difficult and their biological behavior is still controversial. We report the case of a patient with a clinically benign cystic lesion that post-operatively showed to be consistent with an invasive adenocarcinoma arising in a mucinous cystadenoma of the lung, We underline the difficulty of the clinical pre-operative diagnosis of this cystic neoplasia radiologically mimicking a hydatid cyst, and we report the negative TTF1 immunostaining potentially misleading in the differential diagnosis with metastatic mucinous carcinomas. Finallly, we evidence the presence of a pre-existing mucinous benign …

Pulmonary and Respiratory MedicinePathologymedicine.medical_specialtyLung NeoplasmsProliferation indexCystic mucinous adenocarcinoma lungSettore MED/21 - Chirurgia Toracicalcsh:SurgeryEnzyme-Linked Immunosorbent AssayCase ReportSettore MED/08 - Anatomia PatologicaMalignant transformationMetastasislcsh:RD78.3-87.3Diagnosis DifferentialFatal OutcomeCystadenoma MucinousBronchoscopymedicineAdenocarcinoma of the lungHumansMucinous cystadenomabusiness.industrylcsh:RD1-811General MedicineMiddle Agedmedicine.diseaseImmunohistochemistrylcsh:AnesthesiologyCystadenomaAdenocarcinomaSurgeryFemaleRadiologyDifferential diagnosisCardiology and Cardiovascular MedicinebusinessTomography X-Ray ComputedJournal of cardiothoracic surgery
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Age-related and tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-DNA glycosylase (Ogg1) deficient mice.

2001

Mutations that influence the repair of oxidative DNA modifications are expected to increase the steady-state (background) levels of these modifications and thus create a mutator phenotype that predisposes to malignant transformation. We have analysed the steady-state levels and repair kinetics of oxidative DNA modifications in cells of homozygous ogg1(-/-) null mice, which are deficient in Ogg1 protein, a DNA repair glycosylase that removes the miscoding base 8-hydroxyguanine (8-oxoG) from the genome. Oxidative purine modifications including 8-oxoG were quantified by means of an alkaline elution assay in combination with Fpg protein, the bacterial functional analogue of Ogg1 protein. In pri…

PurineMaleCancer ResearchGuanineDNA RepairOxidative phosphorylationBiologymedicine.disease_causeMalignant transformationchemistry.chemical_compoundMiceTranscription (biology)medicineAnimalsN-Glycosyl HydrolasesMice KnockoutCell growthAge FactorsGeneral MedicineDNAFibroblastsMolecular biologyOxygenOxidative StresschemistryDNA-Formamidopyrimidine GlycosylaseDNA glycosylaseOrgan SpecificityImmunologyHepatocytesOxidative stressDNACell DivisionDNA DamageCarcinogenesis
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Entrectinib: a potent new TRK, ROS1, and ALK inhibitor

2015

Abstract: Introduction: Receptor tyrosine kinases (RTKs) and their signaling pathways, control normal cellular processes; however, their deregulation play important roles in malignant transformation. In advanced non-small cell lung cancer (NSCLC), the recognition of oncogenic activation of specific RTKs, has led to the development of molecularly targeted agents that only benefit roughly 20% of patients. Entrectinib is a pan-TRK, ROS1 and ALK inhibitor that has shown potent anti-neoplastic activity and tolerability in various neoplastic conditions, particularly NSCLC. Areas covered: This review outlines the pharmacokinetics, pharmacodynamics, mechanism of action, safety, tolerability, pre-cl…

Receptor Protein-Tyrosine KinasesEntrectinibNTRK1NTRK2NTRK3Receptor tyrosine kinaseEntrectinibMalignant transformationAntineoplastic AgentNeoplasmsProtein-Tyrosine KinaseALK; colorectal cancer; Entrectinib; non-small cell lung cancer; NTRK1; NTRK2; NTRK3; precision medicine; ROS1; salivary gland cancer; TrkA; TrkB; TrkC; Animals; Antineoplastic Agents; Benzamides; Humans; Indazoles; Neoplasms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Receptor; trkA; Receptor; trkB; Receptor; trkC; Pharmacology; Pharmacology (medical)Anaplastic Lymphoma KinasePharmacology (medical)salivary gland cancerProto-Oncogene ProteinbiologyTrkAPharmacology. TherapyTrkCTrkBGeneral MedicineProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinaseBenzamidesmedicine.symptomROS1ReceptorHumanIndazolesmedicine.drug_classprecision medicineAntineoplastic Agentscolorectal cancerBenzamideProto-Oncogene ProteinsmedicineROS1AnimalsHumansReceptor trkBReceptor trkCReceptor trkAnon-small cell lung cancerPharmacologyAnimalReceptor Protein-Tyrosine KinasesALK inhibitorIndazoleMechanism of actionALKTrk receptorbiology.proteinCancer researchNeoplasmALK; colorectal cancer; Entrectinib; non-small cell lung cancer; NTRK1; NTRK2; NTRK3; precision medicine; ROS1; salivary gland cancer; TrkA; TrkB; TrkC; Animals; Antineoplastic Agents; Benzamides; Humans; Indazoles; Neoplasms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Receptor trkA; Receptor trkB; Receptor trkC; Pharmacology; Pharmacology (medical)Expert Opinion on Investigational Drugs
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Controversial issues in soft tissue solitary fibrous tumors: A pathological and molecular review

2019

The clinical evolution of solitary fibrous tumor (SFT) remains unclear. Although various clinical, morphological and molecular criteria may indicate increased risk of malignancy, some SFT can still progress despite having a clearly benign appearance. Various risk stratification systems have been proposed, but unfortunately they are not sufficient to precisely determine the malignant potential. In this review, we discuss current knowledge on SFT, focusing on the following controversial issues: (i) the diverse morphologic spectrum: 'the great simulator;' (ii) malignant transformation or dedifferentiation; (iii) current risk stratification systems; and (iv) molecular factors associated with cl…

Risk0301 basic medicinePathologymedicine.medical_specialtySolitary fibrous tumorMalignancyPathology and Forensic MedicineMalignant transformationDiagnosis Differential03 medical and health sciences0302 clinical medicinemedicineHumansPathologicalbusiness.industrySoft tissueGeneral MedicineCell DedifferentiationPrognosismedicine.diseaseImmunohistochemistryCell Transformation Neoplastic030104 developmental biologyIncreased riskSolitary Fibrous Tumors030220 oncology & carcinogenesisRisk stratificationbusinessPathology International
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