Search results for "Progression"

showing 10 items of 1251 documents

Tumor Hypoxia: Causative Factors, Compensatory Mechanisms, and Cellular Response

2004

Abstract Learning Objectives After completing this course, the reader will be able to: Explain the effect of hypoxia on resistance to treatment. Describe the causes of tumor hypoxia. Characterize cellular response to hypoxia. Access and take the CME test online and receive 1 hour of AMA PRA category 1 credit at CME.TheOncologist.com Hypoxia is a characteristic feature of locally advanced solid tumors resulting from an imbalance between oxygen (O2) supply and consumption. Major causative factors of tumor hypoxia are abnormal structure and function of the microvessels supplying the tumor, increased diffusion distances between the nutritive blood vessels and the tumor cells, and reduced O2 tra…

Cancer ResearchCell SurvivalAnemiamedicine.medical_treatmentPhotodynamic therapyDiseaseNeoplasmsmedicineHumansNeovascularization PathologicTumor hypoxiabusiness.industryAnemiaTumor OxygenationHypoxia (medical)medicine.diseaseAdaptation PhysiologicalCell HypoxiaOxygenRadiation therapyCell Transformation NeoplasticOncologyDrug Resistance NeoplasmImmunologyDisease ProgressionCancer researchHemoglobinmedicine.symptombusinessThe Oncologist
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Pimasertib Versus Dacarbazine in Patients With Unresectable NRAS-Mutated Cutaneous Melanoma: Phase II, Randomized, Controlled Trial with Crossover

2020

This study investigated the efficacy and safety of pimasertib (MEK1/MEK2 inhibitor) versus dacarbazine (DTIC) in patients with untreated NRAS-mutated melanoma. Phase II, multicenter, open-label trial. Patients with unresectable, stage IIIc/IVM1 NRAS-mutated cutaneous melanoma were randomized 2:1 to pimasertib (60 mg

Cancer ResearchGastroenterologypimasertiblaw.invention0302 clinical medicineRandomized controlled triallawClinical endpoint030212 general & internal medicineMalignant melanomaHazard ratioProgression-free survivalSciences bio-médicales et agricoleslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthDacarbazineOncology[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology030220 oncology & carcinogenesismedicine.symptomPimasertibmedicine.drugQuality of lifemedicine.medical_specialtyNauseaDacarbazinemalignant melanomadacarbazine[SDV.CAN]Life Sciences [q-bio]/CancerN-(2 3-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamideNeutropeniaN-(23-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamidelcsh:RC254-282Article03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerInternal medicinemedicineProgression-free survivalAdverse effectbusiness.industry[SDV.MHEP.DERM] Life Sciences [q-bio]/Human health and pathology/Dermatologymedicine.diseaseadverse eventsCancérologiequality of lifeAdverse events[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologybusinessprogression-free survival[SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology
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Lactate enhances motility of tumor cells and inhibits monocyte migration and cytokine release.

2011

In solid malignant tumors, lactate has been identified as a prognostic parameter for metastasis and overall survival of patients. To investigate the effects of lactate on tumor cell migration, Boyden chamber assays were applied. We could show here that lactate enhances tumor cell motility of head and neck carcinoma cell lines significantly in a dose-dependent manner. The changes in tumor cell migration could be attributed to L-lactate or a conversion of lactate to pyruvate, as only these two substances were able to increase migration. Addition of D-lactate or changes in osmolarity or intracellular pH did not alter the migratory potential of the cells investigated. Because lactate was shown …

Cancer ResearchIntegrin beta Chainsmedicine.medical_treatmentPopulationMotilityBiologyMonocytesCell MovementCell Line TumorNeoplasmsmedicineHumansLactic Acideducationeducation.field_of_studyMonocyteCell migrationCell cycleCytokinemedicine.anatomical_structureOncologyTumor progressionImmunologyCancer researchCytokinesTumor necrosis factor alphaInternational journal of oncology
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Temporal molecular and biological assessment of an erlotinib-resistant lung adenocarcinoma model reveals markers of tumor progression and treatment r…

2012

Abstract Patients with lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term with tyrosine kinase inhibitors (TKI), often develop secondary mutations in EGFR associated with resistance. Mice engineered to develop lung adenocarcinomas driven by the human EGFR T790M resistance mutation are similarly resistant to the EGFR TKI erlotinib. By tumor volume endpoint analysis, these mouse tumors respond to BIBW 2992 (an irreversible EGFR/HER2 TKI) and rapamycin combination therapy. To correlate EGFR-driven changes in the lung with response to drug treatment, we conducted an integrative analysis of global transcriptome and metabolite profiling compared wit…

Cancer ResearchLung NeoplasmsCombination therapyAfatinibGene ExpressionAdenocarcinoma of LungCell Growth ProcessesAdenocarcinomaAfatinibArticleErlotinib HydrochlorideMiceAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsEpidermal growth factor receptorLung cancerErlotinib HydrochlorideProtein Kinase InhibitorsSirolimusbiologymedicine.diseaserespiratory tract diseasesErbB ReceptorsOncologyTumor progressionDrug Resistance NeoplasmCancer researchbiology.proteinDisease ProgressionQuinazolinesErlotinibTyrosine kinasemedicine.drugTranscription FactorsCancer research
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Definitive evidence for Club cells as progenitors for mutantKras/Trp53‐deficient lung cancer

2021

Accumulating evidence suggests that both the nature of oncogenic lesions and the cell-of-origin can strongly influence cancer histopathology, tumor aggressiveness and response to therapy. Although oncogenic Kras expression and loss of Trp53 tumor suppressor gene function have been demonstrated to initiate murine lung adenocarcinomas (LUADs) in alveolar type II (AT2) cells, clear evidence that Club cells, representing the second major subset of lung epithelial cells, can also act as cells-of-origin for LUAD is lacking. Equally, the exact anatomic location of Club cells that are susceptible to Kras transformation and the resulting tumor histotype remains to be established. Here, we provide de…

Cancer ResearchLung NeoplasmsLineage (genetic)Tumor suppressor geneCell of originAdenocarcinomaBiologymedicine.disease_causeMicemedicineAnimalsHumansProgenitor cellLung cancerLungMice KnockoutLungCancerEpithelial Cellsmedicine.diseaseGene Expression Regulation NeoplasticMice Inbred C57BLCell Transformation NeoplasticGenes rasmedicine.anatomical_structureOncologyMutationDisease ProgressionCancer researchKRASTumor Suppressor Protein p53International Journal of Cancer
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Patterns of Carbon-Bound Exogenous Compounds in Patients with Lung Cancer and Association with Disease Pathophysiology.

2021

Abstract Asymptomatic anthracosis is the accumulation of black carbon particles in adult human lungs. It is a common occurrence, but the pathophysiologic significance of anthracosis is debatable. Using in situ high mass resolution matrix-assisted laser desorption/ionization (MALDI) fourier-transform ion cyclotron resonance (FT-ICR) mass spectrometry imaging analysis, we discovered noxious carbon-bound exogenous compounds, such as polycyclic aromatic hydrocarbons (PAH), tobacco-specific nitrosamines, or aromatic amines, in a series of 330 patients with lung cancer in highly variable and unique patterns. The characteristic nature of carbon-bound exogenous compounds had a strong association wi…

Cancer ResearchLung NeoplasmsNitrosaminesDNA damageCarcinogenesismedicine.disease_causeMass SpectrometryTobacco UseMetabolomeTumor MicroenvironmentMedicineHumansCarcinogenesis; Carcinoma Squamous Cell/chemically induced; Carcinoma Squamous Cell/metabolism; Carcinoma Squamous Cell/pathology; Humans; Idiopathic Pulmonary Fibrosis/chemically induced; Idiopathic Pulmonary Fibrosis/metabolism; Idiopathic Pulmonary Fibrosis/pathology; Lung Neoplasms/chemically induced; Lung Neoplasms/metabolism; Lung Neoplasms/pathology; Mass Spectrometry; Metabolome; Nitrosamines/adverse effects; Polycyclic Aromatic Hydrocarbons/adverse effects; Retrospective Studies; Tobacco Use; Tumor MicroenvironmentPolycyclic Aromatic HydrocarbonsLung cancer610 Medicine & healthRetrospective StudiesAnthracosisLungbusiness.industrymedicine.diseasePathophysiologyIdiopathic Pulmonary Fibrosismedicine.anatomical_structureOncologyTumor progressionCancer researchCarcinoma Squamous CellMetabolome570 Life sciences; biologybusinessCarcinogenesis
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Expression of Hugl-1 is strongly reduced in malignant melanoma.

2005

The human gene Hugl-1 (Llgl/Lgl1) has significant homology to the Drosophila tumor suppressor gene lethal(2)giant larvae (lgl). The lgl gene codes for a cortical cytoskeleton protein, Lgl, that is involved in maintaining cell polarity and epithelial integrity. We speculate that Hugl-1 might play a role in epithelial-mesenchymal transition (EMT) and that loss of Hugl-1 expression plays a role in the development or progression of malignant melanoma. Thus, we evaluated melanoma cell lines and tissue samples of malignant melanoma for loss of Hugl-1 transcription. We found that Hugl-1 was downregulated or lost in all cell lines and in most of the tumor samples analysed, and that these losses wer…

Cancer ResearchMMP2Tumor suppressor geneMatrix Metalloproteinases Membrane-AssociatedTranscription GeneticCellBlotting WesternDown-RegulationBiologyTransfectionEpitheliumCell MovementCell Line TumorGeneticsmedicineCell AdhesionMatrix Metalloproteinase 14HumansNeoplasm InvasivenessTissue DistributionRNA MessengerCell adhesionMolecular BiologyMelanomaReverse Transcriptase Polymerase Chain ReactionMelanomaProteinsCell migrationmedicine.diseaseCadherinsImmunohistochemistryMatrix MetalloproteinasesGene Expression Regulation NeoplasticCytoskeletal Proteinsmedicine.anatomical_structureMicroscopy FluorescenceCell cultureImmunologyCancer researchDisease ProgressionMMP14Matrix Metalloproteinase 2RNAOncogene
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Biological indicators of prognosis in Ewing's sarcoma: An emerging role for lectin galactoside-binding soluble 3 binding protein (LGALS3BP)

2009

Starting from an experimental model that accounts for the 2 most important adverse processes to successful therapy of Ewing's sarcoma (EWS), chemoresistance and the presence of metastasis at the time of diagnosis, we defined a molecular signature of potential prognostic value. Functional annotation of differentially regulated genes revealed 3 major networks related to cell cycle, cell-to-cell interactions and cellular development. The prognostic impact of 8 genes, representative of these 3 networks, was validated in 56 EWS patients. High mRNA expression levels of HINT1, IFITM2, LGALS3BP, STOML2 and c-MYC were associated with reduced risk to death and lower risk to develop metastasis. At mul…

Cancer ResearchMice NudeEnzyme-Linked Immunosorbent AssaySarcoma EwingBiologyMetastasisMiceAntigens NeoplasmCell Line TumorBiomarkers TumorCell AdhesionmedicineAnimalsHumansGene SilencingRNA MessengerNeoplasm MetastasisGlycoproteinsOligonucleotide Array Sequence AnalysisTumor microenvironmentReverse Transcriptase Polymerase Chain ReactionCell CycleMatricellular proteinEwing's sarcomaCell cyclePrognosismedicine.diseaseImmunohistochemistryOncologyTumor progressionImmunologyGalactoside bindingCancer researchSarcomaCarrier ProteinsSignal TransductionInternational Journal of Cancer
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Comparative study of human colonic tumor-derived endothelial cells (HCTEC) and normal colonic microvascular endothelial cells (HCMEC): Hypoxia-induce…

2009

Colorectal carcinoma growth and progression is dependent on the vasculature of the tumor microenvironment. Tumor-derived endothelial cells differ functionally from their normal counterpart. For this reason we isolated microvascular endothelial cells from human colon cancer tissue (HCTEC) and compared them with endothelial cells from normal colonic tissue (HCMEC) of the same donor. Since hypoxia is a universal hallmark of carcinomas, we examined its effects on HCTEC of five patients in comparison with the corresponding HCMEC, with respect to the secretion of the soluble form of the two important vascular endothelial growth factor (VEGF) receptors, VEGFR-1 and -2. After dissociation by dispas…

Cancer ResearchPathologymedicine.medical_specialtyEndotheliumColonEnzyme-Linked Immunosorbent AssayCell SeparationBiologychemistry.chemical_compoundmedicineHumansCells CulturedTumor microenvironmentVascular Endothelial Growth Factor Receptor-1OncogeneMicrocirculationEndothelial CellsGeneral MedicineVascular Endothelial Growth Factor Receptor-2Cell HypoxiaEndothelial stem cellVascular endothelial growth factormedicine.anatomical_structureOncologychemistryApoptosisTumor progressionColonic NeoplasmsCancer researchTumor necrosis factor alphaOncology Reports
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Hsp60 and Hsp10 down-regulation predicts bronchial epithelial carcinogenesis in smokers with chronic obstructive pulmonary disease.

2006

BACKGROUND. The relation between smoking, chronic obstructive pulmonary disease (COPD), and lung cancer (LC) is an open field of investigation. A higher frequency of adenocarcinoma has been reported in patients with COPD. Heat shock proteins (Hsps) are implicated in tumoral cell growth and differentiation. The aim of the present study was to investigate the expression of Hsp60 and Hsp10 in bronchial biopsies from smokers with COPD and in 10 lung cancer patients and to evaluate the association between Hsps expression and carcinogenetic steps of LC. METHODS. An immunohistochemical study was performed for Hsp60 and Hsp10 in bronchial biopsies from 35 COPD (postbronchodilator forced expiratory …

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsAdenosquamous carcinomaBlotting WesternDown-Regulationchemical and pharmacologic phenomenaRespiratory MucosaAdenocarcinomaCarcinoma AdenosquamousPulmonary Disease Chronic ObstructivemedicineChaperonin 10HumansLung cancerAgedsmoking chaperone expression lung obstruction lung tumorsCOPDSettore BIO/16 - Anatomia Umanabusiness.industryRespiratory diseaseSmokingCancerChaperonin 60Middle Agedmedicine.diseasePrognosisSquamous metaplasiarespiratory tract diseasesCarcinoma BronchogenicOncologyDysplasiaDisease ProgressionAdenocarcinomabusinessCancer
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