Search results for "ADENOCARCINOMA"

showing 10 items of 589 documents

Zeolite-silver-zinc nanoparticles : biocompatibility and their effect on the compressive strength of mineral trioxide aggregate

2016

Background This study was carried out to evaluate the biocompatibility of zeolite-silver-zinc (Ze-Ag-Zn) nanoparticles and their effect on the compressive strength of Mineral Trioxide Aggregate (MTA). Material and Methods Biocompatibility was evaluated by an MTT assay on the pulmonary adenocarcinoma cells with 0.05, 0.1, 0.25, 0.5, 1 and 5 mg/mL concentrations of Ze-Ag-Zn. For compressive strength test, four groups containing 15 stainless-steel cylinders with an internal diameter of 4 and a height of 6 mm were prepared and MTA (groups 1 and 2) or MTA + 2% Ze-Ag-Zn (groups 3 and 4) were placed in the cylinders. The compressive strength was evaluated using a universal testing machine 4 days a…

0106 biological sciencesMineral trioxide aggregateUniversal testing machineBiocompatibilityChemistryResearchPulmonary adenocarcinomaMineralogy030206 dentistryZinc nanoparticles:CIENCIAS MÉDICAS [UNESCO]01 natural sciences03 medical and health sciences0302 clinical medicineCompressive strength010608 biotechnologyBiomaterials and Bioengineering in DentistryUNESCO::CIENCIAS MÉDICASMTT assayZeoliteGeneral DentistryNuclear chemistry
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Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

2016

AbstractA fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved …

0301 basic medicineAcute promyelocytic leukemiaScienceEGFRRetinoic acidMice NudeTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundDifferentiation therapySettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungCell Line TumorGATA6 Transcription FactormedicineRetinoic acidAnimalsHumansLung cancerProtein Kinase InhibitorsWnt Signaling PathwayTranscription factorCell ProliferationMultidisciplinaryQRWnt signaling pathwayCell Differentiationmedicine.diseaseG1 Phase Cell Cycle CheckpointsXenograft Model Antitumor Assaysrespiratory tract diseasesErbB Receptorslung cancerAnimals; Carcinoma Non-Small-Cell Lung; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Drug Resistance Neoplasm; ErbB Receptors; G1 Phase Cell Cycle Checkpoints; GATA6 Transcription Factor; Humans; Mice Nude; Protein Kinase Inhibitors; Signal Transduction; Tretinoin; Wnt Signaling Pathway; Xenograft Model Antitumor Assays030104 developmental biologychemistryDrug Resistance NeoplasmImmunologyCancer researchMedicineAdenocarcinomaEngineering sciences. TechnologyTyrosine kinaseSignal Transduction
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Quantitative patterns of Hsps in tubular adenoma compared with normal and tumor tissues reveal the value of Hsp10 and Hsp60 in early diagnosis of lar…

2016

Large bowel carcinogenesis involves accumulation of genetic alterations leading to transformation of normal mucosa into dysplasia and, lastly, adenocarcinoma. It is pertinent to elucidate the molecular changes occurring in the pre-neoplastic lesions to facilitate early diagnosis and treatment. Heat shock proteins (Hsps), many of which are molecular chaperones, are implicated in carcinogenesis, and their variations with tumor progression encourage their study as biomarkers. There are many reports on Hsps and cancer but none to our knowledge on their systematic quantification in pre-neoplastic lesions of the large bowel. We performed immunohistochemical determinations of Hsp10, Hsp60, Hsp70, …

0301 basic medicineAdenomaMaleDysplasiaPathologymedicine.medical_specialtyColorectal cancerColonLarge bowelChaperoneBiologyAdenocarcinomamedicine.disease_causeBiochemistryMitochondrial Proteins03 medical and health sciencesBiomarker; Chaperone; Dysplasia; Hsps; Large bowel; Tubular adenoma; Biochemistry; Cell Biology0302 clinical medicineTubular adenomaHeat shock proteinmedicineBiomarkers TumorChaperonin 10HspHumansIntestinal MucosaEarly Detection of CancerAgedTubular adenomaAged 80 and overLamina propriaOriginal PaperBiomarkerCell BiologyChaperonin 60Middle Agedmedicine.disease030104 developmental biologymedicine.anatomical_structureDysplasiaTumor progression030220 oncology & carcinogenesisCase-Control StudiesImmunologyAdenocarcinomaFemaleCarcinogenesisColorectal Neoplasms
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FAST: a randomised phase II study of zolbetuximab (IMAB362) plus EOX versus EOX alone for first-line treatment of advanced CLDN18.2-positive gastric …

2021

Claudin 18.2 (CLDN18.2) is contained within normal gastric mucosa epithelial tight junctions; upon malignant transformation, CLDN18.2 epitopes become exposed. Zolbetuximab, a chimeric monoclonal antibody, mediates specific killing of CLDN18.2-positive cells through immune effector mechanisms.The FAST study enrolled advanced gastric/gastro-oesophageal junction and oesophageal adenocarcinoma patients (aged ≥18 years) with moderate-to-strong CLDN18.2 expression in ≥40% tumour cells. Patients received first-line epirubicin + oxaliplatin + capecitabine (EOX, arm 1, n = 84) every 3 weeks (Q3W), or zolbetuximab + EOX (loading dose, 800 mg/mIn the overall population, both PFS [hazard ratio (HR) = 0…

0301 basic medicineAdultmedicine.medical_specialtyAdolescentEsophageal NeoplasmsPopulationMedizinPhases of clinical researchAdenocarcinomaGastroenterologyLoading doseCapecitabine03 medical and health sciences0302 clinical medicineStomach NeoplasmsInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineClinical endpointHumanseducationCapecitabineeducation.field_of_studybusiness.industryHazard ratioAntibodies MonoclonalHematologyOxaliplatin030104 developmental biologyOncology030220 oncology & carcinogenesisClaudinsEsophagogastric Junctionbusinessmedicine.drugEpirubicinAnnals of oncology : official journal of the European Society for Medical Oncology
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The Barrett‐associated variants at GDF 7 and TBX 5 also increase esophageal adenocarcinoma risk

2016

Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) represent two stages within the esophagitis-metaplasia-dysplasia-adenocarcinoma sequence. Previously genetic risk factors have been identified that confer risk to BE and EAC development. However, to which extent the genetic variants confer risk to different stages of the BE/EAC sequence remains mainly unknown. In this study we analyzed three most recently identified BE variants at the genes GDF7 (rs3072), TBX5 (rs2701108), and ALDH1A2 (rs3784262) separately in BE and EAC samples in order to determine their risk effects during BE/EAC sequence. Our data show that rs3072 at GDF7 and rs2701108 at TBX5 are also associated with EAC and …

0301 basic medicineCancer ResearchCase-control studyGenome-wide association studyLocus (genetics)Biologymedicine.diseaseBioinformaticshumanitiesALDH1A203 medical and health sciences030104 developmental biologymedicine.anatomical_structureOncologyGenetic variationCancer researchmedicineAdenocarcinomaRadiology Nuclear Medicine and imagingEsophagusGeneCancer Medicine
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Concepts to Target MYC in Pancreatic Cancer.

2016

Abstract Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792–8. ©2016 AACR.

0301 basic medicineCancer ResearchPoor prognosisPancreatic ductal adenocarcinomaendocrine system diseasesGene regulatory networkAntineoplastic AgentsBiologymedicine.disease_causeBioinformaticsProto-Oncogene Proteins c-myc03 medical and health sciencesPancreatic cancerCarcinomamedicineAnimalsHumansGene Regulatory NetworksMolecular Targeted TherapyProtein Kinase InhibitorsCancerGenetic Variationmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyOncologyCarrier proteinCancer researchKRASCarrier ProteinsCarcinoma Pancreatic DuctalProtein BindingSignal TransductionMolecular cancer therapeutics
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Colorectal Cancer Cell Line SW480 and SW620 Released Extravascular Vesicles: Focus on Hypoxia-induced Surface Proteome Changes

2018

Background/aim Extravascular vesicle (EV) proteome closely reflects the proteome of the cell of origin. Therefore, cancer cell-derived EV proteomic analysis could help in identifying cancer biomarkers. This study's goal was to investigate hypoxia-induced proteomic changes in EV released from hypoxic human isogenic non-metastatic colorectal cancer cells SW480 and metastatic colorectal cancer cells SW620. Materials and methods EV were characterized by western blot, transmission electron microscopy, proteomic analysis using liquid chromatography time-of-flight-mass spectrometry and quantified by an label-free intensity-based absolute quantitation (iBAQ) approach. Results A total of 16 proteins…

0301 basic medicineCancer ResearchProteomeFocus (geometry)Colorectal cancerAdenocarcinomaExtracellular Vesicles03 medical and health sciences0302 clinical medicineWestern blotTandem Mass SpectrometryCell Line TumorBiomarkers TumormedicineHumansmedicine.diagnostic_testChemistryVesicleCancerGeneral MedicineHypoxia (medical)medicine.diseaseMolecular biologyCell HypoxiaNeoplasm Proteins030104 developmental biologyOncology030220 oncology & carcinogenesisProteomeCancer biomarkersmedicine.symptomColorectal NeoplasmsChromatography LiquidAnticancer Research
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HGF/MET Axis Induces Tumor Secretion of Tenascin-C and Promotes Stromal Rewiring in Pancreatic Cancer

2021

Simple Summary It has been previously shown that activation of the MET receptor by its ligand, the hepatocyte growth factor (HGF), modulates the tumor-stroma cross-talk in models of pancreatic cancer. We now wish to cast light on the molecular mechanisms by which this ligand/receptor pair sustains the interaction between cancer cells and the tumor microenviroment. To this end, we compared data obtained by large-scale analysis of gene expression in pancreatic cancer cells grown in the presence of HGF versus cells grown in the presence of HGF and treated with specific inhibitors of HGF/MET signaling. By clustering differentially expressed genes according to functional groups, we identified ca…

0301 basic medicineCancer ResearchStromal cellpancreatic ductal adenocarcinomaArticle03 medical and health sciences0302 clinical medicinePancreatic tumorPancreatic cancerMET oncogenemedicinetumor microenvironmentmetastasisHepatocyte growth factor; MET oncogene; Metastasis; Pancreatic ductal adenocarcinoma; Tenascin C; Tumor microenvironmentRC254-282Tumor microenvironmentbiologyChemistryTenascin Ctenascin CNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyhepatocyte growth factorOncology030220 oncology & carcinogenesisCancer cellHepatic stellate cellbiology.proteinCancer researchHepatocyte growth factormedicine.drugCancers
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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Role of Surgical Versus Clinical Staging in Chemoradiated FIGO Stage IIB-IVA Cervical Cancer Patients—Acute Toxicity and Treatment Quality of the Ute…

2015

The Uterus-11 trial was designed to evaluate the role of surgical staging in patients with cervical cancer before primary chemoradiation therapy (CRT). The present report provides the toxicity data stratified by the treatment arm and technique.A total of 255 patients with carcinoma of the uterine cervix (International Federation of Gynecology and Obstetrics stage IIB-IVA) were randomized to either surgical staging followed by CRT (arm A) or clinical staging followed by CRT (arm B). Patients with para-aortic metastases underwent extended field radiation therapy (RT). Brachytherapy was mandatory. The present report presents the acute therapy-related toxicities stratified by treatment arm and …

0301 basic medicineCancer Researchmedicine.medical_treatmentBrachytherapyUterine Cervical NeoplasmsCarboplatinlaw.invention0302 clinical medicineRandomized controlled trialLeukocytopenialawGermanyProspective StudiesStage (cooking)Cervical cancerRadiationRadiotherapy DosageChemoradiotherapyMiddle AgedOncology030220 oncology & carcinogenesisCarcinoma Squamous CellFemaleAdultmedicine.medical_specialtyBrachytherapyAntineoplastic AgentsContext (language use)AdenocarcinomaDisease-Free SurvivalCarcinoma AdenosquamousYoung Adult03 medical and health sciencesmedicineHumansRadiology Nuclear Medicine and imagingAgedNeoplasm Stagingbusiness.industrymedicine.diseaseSurgeryRadiation therapy030104 developmental biologyGynecologyRadiation OncologyLymph Node ExcisionRadiotherapy Intensity-ModulatedCisplatinbusinessChemoradiotherapyInternational Journal of Radiation Oncology*Biology*Physics
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