Search results for " adenocarcinoma"

showing 10 items of 140 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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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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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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Circulating Tumor DNA Detection by Digital-Droplet PCR in Pancreatic Ductal Adenocarcinoma: A Systematic Review

2021

Simple Summary Pancreatic cancer is a digestive tumor that is most difficult to treat and carries one of the worst prognoses. The anatomical location of the pancreas makes it very difficult to obtain enough tumor material to establish a molecular diagnosis, so knowing the biology of this tumor and implementing new targeted-therapies is still a pending issue. The use of liquid biopsy, a blood sample test to detect circulating-tumor DNA fragments (ctDNA), is key to overcoming this difficulty and improving the evolution of this tumor. Liquid biopsies are equally representative of the tissue from which they come and allow relevant molecular and diagnostic information to be obtained in a faster …

0301 basic medicineCancer Researchpancreatic cancerpancreatic ductal adenocarcinoma (PDAC)lcsh:RC254-28203 medical and health sciences0302 clinical medicineCirculating tumor cellPancreatic cancerBiopsydigital-droplet PCR (ddPCR)MedicineLiquid biopsymedicine.diagnostic_testbusiness.industryctDNAmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMinimal residual disease030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer cellCancer researchBiomarker (medicine)Systematic ReviewbusinessPancreasCancers
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Water: The First Archaic Mutagen of Evolution, the Adoptive Mother of Currently Nucleic Acids

2016

It would be intuitive to think that for the evolutionary onset of nucleic acids, and even before of their monomeric constituents, the water was crucial. Within the series of evolutions which start from the origin of the universe and still cannot, by definition, be considered concluded, certainly among the geothermal evolution end and the beginning of the chemical one, on Earth, the moment was favorable for the arrival of the first proto-nucleotides: from underground deposits of methanehydrate [1] and phosphate, with the support of all known pre-biotic physical-chemical conditions, were made the monomeric components of nucleic acids. The cradle of nucleic acids does not seem to have been so …

0301 basic medicineGeneticsHuman evolutionary geneticsDNA damageMutagenesisMutagenBiologymedicine.disease_causeEvolutionary geneticsSettore BIO/18 - Genetica03 medical and health sciences030104 developmental biologymedicineNucleic acidEvolutionary mutagenesiDuctal adenocarcinomaAdoptive motherCarcinogenesisJournal of Carcinogenesis & Mutagenesis
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Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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Comprehensive Analysis of SWI/SNF Inactivation in Lung Adenocarcinoma Cell Models

2020

Simple Summary: Mammalian SWI/SNF complexes regulate gene expression by reorganizing the way DNA is packaged into chromatin. SWI/SNF subunits are recurrently altered in tumors at multiple levels, including DNA mutations as well as alteration of the levels of RNA and protein. Cancer cell lines are often used to study SWI/SNF function, but their patterns of SWI/SNF alterations can be complex. Here, we present a comprehensive characterization of DNA mutations and RNA and protein expression of SWI/SNF members in 38 lung adenocarcinoma (LUAD) cell lines. We show that over 85% of our cell lines harbored at least one alteration in one SWI/SNF subunit. In addition, over 75% of our cell lines lacked…

0301 basic medicineLung adenocarcinomaCancer ResearchcellsCellgenetic processesmacromolecular substancesBiologylcsh:RC254-282Articlelaw.inventionTranscriptome03 medical and health sciences0302 clinical medicinelawmedicineEpigeneticsMulti-omicsSWI/SNF complexepigeneticsCancermulti-omicslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaselung adenocarcinomaSWI/SNFcell models3. Good healthCell biologyChromatinenzymes and coenzymes (carbohydrates)lung cancer030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell modelSuppressorEpigeneticsbiological phenomena cell phenomena and immunityLung cancerSWI/SNF complex
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PD-L1 in small bowel adenocarcinoma is associated with etiology and tumor-infiltrating lymphocytes, in addition to microsatellite instability

2020

Small bowel adenocarcinomas (SBAs) are often associated with poor prognosis and have limited therapeutic options. Programmed cell death protein-1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway blockade is an effective treatment in many microsatellite instability-high (MSI-H) solid tumors. We aimed at investigating PD-L1 and PD-1 expression in non-hereditary, non-ampullary SBAs, associated with celiac disease (CeD), Crohn’s disease (CrD), or sporadic, recruited through the Small Bowel Cancer Italian Consortium. We assessed PD-L1 and PD-1 by immunohistochemistry in a series of 121 surgically resected SBAs, including 34 CeD-SBAs, 49 CrD-SBAs, and 38 sporadic SBAs. PD-L1 and PD-1 express…

0301 basic medicineMalePD-L1 - small bowel adenocarcinoma - tumor-infiltrating lymphocytes - microsatellite instabilityPathologyBLOCKADEColorectal cancerLymphocyteSmall bowel adenocarcinomaGastroenterologyB7-H1 AntigenSettore MED/120302 clinical medicineCrohn DiseaseIntestine Smallsmall bowel adenocarcinomaSmall bowel adenocarcinomasMEDULLARY CARCINOMA; MORPHOLOGY; EXPRESSION; BLOCKADE; CANCERbiologymicrosatelliteinstabilityMiddle AgedCANCERmedicine.anatomical_structureMedullary carcinomatumor infiltrating lymphocytes030220 oncology & carcinogenesistumor-infiltrating lymphocytesAdenocarcinomaFemaleMicrosatellite InstabilityPD-L1Adultmedicine.medical_specialtysmall bowel adenocarcinoma tumor-infiltrating lymphocytes microsatelliteinstabilitySettore MED/08 - Anatomia PatologicaAdenocarcinomaMEDULLARY CARCINOMAPD-L1 small bowel adenocarcinomaNOPathology and Forensic Medicine03 medical and health sciencesLymphocytes Tumor-InfiltratingInternal medicinePD-L1expressionIntestinal NeoplasmsBiomarkers TumormedicineHumansPD-L1; small bowel adenocarcinoma; tumor infiltrating lymphocytesPD-L1 in small bowel adenocarcinoma MSI-HSmall bowel adenocarcinoma expression microsatellite instability biomarkersAgedRetrospective Studiesbusiness.industryTumor-infiltrating lymphocytesbiomarkersCancerCorrectionMicrosatellite instabilitymedicine.diseaseCeliac Disease030104 developmental biologybiology.proteinEtiologyMORPHOLOGYbusiness
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Early miR-223 Upregulation in Gastroesophageal Carcinogenesis

2017

Objectives: To test miR-223 upregulation during gastric (intestinal-type) and Barrett esophageal carcinogenesis. Methods: miR-223 expression was assessed by quantitative reverse transcription polymerase chain reaction in a series of 280 gastroesophageal biopsy samples representative of the whole spectrum of phenotypic changes involved in both carcinogenetic cascades. The results were further validated by in situ hybridization on multiple tissue specimens obtained from six surgically treated gastroesophageal adenocarcinomas. miR-223 expression was also assessed in plasma samples from 30 patients with early stage (ie, stages I and II) gastroesophageal adenocarcinoma and relative controls. Res…

0301 basic medicineMalePathologyEsophageal NeoplasmsAtrophic gastritisCarcinogenesisPreneoplastic lesionsBarrett carcinogenesisGastroenterology0302 clinical medicineEarly Detection of CancerIn Situ HybridizationBarrett carcinogenesis; Gastric adenocarcinoma; Preneoplastic lesions; microRNA; Adenocarcinoma; Aged; Barrett Esophagus; Biomarkers Tumor; Carcinogenesis; Early Detection of Cancer; Esophageal Neoplasms; Esophagogastric Junction; Female; Humans; In Situ Hybridization; Male; MicroRNAs; Middle Aged; Retrospective Studies; Reverse Transcriptase Polymerase Chain Reaction; Stomach Neoplasms; Up-RegulationTumormedicine.diagnostic_testmicroRNAReverse Transcriptase Polymerase Chain ReactionBarrett carcinogenesiIntestinal metaplasiaGeneral MedicineMiddle AgedUp-RegulationReverse transcription polymerase chain reactionmedicine.anatomical_structure030220 oncology & carcinogenesisAdenocarcinomaBiomarker (medicine)FemaleEsophagogastric Junctionmedicine.medical_specialty2734BiologyAdenocarcinoma03 medical and health sciencesBarrett EsophagusStomach NeoplasmsInternal medicineBiopsyBiomarkers TumormedicineHumansEsophagusAgedRetrospective StudiesGastric adenocarcinomaCancermedicine.diseasedigestive system diseasesBarrett carcinogenesis; Gastric adenocarcinoma; microRNA; Preneoplastic lesions; Adenocarcinoma; Aged; Barrett Esophagus; Biomarkers Tumor; Carcinogenesis; Early Detection of Cancer; Esophageal Neoplasms; Esophagogastric Junction; Female; Humans; In Situ Hybridization; Male; MicroRNAs; Middle Aged; Retrospective Studies; Reverse Transcriptase Polymerase Chain Reaction; Stomach Neoplasms; Up-Regulation; 2734MicroRNAs030104 developmental biologyBiomarkers
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