Search results for "digestive system"

showing 10 items of 1747 documents

Introduction of WT-TP53 into pancreatic cancer cells alters sensitivity to chemotherapeutic drugs, targeted therapeutics and nutraceuticals

2018

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic malignancy and accounts for 85% of pancreatic cancers. PDAC patients have poor prognosis with a five-year survival of only 5–10%. Mutations at the TP53 gene are readily detected in pancreatic tumors isolated from PDAC patients. We have investigated the effects of restoration of wild-type (WT) TP53 activity on the sensitivity of pancreatic cancer cells to: chemotherapy, targeted therapy, as well as, nutraceuticals. Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisp…

0301 basic medicineCancer ResearchPaclitaxelendocrine system diseasesmedicine.medical_treatmentTargeted therapeuticIrinotecanDeoxycytidineTargeted therapyGlycogen Synthase Kinase 303 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorPancreatic cancerGeneticsmedicineHumansDoxorubicinTP53Signal transduction inhibitorneoplasmsMolecular BiologyCell ProliferationCisplatinChemotherapybusiness.industryPancreatic Neoplasmmedicine.diseaseGemcitabinedigestive system diseasesGemcitabinePancreatic NeoplasmsOxaliplatin030104 developmental biologyPaclitaxelchemistryFluorouracil030220 oncology & carcinogenesisCancer researchMolecular MedicineFluorouracilCisplatinbusinessDrug sensitivityHumanSignal Transductionmedicine.drug
researchProduct

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
researchProduct

Molecular Basis of Mismatch Repair Protein Deficiency in Tumors from Lynch Suspected Cases with Negative Germline Test Results

2020

Some 10&ndash

0301 basic medicineCancer Researchcongenital hereditary and neonatal diseases and abnormalitiesCARCINOMADNA mismatch repair3122 Cancerscolorectal cancersuolistosyövätBiologyGene mutationMLH1DIAGNOSISlcsh:RC254-282Article03 medical and health sciencesdeep sequencing0302 clinical medicineGermline mutationFREQUENT CAUSEMANAGEMENTLynchin oireyhtymäneoplasmspaksusuolisyöpäMUTATIONSPoint mutationMLH1METHYLATIONnutritional and metabolic diseasesNONPOLYPOSIS COLORECTAL-CANCERDEFECTSdiagnostiikkalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensdigestive system diseases3. Good healthDNA-metylaatioMSH2MSH6030104 developmental biologyLynch syndromeOncologyMSH3syöpägeenitMSH2030220 oncology & carcinogenesisCancer researchDNA mismatch repairsyöpätauditCancers
researchProduct

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
researchProduct

Abilities of β-Estradiol to interact with chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals and alter the proliferation of pa…

2019

Improving the effects of chemotherapy and reducing the side effects are important goals in cancer research. Various approaches have been examined to enhance the effectiveness of chemotherapy. For example, signal transduction inhibitors or hormonal based approaches have been included with chemo- or radio-therapy. MIA-PaCa-2 and BxPC-3 pancreatic ductal adenocarcinoma (PDAC) cells both express the estrogen receptor (ER). The effects of β-estradiol on the growth of PDAC cells has not been examined yet the ER is expressed in PDAC cells. We have examined the effects of combining β-estradiol with chemotherapeutic drugs, signal transcription inhibitors, natural products and nutraceuticals on PDAC.…

0301 basic medicineCancer Researchendocrine system diseasesβ estradiolmedicine.medical_treatmentβ-EstradiolEstrogen receptorAntineoplastic AgentsNatural product03 medical and health sciencesFood-Drug Interactions0302 clinical medicineNutraceuticalPancreatic cancerCell Line TumorGeneticsmedicineHumansMolecular BiologyChemotherapeutic drugCell ProliferationChemotherapyNatural products?-EstradiolEstradiolbusiness.industryQUIMIOTERÁPICOSChemotherapeutic drugs; Natural products; Nutraceuticals; Pancreatic cancer; β-EstradiolPancreatic cancerMiddle Agedmedicine.diseasedigestive system diseasesPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsCancer researchSettore BIO/14 - FarmacologiaMolecular MedicineChemotherapeutic drugsFemaleChemotherapeutic drugsNutraceuticalsNutraceuticalSignal transductionbusinessHormoneCarcinoma Pancreatic DuctalSignal TransductionAdvances in biological regulation
researchProduct

Analysis of the Gut Microbiota: An Emerging Source of Biomarkers for Immune Checkpoint Blockade Therapy in Non-Small Cell Lung Cancer

2021

Simple Summary The immune checkpoint blockade (ICB), and concretely the blockade of the PD1/PDL1 axis, has opened up a new standard of treatment for non-small cell lung cancer (NSCLC). However, despite substantial advances in clinical care, many patients still remain refractory to these therapies. Biomarkers such as PD-L1 expression and tumor mutational burden have been associated with ICB efficacy, but the mechanisms underlying variable responses are not yet fully understood. Recently, the differential composition of the gut microbiota was studied as one of the variables accounting for interpatient heterogeneity in ICB responses. To better understand the potential role of the gut microbiot…

0301 basic medicineCancer Researchmedicine.drug_classmedicine.medical_treatmentAntibioticsGut floradigestive systemArticle03 medical and health sciences0302 clinical medicinemedicineLung cancerRC254-282non-small cell lung cancerbiologygut microbiotabusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensImmunotherapyimmune checkpoint blockademedicine.diseasebiology.organism_classificationImmune checkpointBlockade030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyBiomarker (medicine)biomarkernext-generation sequencingimmunotherapybusinessProgressive disease
researchProduct

Identification of clinical phenotypes and related survival in patients with large hccs

2021

Background. Hepatocellular carcinoma (HCC) factors, especially maximum tumor diameter (MTD), tumor multifocality, portal vein thrombosis (PVT), and serum alpha-fetoprotein (AFP), influence survival. Aim. To examine patterns of tumor factors in large HCC patients. Methods. A database of large HCC patients was examined. Results. A multiple Cox proportional hazard model on death identified low serum albumin levels and the presence of PVT and multifocality, with each having a hazard ratio ≥2.0. All combinations of these three parameters were examined in relation to survival. Using univariate Cox analysis, the combination of albumin &gt

0301 basic medicineCancer Researchmedicine.medical_specialtyPVTSettore MED/12 - GASTROENTEROLOGIASerum albuminlcsh:RC254-282GastroenterologyArticle03 medical and health sciences0302 clinical medicineInternal medicineMedicinePlateletHCCneoplasmsSurvival ratePVT.biologybusiness.industryProportional hazards modelAlbuminHazard ratioSettore MED/09 - MEDICINA INTERNAAlbuminMultifocalityHCC; large; phenotypes; PVT; multifocality; albuminlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesPortal vein thrombosisAlbumin; HCC; Large; Multifocality; Phenotypes; PVTPhenotypesPhenotype030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinLargebusiness
researchProduct

Carob leaf polyphenols trigger intrinsic apoptotic pathway and induce cell cycle arrest in colon cancer cells

2017

IF 3.973; International audience; Chemoprevention of Colorectal cancer (CRC) is the major concern for improving public health. We investigated the protective effects of carob, Ceratonia siliqua L, leaf polyphenols (CLP) against CRC. Phenolic content analysis showed that CLP is enriched with gallic acid and m-coumaric acid. We observed that CLP exerted a dose dependent cytotoxic effect through the induction of apoptosis on CRC cell lines, with an IC50 around 20 mu g/mL CLP induced intrinsic apoptotic pathway through the caspase-9 activation and PARP cleavage in HCT-116 and CT-26 cells. Moreover, CLP induced cell cycle arrest in the G1 phase through p53 activation. Gallic acid and m-coumaric …

0301 basic medicineCell cycle checkpointanimal diseases[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionMedicine (miscellaneous)ApoptosisPharmacologydigestive systemCell cycle arrest03 medical and health scienceschemistry.chemical_compoundCytotoxic T cellTX341-641Gallic acidIC50CaspaseNutrition and DieteticsbiologyNutrition. Foods and food supplyChemistryCarob (Ceratonia siliqua L.)food and beveragesPolyphenolsbacterial infections and mycosesColorectal cancer3. Good healthstomatognathic diseases030104 developmental biologyBiochemistryCell cultureApoptosisPolyphenolCaspasesbiology.protein[SDV.AEN]Life Sciences [q-bio]/Food and NutritionFood Science
researchProduct

Copper/MYC/CTR1 interplay: A dangerous relationship in hepatocellular carcinoma

2018

Free serum copper correlates with tumor incidence and progression of human cancers, including hepatocellular carcinoma (HCC). Copper extracellular uptake is provided by the transporter CTR1, whose expression is regulated to avoid excessive intracellular copper entry. Inadequate copper serum concentration is involved in the pathogenesis of Non Alcoholic Fatty Liver Disease (NAFLD), which is becoming a major cause of liver damage progression and HCC incidence. Finally, MYC is over-expressed in most of HCCs and is a critical regulator of cellular growth, tumor invasion and metastasis. The purpose of our study was to understand if higher serum copper concentrations might be involved in the prog…

0301 basic medicineCirrhosisCopper; CTR1; Hepatocellular carcinoma; MYC; Non alcoholic fatty liver disease; OncologyMYCMetastasis03 medical and health sciencesmedicineOncogeneCell growthChemistryFatty liverCTR1hepatocellular carcinomaHCCSmedicine.diseasedigestive system diseases3. Good health030104 developmental biologyOncologyHepatocellular carcinomacopperCancer researchCTR1; MYC; copper; hepatocellular carcinoma; non alcoholic fatty liver diseaseLiver cancerResearch Papernon alcoholic fatty liver disease
researchProduct

Dual proteotoxic stress accelerates liver injury via activation of p62‐Nrf2

2021

Protein accumulation is the hallmark of various neuronal, muscular, and other human disorders. It is also often seen in the liver as a major protein-secretory organ. For example, aggregation of mutated alpha1-antitrypsin (AAT), referred to as PiZ, is a characteristic feature of AAT deficiency, whereas retention of hepatitis B surface protein (HBs) is found in chronic hepatitis B (CHB) infection. We investigated the interaction of both proteotoxic stresses in humans and mice. Animals overexpressing both PiZ and HBs (HBs-PiZ mice) had greater liver injury, steatosis, and fibrosis. Later they exhibited higher hepatocellular carcinoma load and a more aggressive tumor subtype. Although PiZ and H…

0301 basic medicineCirrhosisNF-E2-Related Factor 2medicine.disease_causePathology and Forensic MedicineMice03 medical and health sciences0302 clinical medicineSDG 3 - Good Health and Well-beingStress PhysiologicalFibrosisSequestosome-1 ProteinmedicineAnimalsHumansLiver injuryHepatitis B Surface Antigensbusiness.industryLiver DiseasesAutophagyHepatitis Bmedicine.diseasedigestive system diseasesaggregate Hepatitis B Surface Antigens Humans Liver Diseases Mice NF-E2-Related Factor 2 Sequestosome-1 Protein Stress Physiological alpha 1-Antitrypsin cirrhosis inclusionlipophagy oxidative stress SERPINA1 Animals030104 developmental biologyalpha 1-Antitrypsin030220 oncology & carcinogenesisHepatocellular carcinomaCancer researchSteatosisbusinessOxidative stressThe Journal of Pathology
researchProduct