Search results for " Basic"

showing 10 items of 10515 documents

Squamous Cell Tumors Recruit γδ T Cells Producing either IL17 or IFNγ Depending on the Tumor Stage

2017

Abstract The identification of reciprocal interactions between tumor-infiltrating immune cells and the microenviroment may help us understand mechanisms of tumor growth inhibition or progression. We have assessed the frequencies of tumor-infiltrating and circulating γδ T cells and regulatory T cells (Treg) from 47 patients with squamous cell carcinoma (SCC), to determine if they correlated with progression or survival. Vδ1 T cells infiltrated SSC tissue to a greater extent than normal skin, but SCC patients and healthy subjects had similar amounts circulating. However, Vδ2 T cells were present at higher frequencies in circulation than in the tissue of either cancer patients or healthy donor…

Male0301 basic medicineCancer ResearchChemokineCell typeSkin Neoplasmsmedicine.medical_treatmentImmunologyCell03 medical and health sciencesInterleukin 21Lymphocytes Tumor-Infiltrating0302 clinical medicineImmune systemT-Lymphocyte SubsetsTumor MicroenvironmentmedicineHumansCytotoxic T cellImmunology; Cancer ResearchAgedNeoplasm StagingAged 80 and overTumor microenvironmentbiologyImmunotherapyMiddle Aged030104 developmental biologymedicine.anatomical_structureImmunologyCarcinoma Squamous Cellbiology.proteinCytokinesFemale030215 immunologyCancer Immunology Research
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The nucleotide excision repair protein XPC is essential for bulky DNA adducts to promote interleukin-6 expression via the activation of p38-SAPK

2016

Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants, and many are potent carcinogens. Benzo[a]pyrene (B[a]P), one of the best-studied PAHs, is metabolized ultimately to the genotoxin anti-B[a]P-7,8-dihydrodiol-9,10-epoxide (BPDE). BPDE triggers stress responses linked to gene expression, cell death and survival. So far, the underlying mechanisms that initiate these signal transduction cascades are unknown. Here we show that BPDE-induced DNA damage is recognized by DNA damage sensor proteins to induce activation of the stress-activated protein kinase (SAPK) p38. Surprisingly, the classical DNA damage response, which involves the kinases ATM and ATR, is not involved in p38-SA…

Male0301 basic medicineCancer ResearchDNA RepairCarcinogenesisDNA damagep38 mitogen-activated protein kinases78-Dihydro-78-dihydroxybenzo(a)pyrene 910-oxideBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyReal-Time Polymerase Chain ReactionTransfectionp38 Mitogen-Activated Protein KinasesDNA AdductsMice03 medical and health scienceschemistry.chemical_compoundGeneticsmedicinepolycyclic compoundsAnimalsHumansRNA Small InterferingMolecular BiologyCarcinogenMice KnockoutCisplatinInterleukin-6KinaseFibroblastsCell biologyDNA-Binding ProteinsMice Inbred C57BL030104 developmental biologychemistryCarcinogensNIH 3T3 CellsCancer researchComet AssaySignal transductionDNADNA DamageHeLa CellsMutagensSignal Transductionmedicine.drugNucleotide excision repairOncogene
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Deletion of 11q in Neuroblastomas Drives Sensitivity to PARP Inhibition

2017

AbstractPurpose: Despite advances in multimodal therapy, neuroblastomas with hemizygous deletion in chromosome 11q (20%–30%) undergo consecutive recurrences with poor outcome. We hypothesized that patients with 11q-loss may share a druggable molecular target(s) that can be exploited for a precision medicine strategy to improve treatment outcome.Experimental Design: SNP arrays were combined with next-generation sequencing (NGS) to precisely define the deleted region in 17 primary 11q-loss neuroblastomas and identify allelic variants in genes relevant for neuroblastoma etiology. We assessed PARP inhibitor olaparib in combination with other chemotherapy medications using both in vitro and in v…

Male0301 basic medicineCancer ResearchDNA repairAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsKaplan-Meier EstimatePoly(ADP-ribose) Polymerase InhibitorsBiologyModels BiologicalPolymorphism Single NucleotideImmunophenotypingOlaparibNeuroblastoma03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRecurrenceCell Line TumorNeuroblastomaBiomarkers TumormedicineAnimalsHumansAllelesNeoplasm StagingCisplatinTemozolomideChromosomes Human Pair 11High-Throughput Nucleotide SequencingCancerDrug SynergismPrognosismedicine.diseaseXenograft Model Antitumor AssaysMolecular biologyDisease Models Animal030104 developmental biologyOncologychemistryDrug Resistance Neoplasm030220 oncology & carcinogenesisPARP inhibitorCancer researchFemaleChromosome DeletionHaploinsufficiencyBiomarkersmedicine.drugClinical Cancer Research
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EORTC-1203-GITCG - the “INNOVATION”-trial: Effect of chemotherapy alone versus chemotherapy plus trastuzumab, versus chemotherapy plus trastuzumab pl…

2019

10–20% of patients with gastric cancer (GC) have HER2+ tumors. Addition of trastuzumab (T) to cisplatin/fluoropyrimidine-based chemotherapy (CT) improved survival in metastatic, HER2+ GC. When pertuzumab (P) was added to neoadjuvant T and CT, a significant increase in histopathological complete response rate was observed in HER2+ breast cancer. This study aims to investigate the added benefit of using both HER2 targeting drugs (T alone or the combination of T + P), in combination with perioperative CT for localized HER2+ GC. This is a prospective, randomized, open-label, phase II trial. HER2 status from patients with resectable GC (UICC TNM7 tumor stage Ib-III) will be centrally determined.…

Male0301 basic medicineCancer ResearchEsophageal NeoplasmsReceptor ErbB-2SURGERYmedicine.medical_treatmentGastroenterologyStudy ProtocolNEOADJUVANT CHEMOTHERAPYAntineoplastic Agents Immunological0302 clinical medicineFOLFOXAntineoplastic Combined Chemotherapy ProtocolsProspective StudiesOXALIPLATINNetherlandsAged 80 and overDOCETAXELMiddle AgedOPEN-LABELlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensChemotherapy regimenNeoadjuvant TherapyProgression-Free SurvivalTreatment OutcomeOncology030220 oncology & carcinogenesisFemaleGastro-esophageal junction cancerEsophagogastric JunctionFluorouracilPertuzumabmedicine.drugAdultmedicine.medical_specialtyAntineoplastic AgentsCAPECITABINEAdenocarcinomaAntibodies Monoclonal Humanizedlcsh:RC254-282CapecitabineYoung Adult03 medical and health sciencesBreast cancerStomach NeoplasmsInternal medicineHER2Republic of KoreaREGRESSIONGeneticsmedicineHumansBREAST-CANCERPerioperative PeriodAgedCisplatinChemotherapyPerioperative chemotherapyPertuzumabbusiness.industryTrastuzumabmedicine.diseaseOxaliplatin030104 developmental biologyCisplatinbusinessGastric cancerFollow-Up Studies
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Evidence for PTGER4 ,PSCA, and MBOAT7 as risk genes for gastric cancer on the genome and transcriptome level

2018

Genetic associations between variants on chromosome 5p13 and 8q24 and gastric cancer (GC) have been previously reported in the Asian population. We aimed to replicate these findings and to characterize the associations at the genome and transcriptome level. We performed a fine-mapping association study in 1926 GC patients and 2012 controls of European descent using high dense SNP marker sets on both chromosomal regions. Next, we performed expression quantitative trait locus (eQTL) analyses using gastric transcriptome data from 143 individuals focusing on the GC associated variants. On chromosome 5p13 the strongest association was observed at rs6872282 (P = 2.53 x 10(-04)) and on chromosome …

Male0301 basic medicineCancer ResearchGenotypeQuantitative Trait LocieQTL studyBiologyGPI-Linked ProteinsPolymorphism Single NucleotideGenomeTranscriptome03 medical and health sciencesAntigens NeoplasmStomach NeoplasmsGene expressionmedicineHumansSNPGenetic Predisposition to DiseaseRadiology Nuclear Medicine and imagingGeneGenetic Association StudiesOriginal ResearchCancer BiologyGeneticsGene Expression ProfilingChromosome MappingMembrane ProteinsChromosomeCancermedicine.diseaseNeoplasm ProteinsGene Expression Regulation Neoplastic030104 developmental biologyOncologygenetic association studyCase-Control StudiesExpression quantitative trait locigene expressionChromosomes Human Pair 5FemaleReceptors Prostaglandin E EP4 SubtypeAcyltransferasesChromosomes Human Pair 8Cancer Medicine
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The STAT3 Inhibitor Galiellalactone Reduces IL6-Mediated AR Activity in Benign and Malignant Prostate Models

2018

IL6/STAT3 signaling is associated with endocrine therapy resistance in prostate cancer, but therapies targeting this pathway in prostate cancer were unsuccessful in clinical trials so far. The mechanistic explanation for this phenomenon is currently unclear; however, IL6 has pleiotropic effects on a number of signaling pathways, including the androgen receptor (AR). Therefore, we investigated IL6-mediated AR activation in prostate cancer cell lines and ex vivo primary prostate tissue cultures in order to gain a better understanding on how to inhibit this process for future clinical trials. IL6 significantly increased androgen-dependent AR activity in LNCaP cells but importantly did not infl…

Male0301 basic medicineCancer ResearchINTERLEUKIN-6LactonesProstate cancerLIGAND-INDEPENDENT ACTIVATION0302 clinical medicineProstateDEPRIVATIONANDROGEN RECEPTORGLUCOCORTICOID-RECEPTORmedicine.anatomical_structureOncologyReceptors Androgen030220 oncology & carcinogenesisAndrogensSILTUXIMAB CNTO 328GROWTHSIGNAL TRANSDUCERSignal transductionLife Sciences & BiomedicineProtein BindingSignal TransductionSTAT3 Transcription FactorENZALUTAMIDEmedicine.drug_classMice NudeModels BiologicalTMPRSS203 medical and health sciencesProtein DomainsCell Line TumorLNCaPmedicineAnimalsHumansCastrationCANCER CELLSScience & TechnologyInterleukin-6business.industryProstatic NeoplasmsDNAmedicine.diseaseAndrogenXenograft Model Antitumor AssaysAndrogen receptor030104 developmental biologyCancer researchbusinessEx vivo
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Dual disruption of aldehyde dehydrogenases 1 and 3 promotes functional changes in the glutathione redox system and enhances chemosensitivity in nonsm…

2020

AbstractAldehyde dehydrogenases (ALDHs) are multifunctional enzymes that oxidize diverse endogenous and exogenous aldehydes. We conducted a meta-analysis based on The Cancer Genome Atlas and Gene Expression Omnibus data and detected genetic alterations in ALDH1A1, ALDH1A3, or ALDH3A1, 86% of which were gene amplification or mRNA upregulation, in 31% of nonsmall cell lung cancers (NSCLCs). The expression of these isoenzymes impacted chemoresistance and shortened survival times in patients. We hypothesized that these enzymes provide an oxidative advantage for the persistence of NSCLC. To test this hypothesis, we used genetic and pharmacological approaches with DIMATE, an irreversible inhibito…

Male0301 basic medicineCancer ResearchLung NeoplasmsCell- och molekylärbiologiCellAldehyde dehydrogenaseKaplan-Meier EstimateMicechemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsCytotoxicityMiddle AgedAldehyde OxidoreductasesGlutathioneCancer metabolismUp-Regulation3. Good healthCancer therapeutic resistancemedicine.anatomical_structureAlkynes030220 oncology & carcinogenesisFemale[SDV.CAN]Life Sciences [q-bio]/CancerBiologyIsozymeAldehyde Dehydrogenase 1 FamilyArticle03 medical and health sciencesTargeted therapiesDownregulation and upregulationCell Line TumorGeneticsmedicineAnimalsHumansSulfhydryl CompoundsLung cancerMolecular BiologyAgedCancer och onkologiGene AmplificationRetinal DehydrogenaseGlutathioneAldehyde Dehydrogenasemedicine.diseaseXenograft Model Antitumor AssaysALDH1A1030104 developmental biologychemistryDrug Resistance NeoplasmCancer and Oncologybiology.proteinCancer researchCisplatinReactive Oxygen SpeciesCell and Molecular Biologynonsmall cell lung cancer
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Exome Analysis Reveals Genomic Markers Associated with Better Efficacy of Nivolumab in Lung Cancer Patients

2019

Abstract Purpose: Immune checkpoint inhibitors revolutionized the treatment of non-small cell lung cancer (NSCLC). However, only one-quarter of patients benefit from these new therapies. PD-L1 assessment and tumor mutational burden (TMB) are available tools to optimize use of checkpoint inhibitors but novel tools are needed. Exome sequencing could generate many variables but their role in identifying predictors of response is unknown. Experimental Design: We performed somatic and constitutional exome analyses for 77 patients with NSCLC treated with nivolumab. We studied: one-tumor-related characteristics: aneuploidy, CNA clonality, mutational signatures, TMB, mutations in WNT, AKT, MAPK, an…

Male0301 basic medicineCancer ResearchLung NeoplasmsDNA repairAntineoplastic AgentsPembrolizumabAntibodies Monoclonal HumanizedB7-H1 AntigenDisease-Free Survival03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineCarcinoma Non-Small-Cell LungExome SequencingBiomarkers TumorHumansMedicineCTLA-4 AntigenLung cancerExomeExome sequencingAgedRetrospective StudiesAged 80 and overbusiness.industryGenomicsMiddle Agedmedicine.diseaseIpilimumabNivolumabTreatment Outcome030104 developmental biologyOncology030220 oncology & carcinogenesisMutationMonoclonalCancer researchBiomarker (medicine)FemaleNivolumabbusinessClinical Cancer Research
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Absence of germline CDKN2A mutation in Sicilian Patients with Familial Malignant Melanoma: could it be a population-specific genetic signature?

2015

Germline CDKN2A mutations have been described in 25% to 40% of melanoma families from several countries. Sicilian population is genetically different from the people of Europe and Northern Italy because of its historical background, therefore familial melanoma could be due to genes different from high-penetrance CDKN2A gene. Four hundred patients with cutaneous melanoma were observed in a 6-years period at the Plastic Surgery Unit of the University of Palermo. Forty-eight patients have met the criteria of the Italian Society of Human Genetics (SIGU) for the diagnosis of familial melanoma and were screened for CDKN2A and CDK4 mutations. Mutation testing revealed that none of the families car…

Male0301 basic medicineCancer ResearchMutation rateSettore MED/06 - Oncologia MedicaSettore MED/19 - Chirurgia Plasticap14ARFGermline0302 clinical medicineCDKN2ATumor Suppressor Protein p14ARFMedicineMelanomaSicilyfamilial melanomaGeneticseducation.field_of_studyMelanomaMiddle AgedGene Expression Regulation NeoplasticItalyOncologygermline mutation030220 oncology & carcinogenesisMolecular MedicineFemaleResearch PaperSignal TransductionAdultPopulation03 medical and health sciencesCDKN2Acutaneous melanomaGermline mutationp16INK4aHumansGenetic Predisposition to DiseaseeducationneoplasmsCyclin-Dependent Kinase Inhibitor p16Germ-Line MutationAgedPharmacologybusiness.industryGenetic heterogeneityp.R87W mutationmedicine.disease030104 developmental biologyMutationCutaneous melanomaCDKN2A; cutaneous melanoma; familial melanoma; germline mutation; p.R87W mutation; p14ARF; p16INK4a; Cancer Research; Oncology; Molecular Medicine; Pharmacologybusiness
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The genetic tumor background is an important determinant for heterogeneous MYCN ‐amplified neuroblastoma

2016

Amplification of MYCN is the signature genetic aberration of 20–25% of neuroblastoma and a stratifying marker associated with aggressive tumor behavior. The detection of heterogeneous MYCN amplification (hetMNA) poses a diagnostic dilemma due to the uncertainty of its relevance to tumor behavior. Here, we aimed to shed light on the genomic background which permits hetMNA in neuroblastoma and tied the occurrence to other stratifying markers and disease outcome. We performed SNP analysis using Affymetrix Cytoscan HD arrays on 63 samples including constitutional DNA, tumor, bone marrow and relapse samples of 26 patients with confirmed hetMNA by MYCN‐FISH. Tumors of patients ≤18m were mostly an…

Male0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyTumor Markers and Signaturesuniparental disomyAdolescentMYCN amplificationAneuploidyBiologyPolymorphism Single NucleotideN-Myc Proto-Oncogene ProteinBenign tumorGenetic HeterogeneityNeuroblastoma03 medical and health sciences0302 clinical medicineNeuroblastomamedicineHumansChildIn Situ Hybridization FluorescenceChromosome AberrationsOncogene ProteinsN-Myc Proto-Oncogene ProteinGenetic heterogeneityGene AmplificationInfantNuclear ProteinsAneuploidymedicine.diseaseUniparental disomy030104 developmental biologyOncologyChild Preschool030220 oncology & carcinogenesisintratumoral heterogeneityCancer researchFemaleChromosome DeletionTrisomySNP arrayInternational Journal of Cancer
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