Search results for "ONCOLOGIA"

showing 10 items of 386 documents

Driver mutations and differential sensitivity to targeted therapies: a new approach to the treatment of lung adenocarcinoma

2010

The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In th…

Lung NeoplasmsOncogene Proteins FusionSettore MED/06 - Oncologia MedicaEGFRGene ExpressionAdenocarcinomaGene mutationmedicine.disease_causeProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesPredictive Value of TestsProto-Oncogene ProteinsAntineoplastic Combined Chemotherapy ProtocolsmedicineAdenocarcinoma of the lungHumansRadiology Nuclear Medicine and imagingMolecular Targeted TherapyEpidermal growth factor receptorTyrosine kinase inhibitorsMutationbiologybusiness.industryDriver mutationGeneral MedicineProtein-Tyrosine KinasesPrognosismedicine.diseaseErbB ReceptorsTreatment OutcomeOncologyMutationImmunologyras ProteinsCancer researchbiology.proteinAdenocarcinomaKRASCarcinogenesisbusinessTyrosine kinaseAlgorithmsCancer Treatment Reviews
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Novel therapeutic strategies for patients with NSCLC that do not respond to treatment with EGFR inhibitors

2014

Abstract: Introduction: Treatment with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) yields tumour responses in non-small cell lung cancer (NSCLC) patients harbouring activating EGFR mutations. However, even in long-lasting responses, resistance to EGFR TKIs invariably occurs. Areas covered: This review examines resistance mechanisms to EGFR TKI treatment, which mainly arise from secondary EGFR mutations. Other resistance-inducing processes include mesenchymal-epithelial transition factor (MET) amplification, epithelial-mesenchymal transformation, phenotypic change from NSCLC to small-cell lung carcinoma, and modifications in parallel signalling pathways. Current…

Lung NeoplasmsSettore MED/06 - Oncologia MedicaAfatinibNovel therapeutic strategiesLapatinibmedicine.disease_causeNSCLCT790Mchemistry.chemical_compoundErbB ReceptorsCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansRadiology Nuclear Medicine and imagingEpidermal growth factor receptorProtein Kinase InhibitorsEGFR inhibitorsbiologybusiness.industryEGFR mutations; TKI inhibitors resistance; NSCLC; New drugs; Novel therapeutic strategiesGeneral MedicineNew drugEGFR mutationsCombined Modality TherapyDacomitinibrespiratory tract diseasesErbB ReceptorsNew drugsOncologychemistryDrug Resistance NeoplasmCancer researchbiology.proteinKRASHuman medicineEGFR mutationbusinessmedicine.drugTKI inhibitors resistanceCancer Treatment Reviews
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GENETIC AND FUNCTIONAL DISSECTION OF THE MIR-17-92 CLUSTER OF MIRNAS

2011

Background: The miR-17∼92 cluster was among the first cluster of miRNAs to be linked to cancer. It is directly activated by the members of the MYC family of transcription factors and acts as a bona fide oncogene in several types of cancer, including lymphomas. miR-17∼92 is essential for mammalian development. Knockout mice die in utero or at birth with cardiovascular defects and impaired B-cell maturation. Aims: Although miR-17∼92 is important for tumorigenesis and development both the molecular mechanisms and the prominent miRNAs acting in different contexts are still unknown. The main aim of our study was to identify the role played by different members of the miR-17∼92 cluster in B-cell …

MIR-17-92 CLUSTERMIRNASSettore MED/06 - Oncologia MedicaGENETICFUNCTIONAL DISSECTION
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"ONCOGENE ADDICTED SOLID TUMORS: BIOMARKERS PROGNOSTIC AND PREDICTIVE OF RESISTANCE OR SENSITIVITY TO MOLECULAR TARGETED THERAPIES IN CRC

2011

MOLECULARSettore MED/06 - Oncologia MedicaONCOGENETUMORSBIOMARKERS PROGNOSTIC
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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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Male breast cancer in BRCA1 and BRCA2 mutation carriers: pathology data from the Consortium of Investigators of Modifiers of BRCA1/2

2016

Background BRCA1 and, more commonly, BRCA2 mutations are associated with increased risk of male breast cancer (MBC). However, only a paucity of data exists on the pathology of breast cancers (BCs) in men with BRCA1/2 mutations. Using the largest available dataset, we determined whether MBCs arising in BRCA1/2 mutation carriers display specific pathologic features and whether these features differ from those of BRCA1/2 female BCs (FBCs). Methods We characterised the pathologic features of 419 BRCA1/2 MBCs and, using logistic regression analysis, contrasted those with data from 9675 BRCA1/2 FBCs and with population-based data from 6351 MBCs in the Surveillance, Epidemiology, and End Results (…

Male0301 basic medicineGenotype-phenotype correlationPathologygenotype-phenotype correlationsendocrine system diseasesSettore MED/06 - Oncologia MedicaFEATURESmale breast cancerGenotype-phenotype correlationsLogistic regressionHistologic grade610 Medical sciences MedicineBreast cancer0302 clinical medicineEpidemiologyMedicine and Health SciencesPathologypolycyclic compoundsskin and connective tissue diseasesPOPULATIONRISKeducation.field_of_studyBRCA1 ProteinMenSingle NucleotideMiddle Aged3. Good healthGRADE030220 oncology & carcinogenesisMale breast canceroncologyFemaleBreast NeoplasmResearch ArticleHumanAdultmedicine.medical_specialtyCARCINOMAGenotype–phenotype correlations3122 CancersPopulation610Breast NeoplasmsBRCA1/2; genotype-phenotype correlations; histologic grade; male breast cancer; pathology; cancer research; oncologyMale breast cancer BRCA1 BRCA2Polymorphism Single NucleotideCàncer de mamaBreast Neoplasms Male03 medical and health sciencesBreast cancerSDG 3 - Good Health and Well-beingBRCA1/2Journal ArticleCarcinomamedicineHumansGenetic Predisposition to DiseasePolymorphismeducationAgedNeoplasm StagingBRCA2 Proteinbusiness.industryOdds ratiohistologic grademedicine.diseaseConfidence intervalMale breast cancer030104 developmental biologyddc:161HomesMutationcancer researchpathologyBRCA1/2; Genotype-phenotype correlations; Histologic grade; Male breast cancer; Pathology; Adult; Aged; BRCA1 Protein; BRCA2 Protein; Breast Neoplasms; Breast Neoplasms Male; Female; Genetic Predisposition to Disease; Humans; Male; Middle Aged; Mutation; Neoplasm Staging; Polymorphism Single Nucleotide; Oncology; Cancer Researchbusiness
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Neutrophil/lymphocyte ratio helps select metastatic pancreatic cancer patients benefitting from oxaliplatin

2016

BACKGROUND: High Neutrophil/Lymphocyte ratio (NLR), as a measure of enhanced inflammatory response, has been negatively associated with prognosis in patients with localized pancreatic ductal adenocarcinoma (PDA). OBJECTIVE: In the present study, we aimed at investigating the prognostic value of NLR in two homogeneous groups of chemotherapy-na've metastatic PDA patients. Patients were treated with either gemcitabine (GEM) or gemcitabine/ oxaliplatin (GEMOXA). We also assessed whether NLR could identify patients benefiting from the use of oxaliplatin. METHODS: Consecutive PDA patients treated at the Medical Oncology Unit of Tor Vergata University Hospital of Rome with either GEM or GEMOXA wer…

Male0301 basic medicineOncologyCancer ResearchNeutrophil/lymphocyte ratio; gemcitabine; oxaliplatin; pancreatic ductal adenocarcinomaOrganoplatinum CompoundsNeutrophilsSettore MED/06 - Oncologia MedicaLymphocyteAntineoplastic AgentLeukocyte Count0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsLymphocytesNeoplasm MetastasisAged 80 and overNeutrophilPancreatic NeoplasmgemcitabineGeneral MedicineMiddle AgedPrognosisNeoplasm MetastasiTreatment Outcomemedicine.anatomical_structureOncology030220 oncology & carcinogenesisNeutrophil/lymphocyte ratioLymphocyteFemaleHumanCarcinoma Pancreatic Ductalmedicine.drugAdultmedicine.medical_specialtyPancreatic ductal adenocarcinomaPrognosiInflammatory responseeducationpancreatic ductal adenocarcinomaAntineoplastic Agents03 medical and health sciencesGeneticNegatively associatedInternal medicineMetastatic pancreatic cancerGeneticsmedicineHumansIn patientAgedProportional Hazards ModelsSettore MED/04 - Patologia GeneraleAntineoplastic Combined Chemotherapy Protocolbusiness.industryOrganoplatinum CompoundfungioxaliplatinBiomarkerGemcitabineOxaliplatinPancreatic Neoplasms030104 developmental biologyROC CurveProportional Hazards ModelbusinessBiomarkers
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Palbociclib plus endocrine therapy in HER2 negative, hormonal receptor-positive, advanced breast cancer: A real-world experience

2019

Data from 423 human epidermal growth factor receptor 2-negative (HER2−), hormone receptor-positive (HR+) advanced breast cancer (aBC) patients treated with palbociclib and endocrine therapy (ET) were provided by 35 Italian cancer centers and analyzed for treatment outcomes. Overall, 158 patients were treated in first line and 265 in second/later lines. We observed 19 complete responses and 112 partial responses. The overall response rate (ORR) was 31% (95% confidence interval [CI], 26.6–35.4) and clinical benefit was 52.7% (95% CI, 48–57.5). ORR was negatively affected by prior exposure to everolimus/exemestane (p = 0.002) and favorably influenced by early line-treatment (p < 0.0001). At…

Male0301 basic medicineOncologyPyridinesReceptor ErbB-2PhysiologyClinical BiochemistryPiperazineschemistry.chemical_compound0302 clinical medicineExemestaneAntineoplastic Combined Chemotherapy Protocolsadvanced breast cancer; hormonal therapy; endocrine resistance; palbociclib; real-world settingBreastAged 80 and overadvanced breast cancerhormonal therapyadvanced breast cancer hormonal therapy; endocrine resistance; palbociclib; real-world settingMiddle AgedTreatment OutcomeReceptors Estrogen030220 oncology & carcinogenesisToxicityFemaleReceptors Progesteronemedicine.drugAdultadvanced breast cancer hormonal therapy; endocrine resistance; palbociclib; real-world setting; Physiology; Clinical Biochemistry; Cell Biologymedicine.medical_specialtypalbociclibBreast NeoplasmsPalbociclibNeutropeniaadvanced breast cancer hormonal therapyDisease-Free Survivalendocrine resistance03 medical and health sciencesInternal medicinereal-world settingmedicineHumansAgedEverolimusSettore MED/06 - ONCOLOGIA MEDICAbusiness.industryCancerCell Biologymedicine.diseaseConfidence interval030104 developmental biologychemistryMED/06 - ONCOLOGIA MEDICAbusinessHormone
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TNF-alpha gene promoter polymorphisms and risk of venous thromboembolism in gastrointestinal cancer patients undergoing chemotherapy

2013

Abstract Background TNF-α has been proposed as a predictive factor for venous thromboembolism (VTE). Genetic polymorphisms could regulate TNF-α production. However, the relationship between TNFA gene variants and VTE is not clarified. This study aims to investigate the predictive role of five different TNFA gene promoter SNPs, or their haplotype combination(s), for a first VTE episode in gastrointestinal cancer out-patients treated with chemotherapy. Patients and methods Serum TNF-α levels and TNFA -863C/A, -857C/T, -376G/A, -308G/A and -238G/A gene promoter polymorphisms were retrospectively evaluated in 314 subjects, including 157 controls and 157 Caucasian patients with histologically di…

MaleAntimetabolitesSettore MED/06 - Oncologia Medicamedicine.medical_treatmentchemotherapyGastroenterologysingle nucleotide polymorphismschemotherapy; gastrointestinal cancer; single nucleotide polymorphisms; tumour necrosis factor-α; venous thromboembolismsingle nucleotide polymorphismPhytogenic80 and overtumour necrosis factor-αPromoter Regions GeneticGastrointestinal NeoplasmsAged 80 and overHazard ratioSingle NucleotideHematologyMiddle AgedAntineoplasticChemotherapy regimenOncologyFemaleFluorouracilmedicine.drugAdultRiskAntimetabolites Antineoplasticmedicine.medical_specialtygastrointestinal cancervenous thromboembolismAntineoplastic AgentsSingle-nucleotide polymorphismIrinotecanPolymorphism Single NucleotidePromoter RegionsGeneticInternal medicinemedicineHumansGenetic Predisposition to DiseaseGastrointestinal cancercardiovascular diseasesPolymorphismRetrospective StudiesAgedChemotherapyTumor Necrosis Factor-alphabusiness.industryHaplotypeOdds ratiomedicine.diseaseAntineoplastic Agents PhytogenicIrinotecanHaplotypesCase-Control StudiesImmunologyCamptothecinHuman medicinePolymorphism Single Nucleotide; Antimetabolites Antineoplastic; single nucleotide polymorphisms; Humans; Retrospective Studies; Aged; Promoter Regions Genetic; Haplotypes; Aged 80 and over; Adult; gastrointestinal cancer; Genetic Predisposition to Disease; Male; tumour necrosis factor-α; Tumor Necrosis Factor-alpha; Venous Thromboembolism; Camptothecin; chemotherapy; Risk; Fluorouracil; Case-Control Studies; Gastrointestinal Neoplasms; Middle Aged; venous thromboembolism; Antineoplastic Agents Phytogenic; Femalebusiness
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4843delC of the BRCA1 gene is a possible founder mutation in Southern Italy (Sicily).

2007

Various studies have been published in Italy regarding the different BRCA1 mutations, but only the BRCA1-5083del19 mutation is recurrent and specific to individuals of Italian descent with a founder effect on the Calabrian population. In our previous study, BRCA1-5083del19 mutation carriers were found in four index cases of 106 Sicilian patients selected for familial and/or hereditary breast/ovarian cancers. The high frequency rate of this mutation identified in the Sicilian population led us to perform haplotype analysis in all family carriers. Five highly polymorphic microsatellite markers were used (D17S1320, D17S932, D17S1323, D17S1326, D17S1325) to establish whether or not all these fa…

MaleBRCA1 gene Founder mutation Haplotype analysis Hereditary breast and ovarian cancer Sicilian patientsSettore MED/06 - Oncologia MedicaGenetic counselingPopulationDNA Mutational AnalysisGenes BRCA1Single-nucleotide polymorphismBreast NeoplasmsBiologyBRCA1 geneHaplotype analysiHumansAlleleeducationAllelotypeFounder mutationSicilyGeneticsOvarian Neoplasmseducation.field_of_studyHaplotypeHematologylanguage.human_languageFounder EffectPedigreeOncologyHaplotypesHaplotype frequencylanguageFemaleSicilianGene DeletionFounder effectGenetic counselingMicrosatellite Repeats
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