Search results for "Neoplasms"

showing 10 items of 7988 documents

The Clinical Efficacy of Radium-223 for Bone Metastasis in Patients with Castration-Resistant Prostate Cancer: An Italian Clinical Experience.

2017

<b><i>Background/Aim:</i></b> Prostate cancer frequently causes bone metastases and skeletal events that impair quality of life (QoL) and survival. The alpha emitter radium-223 is a new drug that improves treatment in men with castration-resistant prostate cancer (CRPC) and bone metastases. Our aim was to evaluate the effectiveness of radium-223. <b><i>Subjects and Methods:</i></b> In this retrospective study we enrolled 48 subjects. Pain reduction, alkaline phosphatase (ALP), time to first symptomatic skeletal event, and QoL were the variables we evaluated. <b><i>Results:</i></b> Radium-223 was well tolerated, with a m…

0301 basic medicineOncologyDrugRadium-223MaleCancer Researchmedicine.medical_specialtymedia_common.quotation_subjectAntineoplastic AgentsBone NeoplasmsDocetaxel03 medical and health sciencesProstate cancer0302 clinical medicineQuality of lifeInternal medicinemedicineHumansmedia_commonAgedRetrospective StudiesAged 80 and overRadioisotopesbusiness.industryBone metastasisRetrospective cohort studyGeneral MedicineMiddle Agedmedicine.diseaseProstatic Neoplasms Castration-Resistant030104 developmental biologyOncologyDocetaxelItaly030220 oncology & carcinogenesisQuality of LifeAlkaline phosphatasePrednisoneTaxoidsRadium-223 Bone metastasis Prostate cancer Radiopharmaceuticals Metastatic castration-resistant prostate cancer Quality of Lifebusinessmedicine.drugRadiumOncology
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Involvement of non-coding RNAs in chemo- and radioresistance of colorectal cancer

2016

Despite recent progress in understanding the cancer signaling pathways and in developing new therapeutic strategies, however, the resistance of colorectal cancer (CRC) cells to chemo- and radiotherapy represents the main hurdle to the successful treatment, leading to tumor recurrence and, consequently, a poor prognosis. Therefore, overcoming drug and radiation resistance, enhancing drug and radiation sensitivity of CRC cells, and improving the effi cacy of chemo- and radiotherapy have an important signifi cance in the treatment of CRC. The identifi cation of new molecular biomarkers which can predict therapy response and prognosis is one of the most signifi cant aims in pharmacogenomics and…

0301 basic medicineOncologyDrugmedicine.medical_specialtyColorectal cancermedicine.medical_treatmentmedia_common.quotation_subjectTherapy responseBiologyTargeted therapyTargeted therapy03 medical and health sciences0302 clinical medicineRadioresistanceInternal medicinemicroRNAmedicineChemotherapyNon-coding RNAneoplasmsChemoresistance; Chemotherapy; miRNAs; Non-coding RNA; Predictive biomarkers; Radioresistance; Radiotherapy; Targeted therapy; Therapy response; Medicine (all); Biochemistry Genetics and Molecular Biology (all)miRNAmedia_commonChemotherapyBiochemistry Genetics and Molecular Biology (all)RadiotherapyMedicine (all)Radioresistancemedicine.diseaseRadiation therapyPredictive biomarker030104 developmental biology030220 oncology & carcinogenesisPharmacogenomicsChemoresistance
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Recent Insights into the Development of Preclinical Trastuzumab- Resistant HER2+ Breast Cancer Models.

2018

Background: Overexpression and amplification of the human epidermal growth factor receptor 2 (HER2) occur in 20% of total breast carcinomas. HER2-overexpression is implicated in disease initiation and progression and associated with poor prognosis. Trastuzumab, a humanized monoclonal antibody, is the standard HER2-targeted therapy for early and metastatic HER2-amplified breast cancer patients. Trastuzumab has significantly increased clinical benefit in HER2+ metastatic and adjuvant settings; however, it is not effective for many patients due to primary or acquired resistance to the drug. During the last decade, many studies have revealed a number of novel molecular traits of HER2+ breast c…

0301 basic medicineOncologyDrugmedicine.medical_specialtymedicine.drug_classReceptor ErbB-2medicine.medical_treatmentmedia_common.quotation_subjectBreast NeoplasmsDiseaseMonoclonal antibodyBiochemistryTargeted therapy03 medical and health sciences0302 clinical medicineBreast cancerAcquired resistanceAntineoplastic Agents ImmunologicalTrastuzumabInternal medicineCell Line TumorDrug DiscoverymedicineBiomarkers TumorAnimalsHumansskin and connective tissue diseasesneoplasmsmedia_commonPharmacologybusiness.industryOrganic ChemistryTrastuzumabmedicine.diseaseGene Expression Regulation Neoplastic030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisMolecular MedicineFemalebusinessAdjuvantmedicine.drugCurrent medicinal chemistry
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Recommendations for the implementation of BRCA testing in ovarian cancer patients and their relatives

2019

The current availability of new Poly(ADP-ribose) Polymerase (PARP)-inhibitors for the treatment of ovarian cancer patients independently of the presence of a BRCA pathogenic variant, together with the validation of somatic test for the analysis of BRCA1/2 genes, involves the need to optimise the guidelines for BRCA testing. The AIOM-SIGU-SIBIOC-SIAPEC-IAP Italian Scientific Societies, in this position paper, recommend the implementation of BRCA testing with 2 main objectives: the first is the identification of ovarian cancer patients with higher probability of benefit from specific anticancer treatments (test for response to therapy); the second goal, through BRCA testing in the family memb…

0301 basic medicineOncologyGenetic testingendocrine system diseasesSettore MED/03 - GENETICA MEDICAMedical OncologyBiochemistrychemistry.chemical_compound0302 clinical medicineGermline mutationPARP inhibitorsTrabectedinSocieties MedicalOvarian Neoplasmsmedicine.diagnostic_testBRCA1 ProteinHematologyfemale genital diseases and pregnancy complicationsOncologyItaly030220 oncology & carcinogenesisFemalemedicine.drugHumanmedicine.medical_specialtyGenetic counselingOlaparib03 medical and health sciencesGeneticSomatic mutationsOvarian cancerMedicalInternal medicineBRCA1; BRCA2; Genetic testing; Germline mutations; Ovarian cancer; PARP inhibitors; Somatic mutations; BRCA1 Protein; BRCA2 Protein; Biochemistry; Female; Genetic Testing; Genetics; Humans; Italy; Medical Oncology; Ovarian Neoplasms; Germ-Line Mutation; Societies MedicalGeneticsmedicineGenetic predispositionHumansRucaparibGermline mutationsGerm-Line MutationGenetic testingBRCA2 Proteinbusiness.industrySomatic mutationOvarian NeoplasmCancermedicine.diseaseBRCA1BRCA2BRCA1; BRCA2; Genetic testing; Germline mutations; Ovarian cancer; PARP inhibitors; Somatic mutations030104 developmental biologyPARP inhibitorchemistrySocietiesOvarian cancerbusiness
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Anti-angiogenic drugs for second-line treatment of NSCLC patients: just new pawns on the chessboard?

2016

Tumor angiogenesis is one of the main pathways targeted to treat cancer. Bevacizumab added survival benefit when combined with platinum-based chemotherapy in NSCLC. Recently, Phase III trials showed survival benefit when anti-angiogenic drugs are added to docetaxel as second-line treatment for NSCLC. These anti-angiogenic agents include nintedanib and ramucirumab, a tyrosine-kinase inhibitor and a monoclonal antibody, respectively, which target receptors involved in angiogenesis. These studies have some similarities and differences. We propose a new algorithm for treatment sequences in performance status 0-1 patients with non-oncogene-addicted NSCLC type adenocarcinoma. Indeed clearer scien…

0301 basic medicineOncologyIndolesLung NeoplasmsAngiogenesisInvestigationalangiogenesis; docetaxel; nintedanib; NSCLC; ramucirumab; Angiogenesis Inhibitors; Antibodies; Monoclonal; Carcinoma; Non-Small-Cell Lung; Chemotherapy; Adjuvant; Humans; Indoles; Lung Neoplasms; Neovascularization; Pathologic; Practice Guidelines as Topic; Protein Kinase Inhibitors; Taxoids; Therapies; Investigational; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Clinical BiochemistryClinical BiochemistryAngiogenesis InhibitorsNSCLCangiogenesischemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungMonoclonalDrug DiscoverynintedanibdocetaxelNon-Small-Cell LungAdjuvantNeovascularization PathologicTherapies InvestigationalAntibodies MonoclonalDocetaxelChemotherapy Adjuvant030220 oncology & carcinogenesisPractice Guidelines as TopicAdenocarcinomaTaxoidsNintedanibAngiogenesis InhibitorHumanmedicine.drugmedicine.medical_specialtyBevacizumabramucirumabProtein Kinase InhibitorAntibodies Monoclonal HumanizedAntibodiesRamucirumab03 medical and health sciencesTaxoidInternal medicinemedicineChemotherapyHumansProtein Kinase InhibitorsNeovascularizationPathologicPharmacologyPerformance statusbusiness.industryDrug Discovery3003 Pharmaceutical ScienceCarcinomaangiogenesiCancermedicine.diseaseLung Neoplasm030104 developmental biologychemistryIndoleTherapiesangiogenesis; docetaxel; nintedanib; NSCLC; ramucirumab; Angiogenesis Inhibitors; Antibodies Monoclonal; Carcinoma Non-Small-Cell Lung; Chemotherapy Adjuvant; Humans; Indoles; Lung Neoplasms; Neovascularization Pathologic; Practice Guidelines as Topic; Protein Kinase Inhibitors; Taxoids; Therapies Investigational; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Clinical BiochemistrybusinessExpert Opinion on Biological Therapy
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Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets

2019

Idiopathic pulmonary fibrosis (IPF) is the most common idiopathic interstitial pulmonary disease with a median survival of 2–4 years after diagnosis. A significant number of IPF patients have risk factors, such as a history of smoking or concomitant emphysema, both of which can predispose the patient to lung cancer (LC) (mostly non-small cell lung cancer (NSCLC)). In fact, IPF itself increases the risk of LC development by 7% to 20%. In this regard, there are multiple common genetic, molecular, and cellular processes that connect lung fibrosis with LC, such as myofibroblast/mesenchymal transition, myofibroblast activation and uncontrolled proliferation, endoplasmic reticulum stress, alterat…

0301 basic medicineOncologyIndolesLung Neoplasmsnon-small cell lung cancer (NSCLC)Reviewlcsh:Chemistrychemistry.chemical_compoundIdiopathic pulmonary fibrosis0302 clinical medicineCarcinoma Non-Small-Cell LungMyofibroblastslcsh:QH301-705.5SpectroscopyGeneral MedicinePirfenidonerespiratory systemComputer Science Applicationsnon-small cell lung cancer (NSCLC)030220 oncology & carcinogenesisNintedanibidiopathic pulmonary fibrosis (IPF)Myofibroblastmedicine.drugmedicine.medical_specialtyPyridonesAntineoplastic AgentsCatalysisInorganic Chemistry03 medical and health sciencesInternal medicinemedicineAnimalsHumansPhysical and Theoretical ChemistryLung cancerMolecular Biologylung cancer (LC)business.industryOrganic ChemistryMesenchymal stem cellmedicine.diseaseIdiopathic Pulmonary Fibrosisrespiratory tract diseases030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryConcomitantbusinessInternational Journal of Molecular Sciences
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Non-invasive stratification of hepatocellular carcinoma risk in non-alcoholic fatty liver using polygenic risk scores

2021

Background & Aims: Hepatocellular carcinoma (HCC) risk stratification in individuals with dysmetabolism is a major unmet need. Genetic predisposition contributes to non-alcoholic fatty liver disease (NAFLD). We aimed to exploit robust polygenic risk scores (PRS) that can be evaluated in the clinic to gain insight into the causal relationship between NAFLD and HCC, and to improve HCC risk stratification. Methods: We examined at-risk individuals (NAFLD cohort, n = 2,566; 226 with HCC; and a replication cohort of 427 German patients with NAFLD) and the general population (UK Biobank [UKBB] cohort, n = 364,048; 202 with HCC). Variants in PNPLA3-TM6SF2-GCKR-MBOAT7 were combined in a hepatic …

0301 basic medicineOncologyLiver CirrhosisMaleMultifactorial InheritanceCirrhosis0302 clinical medicineRisk FactorsNon-alcoholic Fatty Liver DiseaseHepatic fatAdiposityeducation.field_of_studyFatty liverLiver NeoplasmsMiddle AgedPrognosisEuropeCirrhosisLiverCohort030211 gastroenterology & hepatologyBiomarker; Cirrhosis; Genetics; Hepatic fat; Non-alcoholic fatty liver diseaseFemaleLiver cancerCohort studymedicine.medical_specialtyCarcinoma HepatocellularSettore MED/12 - GASTROENTEROLOGIAPopulationRisk Assessment03 medical and health sciencesBiomarker Cirrhosis Genetics Hepatic fat Non-alcoholic fatty liver disease Cross-Sectional Studies Europe Female Genetic Predisposition to Disease Humans Liver Liver Cirrhosis Male Mediation Analysis Middle Aged Multifactorial Inheritance Predictive Value of Tests Prognosis Risk Assessment Risk Factors Adiposity Carcinoma Hepatocellular Non-alcoholic Fatty Liver DiseaseGeneticPredictive Value of TestsInternal medicinemedicineGenetic predispositionGeneticsHumansGenetic Predisposition to DiseaseeducationCirrhosiMediation AnalysisHepatologybusiness.industryCarcinomaCase-control studyHepatocellularBiomarkermedicine.diseasedigestive system diseases030104 developmental biologyCross-Sectional StudiesbusinessJournal of Hepatology
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EGFR inhibition in NSCLC: New findings…. and opened questions?

2017

The targeted inhibition of epidermal growth factor receptor (EGFR) has represented a milestone in the treatment of lung cancer. Several studies convincingly and consistently demonstrated a significant superiority of EGFR-TKIs over standard platinum-chemotherapy in EGFR-mutated NSCLC patients, leading to the sequential approval of gefitinib, erlotinib and afatinib as new standard first-line clinical treatment. To date we are witnessing a second revolution in the management of EGFR-positive NSCLC thanks to the development of new treatment strategies aiming to overcome acquired resistance to TKIs and ultimately improve patients’ outcomes. In this review we summarize the most important recent f…

0301 basic medicineOncologyLung Neoplasmsmedicine.medical_treatmentAfatinibResistanceTreatment of lung cancerTargeted therapyTargeted therapyAntineoplastic Agent0302 clinical medicineEpidermal growth factorEpidermal growth factor receptorMolecular Targeted TherapybiologyHematologyTKIErbB ReceptorsOncology030220 oncology & carcinogenesisErlotinibReceptorHumanmedicine.drugmedicine.medical_specialtyEGFR; Liquid biopsy; Resistance; Targeted therapy; TKIs; Antineoplastic Agents; Humans; Lung Neoplasms; Molecular Targeted Therapy; Mutation; Protein Kinase Inhibitors; Receptor Epidermal Growth Factor; Hematology; Oncology; Geriatrics and GerontologyEGFRProtein Kinase InhibitorAntineoplastic Agents03 medical and health sciencesGefitinibInternal medicinemedicineHumansLiquid biopsyIntensive care medicineProtein Kinase InhibitorsEGFR; Liquid biopsy; Resistance; Targeted therapy; TKIs; Antineoplastic Agents; Humans; Lung Neoplasms; Molecular Targeted Therapy; Mutation; Protein Kinase Inhibitors; Receptor; Epidermal Growth Factor; Hematology; Oncology; Geriatrics and GerontologyEpidermal Growth FactorLiquid biopsybusiness.industryrespiratory tract diseasesLung Neoplasm030104 developmental biologyTKIsMutationbiology.proteinReceptor Epidermal Growth FactorGeriatrics and Gerontologybusiness
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Detection of MET Alterations Using Cell Free DNA and Circulating Tumor Cells from Cancer Patients

2020

MET alterations may provide a potential biomarker to evaluate patients who will benefit from treatment with MET inhibitors. Therefore, the purpose of the present study is to investigate the utility of a liquid biopsy-based strategy to assess MET alterations in cancer patients. We analyzed MET amplification in circulating free DNA (cfDNA) from 174 patients with cancer and 49 healthy controls and demonstrated the accuracy of the analysis to detect its alteration in patients. Importantly, a significant correlation between cfDNA concentration and MET copy number (CN) in cancer patients (r = 0.57, p &lt

0301 basic medicineOncologyMale<i>MET</i> copy numbermedicine.medical_treatmentproteínas protooncogénicas c-metdosificación génicahumanosresistencia a medicamentosDrug ResistanceGene Dosagecirculating free DNA (cfDNA)<i>MET</i> amplificationTargeted therapyTargeted therapy0302 clinical medicineCirculating tumor cellestudios prospectivosNeoplasmsantineoplásicosProspective Studieslcsh:QH301-705.5Circulating tumor cells (CTCs)neoplasiasGeneral MedicineProto-Oncogene Proteins c-mettargeted therapyNeoplastic Cells CirculatingErbB ReceptorsCell-free fetal DNA030220 oncology & carcinogenesisinhibidores de proteína cinasasBiomarker (medicine)FemaleMET protein expressionCell-Free Nucleic AcidsMET amplificationmedicine.medical_specialtycirculating tumor cells (CTCs)estudios de casos y controlesMet amplificationCirculating free DNA (cfDNA)Antineoplastic AgentsArticle03 medical and health sciencesInternal medicinemedicineBiomarkers TumorHumansLiquid biopsyProtein Kinase InhibitorsRetrospective Studiesbusiness.industryHead and neck cancerestudios retrospectivosLiquid BiopsyCancermedicine.disease030104 developmental biologylcsh:Biology (General)Drug Resistance NeoplasmCase-Control StudiesMET copy numberbusinessCells
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Phospho-Akt overexpression is prognostic and can be used to tailor the synergistic interaction of Akt inhibitors with gemcitabine in pancreatic cancer

2017

Background There is increasing evidence of a constitutive activation of Akt in pancreatic ductal adenocarcinoma (PDAC), associated with poor prognosis and chemoresistance. Therefore, we evaluated the expression of phospho-Akt in PDAC tissues and cells, and investigated molecular mechanisms influencing the therapeutic potential of Akt inhibition in combination with gemcitabine. Methods Phospho-Akt expression was evaluated by immunohistochemistry in tissue microarrays (TMAs) with specimens tissue from radically-resected patients (n = 100). Data were analyzed by Fisher and log-rank test. In vitro studies were performed in 14 PDAC cells, including seven primary cultures, characterized for their…

0301 basic medicineOncologyMaleCancer ResearchBiopsyAKT1ApoptosisAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Hematology; Molecular Biology; Oncology; Cancer ResearchDeoxycytidinePancreatic ductal adenocarcinoma0302 clinical medicineCell MovementTumor Cells CulturedGlucose Transporter Type 1medicine.diagnostic_testChemistryCell CyclePancreatic NeoplasmDrug Synergismlcsh:Diseases of the blood and blood-forming organsHematologyCell cycleMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisOncologyAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Aged; Apoptosis; Biopsy; Carcinoma Pancreatic Ductal; Cell Cycle; Cell Movement; Deoxycytidine; Drug Synergism; Female; Glucose Transporter Type 1; Humans; Male; Middle Aged; Pancreatic Neoplasms; Phosphoproteins; Prognosis; Proto-Oncogene Proteins c-akt; RNA Messenger; Spheroids Cellular; Tumor Cells Cultured; Hematology; Molecular Biology; Oncology; Cancer Research030220 oncology & carcinogenesisPhosphoproteinFemalemedicine.drugHumanCarcinoma Pancreatic Ductalmedicine.medical_specialtyPrognosilcsh:RC254-282Flow cytometry03 medical and health sciencesInternal medicinePancreatic cancerSpheroids CellularmedicineHumansRNA MessengerProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayAgedlcsh:RC633-647.5ResearchAktSynergismApoptosimedicine.diseasePhosphoproteinsGemcitabineGemcitabinePancreatic Neoplasms030104 developmental biologyCancer cellCancer researchProto-Oncogene Proteins c-akt
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