Search results for "Bevacizumab"

showing 10 items of 162 documents

The route to solve the interplay between inflammation, angiogenesis and anti-cancer immune response.

2016

Even though the crucial role played by inflammation in cancer development and progression was first hypothesized by Rudolf Virchow at the beginning of the nineteenth century, only recently inflammation has been recognized as a hallmark of cancer. At present, the biology underlying the humoral and cellular immune-suppressive cancer-associated inflammatory microenvironment is an active area of preclinical and clinical investigation.1, 2 Indeed, the possibility to modulate the inflammatory/immune microenvironment, by either antagonizing the tumor-associated immune-suppression or by enhancing the pre-existing anti-cancer immune response in tumor tissues, is a promising therapeutic option for ca…

0301 basic medicineCancer ResearchBevacizumabAngiogenesisColorectal cancerImmunologyInflammationModels Biologicalimmune responseProinflammatory cytokineImmunomodulation03 medical and health sciencesCellular and Molecular Neuroscienceinflammation angiogenesis and anti-cancer immune response0302 clinical medicineImmune systemNeoplasmsmedicinecancerCytotoxic T cellAnimalsHumansangiogenesis and anti-cancer immune responseNeovascularization Pathologicbusiness.industryangiogenesiFOXP3Cell BiologyNews and Commentarymedicine.diseaseBevacizumab030104 developmental biologyinflammation030220 oncology & carcinogenesisImmunologymedicine.symptombusinessmedicine.drug
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EphrinB2 repression through ZEB2 mediates tumour invasion and anti-angiogenic resistance.

2016

Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion by abrogation of repulsive signals. We demonstrate that ephrinB2 is downregulated in human gliomas as a consequence of promoter hypermethylation and gene deletion. Consistently, genetic deletion of ephrinB2 in a murine high-grade glioma model increases invasion. Importantly, ephrinB2 gene silencing is complemented by a hypoxia-induced transcriptional repression. Mechanistically, hypoxia-inducible facto…

0301 basic medicineCell signalingScienceGeneral Physics and AstronomyRepressorDown-RegulationAngiogenesis InhibitorsEphrin-B2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleNeovascularization03 medical and health sciencesDownregulation and upregulationddc:570GliomamedicineGene silencingAnimalsHumansNeoplasm InvasivenessPsychological repressionZinc Finger E-box Binding Homeobox 2Regulation of gene expressionMice KnockoutMultidisciplinaryNeovascularization PathologicQGeneral ChemistryGliomamedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysCell HypoxiaCell biologyUp-RegulationBevacizumabGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyDrug Resistance Neoplasmmedicine.symptomNature communications
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Bevacizumab diminishes inflammation in an acute endotoxin-induced uveitis model

2017

Este artículo se encuentra disponible en la página web de la revista en la siguiente URL: https://www.frontiersin.org/articles/10.3389/fphar.2018.00649/full Introduction: Uveitis is an eye disease characterized by inflammation of the uvea and an early and exhaustive diagnosis is essential for its treatment. The aim of our study is to assess the potential toxicity and anti-inflammatory efficacy of Bevacizumab in an experimental uveitis model by subcutaneously injecting lipopolysaccharide into Lewis rats and to clarify its mechanism. Material and Methods: Blood–aqueous barrier integrity was assessed 24 h after endotoxin-induced uveitis (EIU) by analyzing two parameters: cell count and protein…

0301 basic medicineChemokineLipopolysaccharidegenetic structuresmedicine.medical_treatmentÚvea - Efectos de los medicamentos.chemokinesPharmacologymedicine.disease_causeendotoxin-induced uveitischemistry.chemical_compound0302 clinical medicineMedicineoxidative stressPharmacology (medical)Bevacizumab - Efectos fisiológicos.Bevacizumab - Efectos secundarios.Uvea - Effect of drugs on.Original ResearchEstrés oxidativo.biologyOxidative stress.medicine.anatomical_structureCytokineToxicityOjos - Enfermedades - Tratamiento.medicine.symptomUveitisPharmacology.InflammationFarmacología.bevacizumabBevacizumab - Physiological effect.Bevacizumab - Side effects.03 medical and health sciencesUveitis - Treatment.Eyes - Diseases - Treatment.Pharmacologybusiness.industrylcsh:RM1-950Uveítis - Tratamiento.Uveamedicine.diseaseeye diseasescytokines030104 developmental biologylcsh:Therapeutics. Pharmacologychemistryinflammation030221 ophthalmology & optometrybiology.proteinsense organsbusinessOxidative stress
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Predictive and prognostic value of magnesium serum level in FOLFIRI plus cetuximab or bevacizumab treated patients with stage IV colorectal cancer: r…

2020

Magnesium wasting is a frequent side effect of epidermal growth factor receptor (EGFR)-antibody treatment as magnesium-absorption mechanisms are dependent on EGFR signaling. EGFR-inhibition results in decreased renal reabsorption. There is evidence that hypomagnesemia during cetuximab treatment correlates with response. The prognostic role of hypomagnesemia during bevacizumab treatment has not been studied yet. Here, we evaluate the prognostic value of hypomagnesemia in patients with metastatic colorectal cancer treated with FOLFIRI plus cetuximab or bevacizumab as first-line therapy. A total of 391 of 752 patients of the firstline irinotecan study population had magnesium levels measured a…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyRenal Tubular Transport Inborn ErrorsBevacizumabSide effectColorectal cancerHypercalciuriaLeucovorinCetuximabIrinotecanGastroenterologyHypomagnesemia03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansPharmacology (medical)MagnesiumAgedRetrospective StudiesPharmacologyCetuximabbusiness.industryHazard ratiomedicine.diseasePrognosisIrinotecanBevacizumabSurvival RateNephrocalcinosis030104 developmental biologyOncology030220 oncology & carcinogenesisFOLFIRICamptothecinFemaleFluorouracilbusinessColorectal Neoplasmsmedicine.drugFollow-Up StudiesAnti-cancer drugs
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Role of RAS mutation status as a prognostic factor for patients with advanced colorectal cancer treated with first-line chemotherapy based on fluorop…

2016

The role of Kirsten rat sarcoma viral oncogene homolog (KRAS) and neuroblastoma RAS viral oncogene homolog (NRAS) mutations as negative predictors for anti-epidermal growth factor receptor (EGFR) therapies in metastatic colorectal cancer (CRC) has been firmly established. However, whether the RAS mutation status plays a role as a biomarker for anti-vascular endothelial growth factor (VEGF) treatment remains controversial. Data from 93 CRC patients who received first-line cytotoxic chemotherapy with fluoropyrimidines and oxaliplatin, with or without bevacizumab, were analyzed. We investigated the association between the RAS mutation status and clinical outcomes in terms of response rate, pro…

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancermedicine.medical_treatmentmedicine.disease_cause03 medical and health sciences0302 clinical medicineInternal medicinemedicineChemotherapyOncogenebusiness.industryCancerArticlesmedicine.diseaseOxaliplatin030104 developmental biologyOncology030220 oncology & carcinogenesisKRASbusinessmedicine.drugMolecular and Clinical Oncology
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Impact of BRAF and RAS mutations on first-line efficacy of FOLFIRI plus cetuximab versus FOLFIRI plus bevacizumab: analysis of the FIRE-3 (AIO KRK-03…

2017

Abstract Background RAS and BRAF mutations have been identified as negative prognostic factors in metastatic colorectal cancer. Efficacy of 5-fluorouracil, leucovorin, irinotecan (FOLFIRI) plus bevacizumab in patients with RAS-mutant tumours needs to be further evaluated. Whether to treat patients with BRAF-mutant tumours with either bevacizumab or anti-epidermal growth factor receptor (EGFR) antibodies remains unclear. Methods Patients treated within the FIRE-3 trial were retrospectively tested for BRAF and RAS mutations using formalin fixated paraffin embedded (FFPE) tumour material applying pyrosequencing for KRAS and NRAS exon 2, 3 and 4 mutations as far as for BRAF mutations. Survival …

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleProto-Oncogene Proteins B-rafCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancerLeucovorinCetuximabmedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansneoplasmsSurvival analysisAgedRetrospective StudiesCetuximabbusiness.industryLiver NeoplasmsExonsMiddle Agedmedicine.diseasedigestive system diseasesIrinotecanBevacizumab030104 developmental biologyTreatment OutcomeOncology030220 oncology & carcinogenesisMutationFOLFIRICamptothecinFemaleKRASFluorouracilbusinessColorectal Neoplasmsmedicine.drugEuropean journal of cancer (Oxford, England : 1990)
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Does bevacizumab impact anti-EGFR therapy efficacy in metastatic colorectal cancer?

2016

IF 5.008; International audience; Anti-EGFR therapy and antiangiogenic therapies are used alone or in combination with chemotherapies to improve survival in metastatic colorectal cancer. However, it is unknown whether pretreatment with antiangiogenic therapy could impact on the efficacy of anti-EGFR therapy. We selected one hundred and twenty eight patients diagnosed with advanced colorectal cancer with a KRAS and NRAS unmutated tumor. These patients were treated with cetuximab or panitumumab alone or with chemotherapy as second or third-line. Univariate and multivariate Cox model analysis were performed to estimate the effect of a previous bevacizumab regimen on progression free survival a…

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleVascular Endothelial Growth Factor AColorectal cancerCetuximabAngiogenesis Inhibitorsmedicine.disease_causeTrialGTP PhosphohydrolasesRas mutations[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsDrug InteractionsAged 80 and overCetuximabPanitumumabAntibodies MonoclonalMiddle Aged3. Good healthErbB ReceptorsOncology030220 oncology & carcinogenesisFemaleKRASColorectal Neoplasms1st-Line treatmentmedicine.drugResearch PaperAdultSTAT3 Transcription Factormedicine.medical_specialtyBevacizumabAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologybevacizumabIrinotecanDisease-Free SurvivalTumor angiogenesisProto-Oncogene Proteins p21(ras)03 medical and health sciencesVEGFRInternal medicineCell Line TumormedicinePanitumumabHumansEndothelial growth-FactorChemotherapyProgression-free survivalAgedbusiness.industry[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMembrane Proteinsmetastatic colon cancerStat-3medicine.diseaseVascular Endothelial Growth Factor Receptor-2IrinotecanRandomized phase-III030104 developmental biologyanti-EGFR therapyFactor receptorCaco-2 Cellsbusiness
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FOLFIRI plus cetuximab versus FOLFIRI plus bevacizumab for metastatic colorectal cancer (FIRE-3): a post-hoc analysis of tumour dynamics in the final…

2016

Summary Background FIRE-3 compared first-line 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI) plus cetuximab with FOLFIRI plus bevacizumab in patients with KRAS exon 2 wild-type metastatic colorectal cancer. The same study also reported an exploratory analysis of a subgroup of patients with tumours that were wild-type at other RAS genes ( KRAS and NRAS exons 2–4). We report here efficacy results for the FIRE-3 final RAS ( KRAS/NRAS , exons 2–4) wild-type subgroup. Moreover, new metrics of tumour dynamics were explored during a centralised radiological review to investigate how FOLFIRI plus cetuximab conferred overall survival benefit in the absence of differences in investigator-assess…

0301 basic medicineOncologyAdultMalemedicine.medical_specialtyBevacizumabColorectal cancerPopulationLeucovorinCetuximabmedicine.disease_cause03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansNeoplasm MetastasiseducationResponse Evaluation Criteria in Solid TumorsAgededucation.field_of_studyCetuximabbusiness.industryMiddle Agedmedicine.diseaseIrinotecanBevacizumab030104 developmental biologyGenes rasOncologyResponse Evaluation Criteria in Solid Tumors030220 oncology & carcinogenesisFOLFIRICamptothecinFemaleKRASFluorouracilbusinessColorectal NeoplasmsTomography X-Ray Computedmedicine.drugThe Lancet. Oncology
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Aurora Kinase A expression predicts platinum-resistance and adverse outcome in high-grade serous ovarian carcinoma patients

2016

High-Grade Serous Ovarian Carcinoma (HGSOC) is the predominant histotype of epithelial ovarian cancer (EOC), characterized by advanced stage at diagnosis, frequent TP53 mutation, rapid progression, and high responsiveness to platinum-based-chemotherapy. To date, standard first-line-chemotherapy in advanced EOC includes platinum salts and paclitaxel with or without bevacizumab. The major prognostic factor is the response duration from the end of the platinum-based treatment (platinum-free interval) and about 10–0 % of EOC patients bear a platinum-refractory disease or develop early resistance (platinum-free interval shorter than 6 months). On these bases, a careful selection of patients who …

0301 basic medicineOncologyAdultmedicine.medical_specialtyBevacizumabendocrine system diseasesPrognosimedicine.medical_treatmentHigh-grade serous ovarian carcinoma (HGSOC)Gene ExpressionAntineoplastic AgentsKaplan-Meier EstimateBrief Communication03 medical and health sciences0302 clinical medicineOvarian carcinomaInternal medicineObstetrics and GynaecologyMedicineHumansPlatinumAgedAurora Kinase ANeoplasm StagingGynecologyAged 80 and overOvarian NeoplasmsChemotherapyAURKAbusiness.industryObstetrics and GynecologyRetrospective cohort studyMiddle AgedPrognosisImmunohistochemistryfemale genital diseases and pregnancy complicationsCystadenocarcinoma SerousClinical trialSerous fluid030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisFemaleAurora Kinase APersonalized medicineTherapybusinessmedicine.drugJournal of Ovarian Research
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Accumulation of MDSC and Th17 Cells in Patients with Metastatic Colorectal Cancer Predicts the Efficacy of a FOLFOX-Bevacizumab Drug Treatment Regimen

2016

Abstract Host immunity controls the development of colorectal cancer, and chemotherapy used to treat colorectal cancer is likely to recruit the host immune system at some level. Athough preclinical studies have argued that colorectal cancer drugs, such as 5-fluorouracil (5-FU) and oxaliplatin, exert such effects, their combination as employed in the oncology clinic has not been evaluated. Here, we report the results of prospective immunomonitoring of 25 metastatic colorectal cancer (mCRC) patients treated with a first-line combination regimen of 5-FU, oxaliplatin, and bevacizumab (FOLFOX–bevacizumab), as compared with 20 healthy volunteers. Before this therapy was initiated, T regulatory ce…

0301 basic medicineOncologyCancer ResearchOrganoplatinum CompoundsColorectal cancermedicine.medical_treatmentLeucovorinKaplan-Meier EstimatePolymerase Chain ReactionSuppressor-Cells[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineFOLFOXAntineoplastic Combined Chemotherapy ProtocolsProspective StudiesProgressionFlow Cytometry3. Good healthBevacizumabOncology030220 oncology & carcinogenesisFluorouracilColorectal Neoplasmsmedicine.drugmedicine.medical_specialtyBevacizumabT-Cells[SDV.CAN]Life Sciences [q-bio]/CancerDisease-Free Survival03 medical and health sciencesInternal medicinemedicineCarcinomaHumansChemotherapyTumorsInflammationChemotherapyAntitumor Immunitybusiness.industryMyeloid-Derived Suppressor CellsCarcinomaCancermedicine.diseasedigestive system diseasesOxaliplatinRegimen030104 developmental biologyTherapiesImmunologyTh17 CellsPoor-Prognosisbusiness
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