Search results for "KRAS"

showing 10 items of 232 documents

Estudio de acetilación de proteínas en líneas celulares humanas de cáncer colorectal KRAS mutado y salvaje

2016

El estado mutacional de KRAS es el principal predictor negativo de respuesta a terapias anti-factor de crecimiento epidérmico (EGFR) en pacientes diagnosticados de cáncer colorectal avanzado (CRC). Sin embargo existe datos contradictorios sobre las causas de la respuesta variable a estos fármacos diana de acuerdo con la presencia de mutaciones, de hecho publicaciones recientes han presentado datos no concluyentes sobre los pacientes portadores de mutaciones en el codón 13. En nuestro trabajo, hemos estudiado el impacto de la presencia de mutaciones en KRAS en proteínas intracelulares no histónicas. Para ello hemos utilizado diferentes líneas celulares de cáncer colorectal portadoras de dife…

Líneas celularesCancer ColorectalAcetilación proteícaKRASFármacos anti factor de crecimiento epidérmico
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Jūras krastā izskaloto aļģu biomasas ķīmiskā sastāva izvērtējums Kurzemes piekrastē

2021

Jūras krastā izskaloto aļģu biomasas ķīmiskā sastāva izvērtējums Kurzemes piekrastē. Butkus D., darba vadītāji Dr. chem. Rudoviča V. un Dr. chem. Bikovens O. Maģistra darbs, 53 lappuses, 23 attēli, 18 tabulas, 37 literatūras avoti, 7 pielikumi. Latviešu valodā. Maģistra darbā ir veikta izskaloto jūras aļģu biomasas izpēte. Aļģu paraugi tika ievākti Baltijas jūras Kurzemes piekrastē Liepājas un Pāvilostas pludmalēs 2020. gadā vasaras un rudens sezonā. Izskalotās jūras aļģes tika raksturotas pēc botāniskā sastāva un noteiktā ķīmiskā elementu satura tajās. Izvērtēta jūras aļģu izmantošanas iespēja lauksaimniecībā mēslošanas nolūkos. MAKRO-, MIKRO-, RETZEMJU ELEMENTI, JŪRAS AĻĢES, KURZEMES JŪRA…

MAKRO- MIKRO- RETZEMJU ELEMENTIKURZEMES JŪRAS PIEKRASTEINDUKTĪVI SAISTĪTĀS PLAZMAS MASSPEKTROMETRIJAJŪRAS AĻĢESĶīmija
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Roles of EGFR and KRAS and their downstream signaling pathways in pancreatic cancer and pancreatic cancer stem cells

2015

Pancreatic cancer is currently the fourth most common cancer, is increasing in incidence and soon will be the second leading cause of cancer death in the USA. This is a deadly malignancy with an incidence that approximates the mortality with 44,000 new cases and 36,000 deaths each year. Surgery, although only modestly successful, is the only curative option. However, due the locally aggressive nature and early metastasis, surgery can be performed on less than 20% of patients. Cytotoxic chemotherapy is palliative, has significant toxicity and improves survival very little. Thus new treatment paradigms are needed desperately. Due to the extremely high frequency of KRAS gene mutations (>90%) d…

MAPK/ERK pathwayCancer ResearchmiRsEGFRmedicine.disease_causeMetastasisProto-Oncogene Proteins p21(ras)Glycogen Synthase Kinase 3GeneticCancer stem cellKRaPancreatic cancerKRasGeneticsmedicineAnimalsHumansPTENEpidermal growth factor receptorMolecular BiologyPI3K/AKT/mTOR pathwayGSK-3biologyCancer stem cellsCancer stem cellmiRCancer stem cells; Drug resistance; EGFR; GSK-3; KRas; Metformin; miRsmedicine.diseaseMetforminErbB ReceptorsPancreatic NeoplasmsDrug resistanceNeoplastic Stem Cellsbiology.proteinCancer researchMolecular MedicineKRASSignal TransductionAdvances in Biological Regulation
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Sensitivity of pancreatic cancer cells to chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals can be regulated by WT-TP53

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic malignancy. Approximately 85% of pancreatic cancers are classified as PDACs. The survival of PDAC patients is very poor and only 5–10% of patients survive 5 years after diagnosis. Mutations at the KRAS and TP53 gene are frequently observed in PDAC patients. The PANC-28 cell line lacks wild-type (WT) TP53. In the following study, we have investigated the effects of restoration of WT TP53 activity on the sensitivity of PANC-28 pancreatic cancer cells to various drugs which are used to treat PDAC patients as well as other cancer patients. In addition, we have examined the effects of signal transduction inhibitors which tar…

Male0301 basic medicineDrugCancer ResearchmiRsendocrine system diseasesmedia_common.quotation_subjectSignal transduction inhibitorsTargeted therapeuticAntineoplastic AgentsMalignancymedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineChloroquinePancreatic cancerGeneticsmedicineHumansTP53Molecular BiologyneoplasmsSignal transduction inhibitorTargeted therapeuticsCell Proliferationmedia_commontarget therapeuticsCell growthbusiness.industryCancermedicine.diseasedigestive system diseasesMetforminPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsMutationCancer researchmiRs.Molecular MedicineFemaleKRASTumor Suppressor Protein p53businessSignal Transductionmedicine.drugDrug sensitivity
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Small Bowel Carcinomas in Coeliac or Crohn’s Disease: Clinico-pathological, Molecular, and Prognostic Features. A Study From the Small Bowel Cancer I…

2017

Background and aims An increased risk of small bowel carcinoma [SBC] has been reported in coeliac disease [CD] and Crohn's disease [CrD]. We explored clinico-pathological, molecular, and prognostic features of CD-associated SBC [CD-SBC] and CrD-associated SBC [CrD-SBC] in comparison with sporadic SBC [spo-SBC]. Methods A total of 76 patients undergoing surgical resection for non-familial SBC [26 CD-SBC, 25 CrD-SBC, 25 spo-SBC] were retrospectively enrolled to investigate patients' survival and histological and molecular features including microsatellite instability [MSI] and KRAS/NRAS, BRAF, PIK3CA, TP53, HER2 gene alterations. Results CD-SBC showed a significantly better sex-, age-, and st…

Male0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologySurvivalReceptor ErbB-2Colorectal cancermedicine.disease_causeInflammatory bowel diseaseInflammatory bowel diseasetumour-infiltrating lymphocyteErbB-20302 clinical medicineCrohn DiseaseRetrospective StudieRisk Factors80 and overChildClass I Phosphatidylinositol 3-KinaseAged 80 and overColonic NeoplasmSettore MED/12 - GastroenterologiaCrohn's diseaseMLH1 methylationTumour-infiltrating lymphocytesGastroenterologyGeneral MedicineMiddle AgedPrognosisInflammatory bowel disease; Microsatellite instability; MLH1 promoter methylation; Survival; Tumour-infiltrating lymphocytes; Gastroenterology030220 oncology & carcinogenesisColonic NeoplasmsSurvival AnalysiKRASHumanReceptorAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyPrognosiClass I Phosphatidylinositol 3-KinasesSettore MED/08 - Anatomia PatologicaNOProto-Oncogene Proteins p21(ras)MLH1 promoter methylationYoung Adult03 medical and health sciencesInternal medicinemedicineCarcinomaHumansMLH1 methylation; inflammatory bowel disease; microsatellite instability; survival; tumour-infiltrating lymphocytesneoplasmsAgedRetrospective StudiesInflammatory bowel disease; Microsatellite instability; MLH1 promoter methylation; Survival; Tumour-infiltrating lymphocytes; Adult; Aged; Aged 80 and over; Celiac Disease; Child; Class I Phosphatidylinositol 3-Kinases; Colonic Neoplasms; Crohn Disease; Humans; Male; Microsatellite Instability; Middle Aged; Prognosis; Proto-Oncogene Proteins B-raf; Proto-Oncogene Proteins p21(ras); Receptor ErbB-2; Retrospective Studies; Risk Factors; Survival Analysis; Tumor Suppressor Protein p53; Young Adult; Gastroenterologybusiness.industryTumour-infiltrating lymphocyteRisk FactorCancerMicrosatellite instabilityinflammatory bowel disease; microsatellite instability; MLH1 promoter methylation; tumour-infiltrating lymphocytes; survivalmedicine.diseaseSurvival Analysiseye diseasesdigestive system diseasesCeliac Disease030104 developmental biologyMicrosatellite instabilityTumor Suppressor Protein p53businessJournal of Crohn's and Colitis
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Prognostic and predictive value of primary tumour side in patients with RAS wild-type metastatic colorectal cancer treated with chemotherapy and EGFR…

2017

BACKGROUND: There is increasing evidence that metastatic colorectal cancer (mCRC) is a genetically heterogeneous disease and that tumours arising from different sides of the colon (left versus right) have different clinical outcomes. Furthermore, previous analyses comparing the activity of different classes of targeted agents in patients with KRAS wild-type (wt) or RAS wt mCRC suggest that primary tumour location (side), might be both prognostic and predictive for clinical outcome. METHODS: This retrospective analysis investigated the prognostic and predictive influence of the localization of the primary tumour in patients with unresectable RAS wt mCRC included in six randomized trials (CRY…

Male0301 basic medicineOncologyColorectal cancermedicine.medical_treatmentCetuximabmedicine.disease_causeEGFR Antibody0302 clinical medicineAntineoplastic Agents ImmunologicalNeoplasias ColorrectaisMedicineNeoplasm MetastasisRandomized Controlled Trials as Topicpredictive valuePanitumumabHazard ratiotumour sideAntibodies MonoclonalHematologyPrognosisChemotherapy regimenErbB ReceptorsBevacizumabTreatment OutcomeOncology030220 oncology & carcinogenesisFemaleKRASColorectal Neoplasmsmedicine.drugmedicine.medical_specialtyBevacizumabcolorectal cancerGenes ras03 medical and health sciencesAnticorpos MonoclonaisInternal medicineHumansChemotherapybusiness.industryAntineoplásicos ImunológicosOdds ratiomedicine.diseaserandomised trial030104 developmental biologyGenes rasHuman medicinebusinessprognosticanti-EGFR treatment
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A Phase Ib Dose-Escalation Study of the Safety, Tolerability, and Pharmacokinetics of Cobimetinib and Duligotuzumab in Patients with Previously Treat…

2017

Abstract Lessons Learned Cobimetinib and duligotuzumab were well tolerated as single agents and in combination with other agents. The cobimetinib and duligotuzumab combination was associated with increased toxicity, most notably gastrointestinal, and limited efficacy in the patient population tested. Background KRAS-mutant tumors possess abnormal mitogen-activated protein kinases (MAPK) pathway signaling, leading to dysregulated cell proliferation. Cobimetinib blocks MAPK signaling. The dual-action antibody duligotuzumab (MEHD7945A) inhibits ligand binding to both epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 3 (HER3). Blockade of EGFR/HER3 and inhibitio…

Male0301 basic medicineOncologyMAPK/ERK pathwayCancer ResearchReceptor ErbB-3MAP Kinase Kinase 1Administration Oralmedicine.disease_causechemistry.chemical_compound0302 clinical medicinePiperidinesAntineoplastic Combined Chemotherapy ProtocolsMedicineProspective StudiesEpidermal growth factor receptor31biologyMiddle AgedErbB ReceptorsTreatment OutcomeOncologyTolerability030220 oncology & carcinogenesisFemaleDrug EruptionsKRASmedicine.symptomColorectal NeoplasmsSignal TransductionAdultmedicine.medical_specialty4HypokalemiaAcneiform eruptionProto-Oncogene Proteins p21(ras)03 medical and health sciencesAcneiform EruptionsInternal medicineHumansAdverse effectAgedNeoplasm StagingCobimetinibDose-Response Relationship Drugbusiness.industryClinical Trial Resultsmedicine.disease030104 developmental biologychemistryAstheniaImmunoglobulin Gbiology.proteinAzetidinesbusinessProgressive diseaseThe Oncologist
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EGFR gene copy number decreases during anti-EGFR antibody therapy in colorectal cancer

2018

Epidermal growth factor receptor (EGFR) gene copy number (GCN) increase is associated with a favorable anti-EGFR antibody treatment response in RAS wild-type metastatic colorectal cancer. However, there are limited and comparative data regarding the EGFR GCN in primary colorectal cancer tumors and corresponding metastases or the effect of anti-EGFR antibody treatment on EGFR GCN in recurrent disease. In addition, little is known about the potential EGFR GCN changes during anti-EGFR therapy in comparison with other treatment regimens. EGFR GCN was analyzed by EGFR immunohistochemistry-guided silver in situ hybridization in primary and corresponding recurrent local or metastatic tumors from 8…

Male0301 basic medicineTime FactorsColorectal cancerBLOCKADEGene DosageCetuximabmedicine.disease_causeAntineoplastic Agents Immunological0302 clinical medicinePREDICTS RESPONSEMedicineHETEROGENEITYBENEFITCopy-number variationEpidermal growth factor receptorIn Situ Hybridization FluorescenceAged 80 and overbiologyPanitumumabvasta-aineetMiddle AgedImmunohistochemistry3. Good healthErbB ReceptorsGene Expression Regulation NeoplasticTreatment OutcomeRAS MUTATIONSChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleKRASAntibodyColorectal NeoplasmsAdultgene copy numbermedicine.drug_classCETUXIMAB THERAPY3122 Cancerssilver in situ hybridizationDown-Regulationcolorectal cancerIn situ hybridizationAdenocarcinomaMonoclonal antibodyta3111Pathology and Forensic MedicineProto-Oncogene Proteins p21(ras)03 medical and health sciencesKRASHumansWILD-TYPEMETAANALYSISAgedRetrospective Studiessyöpähoidotbusiness.industrymedicine.diseaseta3122Blockadeperäsuolisyöpä030104 developmental biologymonoclonal antibodyMutationCancer researchbiology.protein3111 BiomedicineNeoplasm Recurrence Localbusinessepidermal growth factor receptorACQUIRED-RESISTANCEHuman Pathology
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Clinical parameters to guide decision-making in elderly metastatic colorectal CANCER patients treated with intensive cytotoxic and anti-angiogenic th…

2017

// Gemma Bruera 1, 2 , Antonio Russo 3 , Antonio Galvano 3 , Sergio Rizzo 3 and Enrico Ricevuto 1, 2 1 Oncology Territorial Care, S. Salvatore Hospital, Oncology Network ASL1 Abruzzo, University of L’Aquila, L’Aquila, Italy 2 Department of Biotechnological and Applied Clinical Sciences, University of L’Aquila, L’Aquila, Italy 3 Medical Oncology, Department of Surgical, Oncological and Stomatological Sciences, University of Palermo, Palermo, Italy Correspondence to: Antonio Russo, email: antonio.russo@usa.net Keywords: elderly, intensive treatment, metastatic colorectal cancer, triplet chemotherapy plus bevacizumab, unfit Received: June 07, 2016     Accepted: November 24, 2016     Published:…

Male0301 basic medicineUnfitmedicine.medical_specialtyBevacizumabColorectal cancerDecision MakingAngiogenesis InhibitorsNeutropeniamedicine.disease_cause03 medical and health sciences0302 clinical medicineElderlyInternal medicinemedicineMucositisHumansNeoplasm MetastasisAgedRetrospective StudiesTriplet chemotherapy plus bevacizumabbusiness.industryMetastatic colorectal cancerelderly; intensive treatment; metastatic colorectal cancer; triplet chemotherapy plus bevacizumab; unfitRetrospective cohort studymedicine.diseaseComorbiditySurgeryRegimenTreatment Outcome030104 developmental biologyOncology030220 oncology & carcinogenesisFemaleIntensive treatmentKRASClinical Research PaperColorectal NeoplasmsbusinessElderly; Intensive treatment; Metastatic colorectal cancer; Triplet chemotherapy plus bevacizumab; Unfit; Oncologymedicine.drug
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Phase I study of FOLFIRI plus pimasertib as second-line treatment for KRAS-mutated metastatic colorectal cancer

2015

BACKGROUND: The mitogen-activated protein kinase (MAPK) pathway has been implicated in the molecular pathogenesis of human cancers, including metastatic colorectal cancer (mCRC). This provides a rationale for the development of MAPK-targeted agents such as pimasertib. METHODS: Patients with KRAS mutant mCRC were treated in the second-line setting with FOLFIRI (5-fluorouracil/folinic acid/irinotecan) plus pimasertib. The primary objective of the safety run-in phase was to determine the maximum-tolerated dose (MTD) and the recommended phase II dose of pimasertib combined with FOLFIRI. RESULTS: Sixteen patients were enrolled in the trial. Ten and six patients were treated daily with 45 and 60 …

MaleCancer ResearchColorectal cancermedicine.medical_treatmentLeucovorinColorectal NeoplasmPharmacologymedicine.disease_causepimasertibcombination therapyAntineoplastic Combined Chemotherapy ProtocolsNeoplasm Metastasiscombination therapy second-line treatmentAged 80 and overProto-Oncogene ProteinCetuximabKRAS-mutated metastatic colorectal cancerMedicine (all)MEK inhibitorMiddle AgedNeoplasm MetastasiTreatment OutcomeOncologyFluorouracilFOLFIRISecond-line treatmentFemaleFluorouracilKRASColorectal NeoplasmsPimasertibHumanmedicine.drugNiacinamideProto-Oncogene Proteins p21(ras)FOLFIRIProto-Oncogene ProteinsmedicineHumansCombination therapyneoplasmsAgedChemotherapyMEK inhibitorAntineoplastic Combined Chemotherapy Protocolbusiness.industryKRAS -mutated metastatic colorectal cancerGenes raras Proteinmedicine.diseasedigestive system diseasesGenes rassecond-line treatmentMutationras ProteinsClinical StudyCancer researchCamptothecinHuman medicinebusinessCamptothecinThe British journal of cancer
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