Search results for "mutation."

showing 10 items of 2808 documents

The impact of TP53 mutation on high-risk rectal cancer patients treated within the EXPERT-C trial, a randomized phase II study of neoadjuvant oxalipl…

2012

e14088 Background: The EXPERT-C trial randomised 165 patients into neoadjuvant CAPOX and CRT ± cetuximab and demonstrated a significant increase in radiological response (RR) and overall survival (OS) with cetuximab in KRAS/BRAF wild type (WT) rectal cancer (Dewdney et al JCO in press). TP53 mutation has been associated with worse CRT response and survival in rectal cancer and could lead to stimulation of PI3K signalling pathway, thus potential resistance to cetuximab. This analysis evaluates the impact of TP53 mutation in the EXPERT-C trial. Methods: FFPE tissue from biopsy (n=102) and resection specimens (n=99) were analysed for TP53 mutations (exons 5-8) using a multiplex PCR method fol…

OncologyCancer Researchmedicine.medical_specialtyCetuximabbusiness.industryColorectal cancerPhases of clinical researchmedicine.diseaseTp53 mutationOxaliplatinCapecitabineOncologyInternal medicinemedicineOverall survivalbusinessneoplasmsmedicine.drugJournal of Clinical Oncology
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Mutational analysis of plasma DNA from patients (pts) in the phase III GRID study of regorafenib (REC) versus placebo (PL) in tyrosine kinase inhibit…

2013

10503 Background: The phase III GRID study showed that REG provides a significant improvement in progression-free survival (PFS) compared with PL in pts with advanced gastrointestinal stromal tumors (GIST) following failure of at least imatinib (IM) and sunitinib (SU; HR 0.27, p<0.0001). Determining GIST genotype in TKI-refractory disease has proven challenging due to inter-tumoral heterogeneity and pt preference to avoid serial biopsies. To overcome this, we analysed circulating DNA in plasma as a source of tumor DNA and studied the correlation between mutational status and clinical outcome. Methods: DNA was isolated from both archival tumor tissue (n=102) and plasma at baseline (n=163…

OncologyCancer Researchmedicine.medical_specialtyGiSTbusiness.industrymedicine.drug_classBioinformaticsPlacebodigestive system diseasesTyrosine-kinase inhibitorMutational analysischemistry.chemical_compoundOncologyRefractorychemistryInternal medicineRegorafenibGenotypeMedicineStromal tumorbusiness
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High-dose radiotherapy for oligo-progressive NSCLC receiving EGFR tyrosine kinase inhibitors: Real world data

2020

Background/aim Local ablative treatments for oligo-progressive, EGFR mutated non-small cell lung cancer (mut-NCSLC) may improve long-term disease control and survival. We analyzed the efficacy of hypo-fractionated, high-dose radiation therapy (HDRT), in association with prolonged EGFR tyrosine kinase inhibitors (TKI) in oligo-progressive, EGFR mutant-NSCLC. Patients and methods Progression-free survival-1 (PFS-1, date from initiation of TKI therapy until oligo-progression or death), and progression-free survival-2 (PFS-2, date of focal progression until further progression or death) were evaluated. Results Thirty-six patients were analyzed. The median PFS 1 was 12.5 months. HDHRT consisted …

OncologyCancer Researchmedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentEGFR high-dose radiotherapy Non-small cell lung cancer oligo-progressionEGFRGeneral Biochemistry Genetics and Molecular Biologyoligo-progression03 medical and health sciences0302 clinical medicineNon-small cell lung cancerCarcinoma Non-Small-Cell LungInternal medicinemedicineOverall survivalHumansProtein Kinase InhibitorsRetrospective StudiesPharmacologybusiness.industryEGFR Non-small cell lung cancer high-dose radiotherapy oligo-progressionEGFR; High-dose radiotherapy; Non-small cell lung cancer; Oligo-progressionEGFR Tyrosine Kinase Inhibitorshigh-dose radiotherapyDisease controlProgression-Free SurvivalErbB ReceptorsRadiation therapy030220 oncology & carcinogenesisMutationNon small cellbusinessReal world dataResearch Article
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Abstract CT022: IVAC® MUTANOME - A first-in-human phase I clinical trial targeting individual mutant neoantigens for the treatment of melanoma

2016

Abstract One of the hallmarks of cancer is the inherent instability of the genome leading to multiple genomic alterations and epigenetic changes that ultimately drive carcinogenesis. These processes lead to a unique molecular profile of every given tumor and to substantial intratumoral heterogeneity of cancer tissues. Recently, a series of independent reports revealed that pre-formed neoantigen specific T-cell responses are of crucial relevance for the clinical efficacy of immune checkpoint inhibitors. However, spontaneous immune recognition of neoantigens seems to be a rare event with only less than 1% of mutations inducing a T-cell response in the tumor-bearing patient. Accordingly, only …

OncologyCancer Researchmedicine.medical_specialtyMutationbusiness.industryImmunogenicityMelanomaCancermedicine.diseasemedicine.disease_causeClinical trialThe Hallmarks of CancerOncologyInternal medicineImmunologymedicineCancer vaccinebusinessCarcinogenesisCancer Research
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Genotyping analysis and 18FDG uptake in breast cancer patients: a preliminary research

2013

Background: Diagnostic imaging plays a relevant role in the care of patients with breast cancer (BC). Positron Emission Tomography (PET) with 18F-fluoro-2-deoxy-D-glucose (FDG) has been widely proven to be a clinical tool suitable for BC detection and staging in which the glucose analog supplies metabolic information about the tumor. A limited number of studies, sometimes controversial, describe possible associations between FDG uptake and single nucleotide polymorphisms (SNPs). For this reason this field has to be explored and clarified. We investigated the association of SNPs in GLUT1, HIF-1a, EPAS1, APEX1, VEGFA and MTHFR genes with the FDG uptake in BC. Methods: In 26 caucasian individu…

OncologyCancer Researchmedicine.medical_specialtyPathologydbSNPGenotypePET-CTSingle-nucleotide polymorphismStandardized uptake valueBreast NeoplasmsGene mutationMultimodal ImagingPolymorphism Single NucleotideBreast cancerBreast cancerFluorodeoxyglucose F18Internal medicinemedicineHumansPET-CTSUVpvcbiologybusiness.industryResearchGlucose analogSUVmaxSingle nucleotide polymorphismsmedicine.diseaseSingle nucleotide polymorphismBreast cancer Single nucleotide polymorphisms PET-CT SUVmax SUVpvcOncologyMethylenetetrahydrofolate reductasePositron-Emission Tomographybiology.proteinFemaleRadiopharmaceuticalsbusinessTomography X-Ray Computed
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Do BARD1 Mutations Confer an Elevated Risk of Prostate Cancer?

2021

Simple Summary Current cancer testing gene panels tend to be comprehensive. One of the genes commonly included in the testing panels is BARD1. To establish whether BARD1 mutations predispose to prostate cancer, we sequenced BARD1 in 390 hereditary prostate cancer cases, genotyped 5715 men with unselected prostate cancer and 10,252 controls for three recurrent rare BARD1 variants in Poland. We did not see an elevated prostate risk cancer given p.Q564X truncating mutation, p.R658C missense mutation and p.R659= synonymous variant. Neither variant influenced prostate cancer characteristics or survival. Our study is the first to evaluate the association between BARD1 mutations and prostate cance…

OncologyCancer Researchmedicine.medical_specialtySusceptibility genemedicine.disease_causesurvivalArticleProstate cancerBreast cancerBARD1; mutation; prostate cancer; risk; survivalInternal medicineBARD1medicineBARD1GeneRC254-282riskProstate cancer riskMutationbusiness.industryCancerNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseprostate cancerOncology<i>BARD1</i>mutationbusinessCancers
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Evaluation of survival across several treatment lines in metastatic colorectal cancer: Analysis of the FIRE-3 trial (AIO KRK0306).

2017

Abstract Background We explored the impacts of sequential application of various treatment lines on survival kinetics. Therefore, differences in overall survival (OS) observed in FIRE-3 were investigated in the context of time and exposure to applied treatment. Patients and methods OS analyses (stratified by treatment with FOLFIRI plus either cetuximab or bevacizumab) were performed according to time intervals as well as using a Cox model to define changes of hazard ratio (HR) over time. Results The fraction of patients with systemic treatment and time on treatment markedly decreases over treatment lines and time. OS evaluation by a Cox model indicated a trend towards a non-proportional haz…

OncologyCancer Researchmedicine.medical_specialtyTime FactorsBevacizumabLeucovorinCetuximabContext (language use)Angiogenesis InhibitorsKaplan-Meier Estimatemedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineRisk FactorsInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineBiomarkers TumorHumans030212 general & internal medicineNeoplasm MetastasisSurvival analysisProportional Hazards ModelsCetuximabProportional hazards modelbusiness.industryHazard ratioIntention to Treat AnalysisBevacizumabTreatment OutcomeOncology030220 oncology & carcinogenesisMutationFOLFIRICamptothecinKRASFluorouracilbusinessColorectal Neoplasmsmedicine.drugEuropean journal of cancer (Oxford, England : 1990)
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LGG-16. PREDICTORS OF OUTCOME IN BRAF-V600E PEDIATRIC GLIOMAS TREATED WITH BRAF INHIBITORS: A REPORT FROM THE PLGG TASKFORCE

2019

The BRAF-V600E mutation is found in 15–20% of pediatric low grade gliomas (PLGG) and result in worse outcome and higher risk of transformation to high grade gliomas (PHGG). Although ongoing trials are assessing the role of BRAF inhibitors (BRAFi) in these children, data are still limited. We aimed to report overall response rates and predictors of outcome in childhood BRAF-V600E gliomas. We collected clinical, imaging and molecular information of patients treated with BRAFi outside trials from centers participating in the PLGG taskforce. Response was calculated by RANO criteria and follow up data were collected for all patients. Sixty-six patients were treated with BRAFi (55 PLGG and 11 PHG…

OncologyCancer Researchmedicine.medical_specialtybusiness.industryLow Grade Gliomamedicine.diseaseChemotherapy regimenBRAF V600EOncologyInternal medicineGliomaMutation (genetic algorithm)MedicineLow-Grade GliomaNeurology (clinical)businessneoplasmsNeuro-Oncology
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Distinct Mutational Profile of Lynch Syndrome Colorectal Cancers Diagnosed under Regular Colonoscopy Surveillance

2021

Regular colonoscopy even with short intervals does not prevent all colorectal cancers (CRC) in Lynch syndrome (LS). In the present study, we asked whether cancers detected under regular colonoscopy surveillance (incident cancers) are phenotypically different from cancers detected at first colonoscopy (prevalent cancers). We analyzed clinical, histological, immunological and mutational characteristics, including panel sequencing and high-throughput coding microsatellite (cMS) analysis, in 28 incident and 67 prevalent LS CRCs (n total = 95). Incident cancers presented with lower UICC and T stage compared to prevalent cancers (p &lt

OncologyColorectal cancerColonoscopybiomarkkeritHEREDITARYGUIDELINESTp53 mutationmedicine.disease_causeMolecular level0302 clinical medicineRISKincident cancercancer preventionmedicine.diagnostic_testRGeneral MedicineTUMORSLynch syndrome3. Good healthsyöpäsolutCARCINOMAS030220 oncology & carcinogenesisMedicineDNA mismatch repair030211 gastroenterology & hepatologyKRAScarcinogenesiskoloskopiamedicine.medical_specialtyDATABASEcolorectal cancersuolistosyövätmikrosatelliititArticle03 medical and health sciencescolonoscopy screeningInternal medicinemutational profilingmedicineLynchin oireyhtymäPathologicalpaksusuolisyöpäCancer preventionmismatch repair deficiencybusiness.industryMicrosatellite instabilitySCREENING INTERVAL3126 Surgery anesthesiology intensive care radiologymedicine.diseasedigestive system diseasesMSH2Lynch syndromeMSH23121 General medicine internal medicine and other clinical medicineT-stageCLINICAL MANAGEMENTmicrosatellite instabilitymutaatiotbusinessJournal of Clinical Medicine
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Prognostic vs predictive molecular biomarkers in colorectal cancer: is KRAS and BRAF wild type status required for anti-EGFR therapy?

2010

An important molecular target for metastatic CRC treatment is the epidermal growth factor receptor (EGFR). Many potential biomarkers predictive of response to anti-EGFR monoclonal antibodies (cetuximab and panitumumab) have been retrospectively evaluated, including EGFR activation markers and EGFR ligands activation markers. With regard to the "negative predictive factors" responsible for primary or intrinsic resistance to anti-EGFR antibodies a lot of data are now available. Among these, KRAS mutations have emerged as a major predictor of resistance to panitumumab or cetuximab in the clinical setting and several studies of patients receiving first and subsequent lines of treatment have sho…

OncologyColorectal cancerSettore MED/06 - Oncologia MedicaCetuximabDrug resistancemedicine.disease_causeEpidermal growth factor receptorEGFR; KRAS; Driver mutations; Monoclonal antibodiesCetuximabbiologyPanitumumabAntibodies MonoclonalGeneral MedicinePrognosisAntibodies Anti-IdiotypicErbB ReceptorsGene Expression Regulation NeoplasticOncologyMonoclonalKRASColorectal Neoplasmsmedicine.drugProto-Oncogene Proteins B-rafmedicine.medical_specialtymedicine.drug_classEGFRMonoclonal antibodyAntibodies Monoclonal HumanizedProto-Oncogene Proteins p21(ras)Predictive Value of TestsInternal medicineProto-Oncogene ProteinsmedicineBiomarkers TumorKRASPanitumumabHumansRadiology Nuclear Medicine and imagingneoplasmsbusiness.industryPTEN PhosphohydrolaseMembrane ProteinsDriver mutationmedicine.diseasedigestive system diseasesDrug Resistance NeoplasmMutationCancer researchbiology.proteinras ProteinsMonoclonal antibodiesbusiness
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