Search results for "suolistosyövät"

showing 10 items of 28 documents

Lack of association between screening interval and cancer stage in Lynch syndrome may be accounted for by over-diagnosis; a prospective Lynch syndrom…

2019

Background Recent epidemiological evidence shows that colorectal cancer (CRC) continues to occur in carriers of pathogenic mismatch repair (path_MMR) variants despite frequent colonoscopy surveillance in expert centres. This observation conflicts with the paradigm that removal of all visible polyps should prevent the vast majority of CRC in path_MMR carriers, provided the screening interval is sufficiently short and colonoscopic practice is optimal. Methods To inform the debate, we examined, in the Prospective Lynch Syndrome Database (PLSD), whether the time since last colonoscopy was associated with the pathological stage at which CRC was diagnosed during prospective surveillance. Path_MMR…

0301 basic medicineCOLONOSCOPIC SURVEILLANCEColorectal cancerColonoscopy030105 genetics & hereditycomputer.software_genreFAMILIESCOLORECTAL-CANCERBreast cancer screening0302 clinical medicine610 Medical sciences MedicineEpidemiologytähystysStage (cooking)Hereditary nonpolyposis colorectal cancerMUTATIONGenetics (clinical)RISKSurveillanceDatabasemedicine.diagnostic_testIncidence (epidemiology)Colonoscopylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensLynch syndrome3. Good healthOncology030220 oncology & carcinogenesisendoskopiaScreeningsyöpätauditkoloskopiamedicine.medical_specialtylcsh:QH426-4703122 Cancers610suolistosyövätmikrosatelliititlcsh:RC254-282Mismatch repair03 medical and health sciencesCàncer colorectalmedicineEndoscòpiaLynchin oireyhtymäperinnölliset tauditseulontatutkimusbusiness.industryResearchColonoscòpiaMicrosatellite instabilityEndoscopyDNAdiagnostiikkamedicine.diseaseColorectal cancerdigestive system diseasesHereditary cancerADENOMAlcsh:GeneticsLynch syndromeOver-diagnosisMicrosatellite instabilitytarkkailubusinesscomputer
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Molecular Basis of Mismatch Repair Protein Deficiency in Tumors from Lynch Suspected Cases with Negative Germline Test Results

2020

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0301 basic medicineCancer Researchcongenital hereditary and neonatal diseases and abnormalitiesCARCINOMADNA mismatch repair3122 Cancerscolorectal cancersuolistosyövätBiologyGene mutationMLH1DIAGNOSISlcsh:RC254-282Article03 medical and health sciencesdeep sequencing0302 clinical medicineGermline mutationFREQUENT CAUSEMANAGEMENTLynchin oireyhtymäneoplasmspaksusuolisyöpäMUTATIONSPoint mutationMLH1METHYLATIONnutritional and metabolic diseasesNONPOLYPOSIS COLORECTAL-CANCERDEFECTSdiagnostiikkalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensdigestive system diseases3. Good healthDNA-metylaatioMSH2MSH6030104 developmental biologyLynch syndromeOncologyMSH3syöpägeenitMSH2030220 oncology & carcinogenesisCancer researchDNA mismatch repairsyöpätauditCancers
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Genetic and Epigenetic Characteristics of Inflammatory Bowel Disease-Associated Colorectal Cancer.

2021

doi: 10.1053/j.gastro.2021.04.042 Background & Aims Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disorder associated with an elevated risk of colorectal cancer (CRC). IBD-associated CRC (IBD-CRC) may represent a distinct pathway of tumorigenesis compared to sporadic CRC (sCRC). Our aim was to comprehensively characterize IBD-associated tumorigenesis integrating multiple high-throughput approaches, and to compare the results with in-house data sets from sCRCs. Methods Whole-genome sequencing, single nucleotide polymorphism arrays, RNA sequencing, genome-wide methylation analysis, and immunohistochemistry were performed using fresh-frozen and formalin-fixed tissue sam…

0301 basic medicineEpigenomicsMaleColorectal cancerDNA Mutational AnalysisPHENOTYPEmedicine.disease_causeEpigenesis GeneticPATHWAY0302 clinical medicineMUTATIONAL PROCESSESDRIVERSTumor MicroenvironmentFinlandOligonucleotide Array Sequence AnalysisAged 80 and overDNA methylationMETHYLATIONGastroenterologyWnt signaling pathwaytulehdukselliset suolistosairaudetHigh-Throughput Nucleotide SequencingMiddle AgedDNA-metylaatio3. Good healthCell Transformation NeoplasticepigenetiikkaDNA methylationCONSENSUS MOLECULAR SUBTYPES030211 gastroenterology & hepatologyFemaleconsensus molecular subtypeKRASgeneettiset tekijätAdultEpithelial-Mesenchymal TransitionINTESTINAL INFLAMMATIONConsensus Molecular Subtype3122 Cancersepithelial-mesenchymal transitioncolorectal cancersuolistosyövätBiology3121 Internal medicinePolymorphism Single Nucleotide03 medical and health sciencesinflammatory bowel diseaseCOLONAXIN2medicineBiomarkers TumorHumansEpithelial–mesenchymal transitionEpigeneticsneoplasmsSIGNATURESAgedNeoplasm StagingColorectal CancerHepatologyWhole Genome SequencingSequence Analysis RNAGene Expression ProfilingInflammatory Bowel DiseaseDNA Methylationmedicine.diseaseInflammatory Bowel DiseasesEVOLUTIONdigestive system diseases030104 developmental biologyMutationCancer research3111 BiomedicineColitis-Associated NeoplasmsNeoplasm GradingCarcinogenesisTranscriptomeGastroenterology
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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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Retrotransposon insertions can initiate colorectal cancer and are associated with poor survival

2019

Genomic instability pathways in colorectal cancer (CRC) have been extensively studied, but the role of retrotransposition in colorectal carcinogenesis remains poorly understood. Although retrotransposons are usually repressed, they become active in several human cancers, in particular those of the gastrointestinal tract. Here we characterize retrotransposon insertions in 202 colorectal tumor whole genomes and investigate their associations with molecular and clinical characteristics. We find highly variable retrotransposon activity among tumors and identify recurrent insertions in 15 known cancer genes. In approximately 1% of the cases we identify insertions in APC, likely to be tumor-initi…

0301 basic medicineMaleGenome instabilityMICROSATELLITE INSTABILITYHYPOMETHYLATIONCarcinogenesisColorectal cancergenetic processestransposonitGeneral Physics and AstronomyRetrotransposon02 engineering and technologyKaplan-Meier EstimateGenome0302 clinical medicineCancer genomicslcsh:ScienceGenetics0303 health sciencesGastrointestinal tractMultidisciplinaryQISLAND METHYLATOR PHENOTYPEGastroenterologyfood and beveragesgenomiikkaMiddle Aged021001 nanoscience & nanotechnology3. Good healthGene Expression Regulation NeoplasticCpG sitesyöpägeenit030220 oncology & carcinogenesisDNA methylationAllelic ImbalanceWHOLE-GENOMEFemaleSVA ELEMENTS0210 nano-technologyColorectal NeoplasmsScience3122 Cancersinformation scienceGenomicssuolistosyövätBiologyGeneral Biochemistry Genetics and Molecular BiologyArticleGenomic Instability03 medical and health sciencesCell Line TumormedicineHumansAged030304 developmental biologySOMATIC L1 RETROTRANSPOSITIONCpG Island Methylator PhenotypeGene Expression ProfilingfungiMicrosatellite instabilityGeneral ChemistryDNA Methylationmedicine.diseaseGENEMutagenesis Insertional030104 developmental biologyLong Interspersed Nucleotide ElementsCPGhealth occupationsCancer researchlcsh:QCpG Islands3111 BiomedicineCaco-2 Cells
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DNA methylation changes and somatic mutations as tumorigenic events in Lynch syndrome-associated adenomas retaining mismatch repair protein expression

2018

Background: DNA mismatch repair (MMR) defects are a major factor in colorectal tumorigenesis in Lynch syndrome (LS) and 15% of sporadic cases. Some adenomas from carriers of inherited MMR gene mutations have intact MMR protein expression implying other mechanisms accelerating tumorigenesis. We determined roles of DNA methylation changes and somatic mutations in cancer-associated genes as tumorigenic events in LS-associated colorectal adenomas with intact MMR. Methods: We investigated 122 archival colorectal specimens of normal mucosae, adenomas and carcinomas from 57 LS patients. MMR-deficient (MMR-D, n 49) and MMR-proficient (MMR-P, n 18) adenomas were of particular interest and were inter…

0301 basic medicineMaleResearch paperMICROSATELLITE INSTABILITYHYPOMETHYLATIONDNA mismatch repairPHENOTYPEmedicine.disease_causeEpigenesis Genetic0302 clinical medicineCOLORECTAL ADENOMASCDKN2APromoter Regions Geneticcolorectal adenomaDNA methylationLINE-1 methylationTumor suppressorGeneral MedicineMethylationMiddle AgedCANCERTUMORSLynch syndromeDNA-metylaatio3. Good healthDEFICIENCY030220 oncology & carcinogenesisDNA methylationsyöpätauditFemaleColorectal adenomaAdultcongenital hereditary and neonatal diseases and abnormalitiesAdenomatumor suppressorsuolistosyövätColorectal adenomaBiologycomplex mixturesGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesBRAF MUTATIONmedicineHumansLynchin oireyhtymäAgedTumor Suppressor ProteinsMicrosatellite instabilityDNAUNE-1 methylationta3122medicine.diseaseGENEColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasestumorigenesisCOPY NUMBER030104 developmental biologyLynch syndromeLong Interspersed Nucleotide Elements3121 General medicine internal medicine and other clinical medicineMutationTumorigenesisCancer research3111 BiomedicineTumotigenesismutationCarcinogenesisEBioMedicine
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The shared frameshift mutation landscape of microsatellite-unstable cancers suggests immunoediting during tumor evolution

2020

The immune system can recognize and attack cancer cells, especially those with a high load of mutation-induced neoantigens. Such neoantigens are abundant in DNA mismatch repair (MMR)-deficient, microsatellite-unstable (MSI) cancers. MMR deficiency leads to insertion/deletion (indel) mutations at coding microsatellites (cMS) and to neoantigen-inducing translational frameshifts. Here, we develop a tool to quantify frameshift mutations in MSI colorectal and endometrial cancer. Our results show that frameshift mutation frequency is negatively correlated to the predicted immunogenicity of the resulting peptides, suggesting counterselection of cell clones with highly immunogenic frameshift peptid…

0301 basic medicineMutation rateGeneral Physics and Astronomymedicine.disease_causeCOLORECTAL-CANCER0302 clinical medicineINDEL MutationMutation RateimmunologiaHLA AntigensNeoplasmsFrameshift Mutationlcsh:ScienceImmunologic SurveillanceGeneticsMutationMultidisciplinaryMISMATCH REPAIR DEFICIENCYQPEPTIDES3. Good healthkohdunrungon syöpäsyöpäsolutimmuunivaste030220 oncology & carcinogenesisTumour immunologyMicrosatellite InstabilityDNA mismatch repairINDEL MutationEXPRESSIONcongenital hereditary and neonatal diseases and abnormalitieskasvaimetDATABASESciencegastrointestinal cancerINSTABILITY3122 CancerssuolistosyövätBiologycomplex mixturesArticleGeneral Biochemistry Genetics and Molecular BiologyFrameshift mutationGastrointestinal cancer03 medical and health sciencesAntigens NeoplasmCOLONmedicineHumansCELLSelection GeneticIndelSIGNATUREStumour immunologyMicrosatellite instabilityGeneral ChemistryDNAmedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseases030104 developmental biologyImmunoeditinglcsh:Qmutaatiotbeta 2-MicroglobulinMicrosatellite Repeats
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Prognostic Value of Immune Environment Analysis in Small Bowel Adenocarcinomas with Verified Mutational Landscape and Predisposing Conditions

2020

Background: Small bowel adenocarcinoma (SBA) is a rare yet insidious cancer with poor survival. The abundance of tumour-infiltrating lymphocytes is associated with improved survival, but the role of the programmed death-1/programmed death ligand-1 (PD-1/PD-L1) pathway in tumour escape is controversial. We evaluated immune cell infiltration, PD1/PD-L1 expression and their prognostic value in a series of SBAs with previously verified predisposing conditions and exome-wide somatic mutation characterization. Methods: Formalin-fixed paraffin-embedded tissue sections stained for CD3, CD8, PD-L1 and PD-1 were analysed from 94 SBAs. An immune cell score (ICS) was formed from the amount of the CD3 a…

0301 basic medicineOncologyPD-L1Cancer Researchmedicine.medical_specialtyadenokarsinoomabiomarkkeritsuolistosyövätlcsh:RC254-282ArticlePathogenesis03 medical and health sciencestumour infiltrating lymphocytesohjelmoitunut solukuolema0302 clinical medicineGermline mutationImmune systemPD-L1Internal medicinesmall bowelPD-1medicineStage (cooking)adenocarcinomabiologybusiness.industryCancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease3. Good health030104 developmental biologyOncologyimmuunijärjestelmä030220 oncology & carcinogenesisbiology.proteinAdenocarcinomaohutsuolisyöpätauditproteiinitlymfosyytitbusinessCD8
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WNT2 activation through proximal germline deletion predisposes to small intestinal neuroendocrine tumors and intestinal adenocarcinomas

2021

Abstract Many hereditary cancer syndromes are associated with an increased risk of small and large intestinal adenocarcinomas. However, conditions bearing a high risk to both adenocarcinomas and neuroendocrine tumors are yet to be described. We studied a family with 16 individuals in four generations affected by a wide spectrum of intestinal tumors, including hyperplastic polyps, adenomas, small intestinal neuroendocrine tumors, and colorectal and small intestinal adenocarcinomas. To assess the genetic susceptibility and understand the novel phenotype, we utilized multiple molecular methods, including whole genome sequencing, RNA sequencing, single cell sequencing, RNA in situ hybridization…

AdenomaAcademicSubjects/SCI01140DOMAINSadenokarsinoomaCANCER-RISKIn situ hybridizationsuolistosyövätAdenocarcinomaBiologyNeuroendocrine tumorsGermlineWnt2 Proteinperinnöllinen alttius03 medical and health sciences0302 clinical medicineWNT2GeneticsGenetic predispositionmedicineHumansIntestinal MucosaMUTATIONMolecular BiologyGenetics (clinical)030304 developmental biologypaksusuolisyöpäCARCINOID-TUMORS0303 health sciencesperinnölliset tauditCYSTIC-FIBROSISGeneral MedicineNATIONWIDEmedicine.diseaseIntestinal epithelium3. Good healthGENOMENeuroendocrine TumorsHyperplastic PolypSingle cell sequencing3121 General medicine internal medicine and other clinical medicine030220 oncology & carcinogenesisMAPCancer researchsyöpätaudit3111 BiomedicineGeneral Articlegeneettiset tekijätColorectal Neoplasms
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The “unnatural” history of colorectal cancer in Lynch syndrome : lessons from colonoscopy surveillance

2021

Individuals with Lynch syndrome (LS), one of the most common inherited cancer syndromes, are at increased risk of developing malignancies, in particular colorectal cancer (CRC). Regular colonoscopy with polypectomy is recommended to reduce CRC risk in LS individuals. However, recent independent studies demonstrated that a substantial proportion of LS individuals develop CRC despite regular colonoscopy. The reasons for this surprising observation confirmed by large prospective studies are a matter of debate. In this review, we collect existing evidence from clinical, epidemiological and molecular studies and interpret them with regard to the origins and progression of LS-associated CRC. Alon…

Cancer ResearchColorectal cancermedicine.medical_treatmentColonoscopyDNA Mismatch RepairADENOMA DETECTION0302 clinical medicineRisk FactorsEpidemiologyMass ScreeningProspective cohort studyMUTATIONRISKmedicine.diagnostic_testincident cancer riskColonoscopyTUMORSLynch syndrome3. Good healthOncology030220 oncology & carcinogenesisPopulation SurveillancesyöpätauditColorectal Neoplasmskoloskopiamedicine.medical_specialtyLONG-TERM3122 Cancerscolorectal cancersuolistosyövätINTERVAL CANCERS03 medical and health sciencesINTESTINAL MICROBIOTACàncer colorectalCOLONmedicineMANAGEMENTHumansLynchin oireyhtymäIntensive care medicinepaksusuolisyöpäperinnölliset tauditseulontatutkimusbusiness.industrymismatch repair deficiencyMicrosatellite instabilityCancerColonoscòpiamedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisPolypectomydigestive system diseasesDNA Repair EnzymesLynch syndromemicrosatellite instabilitybusinesscolonoscopy surveillance
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