2021
Molecular drivers of tumor progression in microsatellite stable APC mutation-negative colorectal cancers
Grant A, Xicola RM, Nguyen V, Lim J, Thorne C, Salhia B, Llor X, Ellis N, Padi M. Molecular drivers of tumor progression in microsatellite stable APC mutation-negative colorectal cancers. Scientific Reports 2021, 11: 23507. PMID: 34873211, PMCID: PMC8648784, DOI: 10.1038/s41598-021-02806-x.Peer-Reviewed Original ResearchMeSH KeywordsAdenomatous Polyposis ColiAdenomatous Polyposis Coli ProteinColorectal NeoplasmsDisease ProgressionDNA Copy Number VariationsDNA MethylationGenes, APCHumansMicrosatellite InstabilityMicrosatellite RepeatsMutationNeoplastic ProcessesPhenotypePromoter Regions, GeneticWnt Signaling PathwayConceptsAdenomatous polyposis coliMitochondrial activationDNA methylation profilesTumor suppressor gene adenomatous polyposis coliRNA expressionExpression of Axin2Cancer Genome AtlasIntracellular WntMethylation profilesAberrant regulationGene fusionsGenetic inactivationExtracellular WntNumber variationsGenome AtlasPolyposis coliSomatic mutationsAPC mutationsMutationsMolecular driversMutations of BRAFWntRSPO3Tumor progressionExpressionPATH-38. APC MUTATION AS A DRIVER ONCOGENE IN NON-CTNNB1 MUTANT ADAMANTINOMATOUS CRANIOPHARYNGIOMAS
Hong C, Erson-Omay Z, Omay S. PATH-38. APC MUTATION AS A DRIVER ONCOGENE IN NON-CTNNB1 MUTANT ADAMANTINOMATOUS CRANIOPHARYNGIOMAS. Neuro-Oncology 2021, 23: vi123-vi123. PMCID: PMC8598823, DOI: 10.1093/neuonc/noab196.490.Peer-Reviewed Original ResearchAdamantinomatous craniopharyngiomaInstitutional review board-approved protocolCTNNB1 mutationsFamilial adenomatous polyposisWhole-exome sequencingAPC mutationsNeurological deficitsVentricular involvementOptic apparatusClassic subtypeStop codon mutationMalignant tumorsThird ventricleBRAF inhibitorsCraniopharyngeal ductDriver oncogenesTherapeutic strategiesMAP kinase/ERKCraniopharyngiomaGermline APC mutationsPapillary craniopharyngiomasPituitary glandAdenomatous polyposisPathogenic variantsEmbryonic remnants
2019
APC mutational patterns in gastric adenocarcinoma are enriched for missense variants with associated decreased survival
Rubinstein JC, Khan SA, Christison‐Lagay E, Cha C. APC mutational patterns in gastric adenocarcinoma are enriched for missense variants with associated decreased survival. Genes Chromosomes And Cancer 2019, 59: 64-68. PMID: 31353684, DOI: 10.1002/gcc.22792.Peer-Reviewed Original ResearchGenomic Data CommonsSingle nucleotide variantsAPC mutationsMutational patternsMissense mutationsSpecific APC mutationsMissense variantsRecurrent somatic eventsProtein dysfunctionAdenomatous polyposis coli (APC) mutationsNucleotide variantsSpecific mutational patternsSomatic eventsMutationsNumerous tumor typesResultant clinical manifestationsDifferent mutationsFuture risk stratification strategiesFamilial adenomatous polyposisData CommonsVariantsColon adenocarcinomaColon cancerGenesColon tumors
1997
Familial colorectal cancer in Ashkenazim due to a hypermutable tract in APC
Laken S, Petersen G, Gruber S, Oddoux C, Ostrer H, Giardiello F, Hamilton S, Hampel H, Markowitz A, Klimstra D, Jhanwar S, Winawer S, Offit K, Luce M, Kinzler K, Vogelstein B. Familial colorectal cancer in Ashkenazim due to a hypermutable tract in APC. Nature Genetics 1997, 17: 79-83. PMID: 9288102, DOI: 10.1038/ng0997-79.Peer-Reviewed Original ResearchConceptsHereditary non-polyposis colorectal cancerFamilial adenomatous polyposisNon-polyposis colorectal cancerDefective mismatch repair genesFamilial colorectal cancerColorectal cancerMismatch repair genesAdenomatous polyposisFamily historyTruncating APC mutationsAshkenazi JewsI cancerCancer predispositionAPC mutationsRepair genesUnited StatesAshkenazimCancerFamilial casesAshkenaziPolyposisEncode proteinsHypermutable regionFamilyGenes
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