2022
Mutational signature profiling classifies subtypes of clinically different mismatch-repair-deficient tumours with a differential immunogenic response potential
Giner-Calabuig M, De Leon S, Wang J, Fehlmann TD, Ukaegbu C, Gibson J, Alustiza-Fernandez M, Pico MD, Alenda C, Herraiz M, Carrillo-Palau M, Salces I, Reyes J, Ortega SP, Obrador-Hevia A, Cecchini M, Syngal S, Stoffel E, Ellis NA, Sweasy J, Jover R, Llor X, Xicola RM. Mutational signature profiling classifies subtypes of clinically different mismatch-repair-deficient tumours with a differential immunogenic response potential. British Journal Of Cancer 2022, 126: 1595-1603. PMID: 35197584, PMCID: PMC9130322, DOI: 10.1038/s41416-022-01754-1.Peer-Reviewed Original ResearchConceptsLynch-like syndromeMMR-deficient tumorsLynch syndromeMicrosatellite instabilityPercent of tumorsMSH2/MSH6 expressionColorectal cancer tumorsPMS2 protein expressionMutational signaturesResultsFifty-three percentClinical managementNeoantigen presentationMSH6 expressionHallmark of tumorsTumor behaviorMMR deficiencyClinical phenotypeDeficient tumorsTumorsSporadic tumorsCancer tumorsMutational profileProtein expressionRepair deficiencySyndrome
2021
Yale Cancer Center Precision Medicine Tumor Board: molecular findings alter a diagnosis and treatment plan
Gibson JA, Finberg KE, Nalbantoglu I, Cecchini M, Ganzak A, Walther Z, Sklar JL, Eder JP, Goldberg SB. Yale Cancer Center Precision Medicine Tumor Board: molecular findings alter a diagnosis and treatment plan. The Lancet Oncology 2021, 22: 306-307. PMID: 33662283, DOI: 10.1016/s1470-2045(20)30683-5.Peer-Reviewed Original Research
2012
BRAF V600E mutation in papillary thyroid microcarcinoma: a genotype–phenotype correlation
Virk RK, Van Dyke AL, Finkelstein A, Prasad A, Gibson J, Hui P, Theoharis CG, Carling T, Roman SA, Sosa JA, Udelsman R, Prasad ML. BRAF V600E mutation in papillary thyroid microcarcinoma: a genotype–phenotype correlation. Modern Pathology 2012, 26: 62-70. PMID: 22918165, DOI: 10.1038/modpathol.2012.152.Peer-Reviewed Original ResearchConceptsPapillary thyroid microcarcinomaThyroid microcarcinomaPapillary thyroid carcinomaFollicular variantThyroid carcinomaLateral cervical node metastasesOsteoclastic-type giant cellsCervical node metastasisInfiltrative tumor borderGroup of tumorsBRAF V600E mutationClassic nuclear featuresGenotype-phenotype correlationStromal calcificationLymphovascular invasionNode metastasisClinicopathologic featuresLymphocytic infiltrationAggressive featuresTumor sizeCystic changesPapillary microcarcinomaAbsence of mutationsHigh prevalenceMicrocarcinoma
2001
A Conserved α-Helical Motif Mediates the Interaction of Sp1-Like Transcriptional Repressors with the Corepressor mSin3A
Zhang J, Moncrieffe M, Kaczynski J, Ellenrieder V, Prendergast F, Urrutia R. A Conserved α-Helical Motif Mediates the Interaction of Sp1-Like Transcriptional Repressors with the Corepressor mSin3A. Molecular And Cellular Biology 2001, 21: 5041-5049. PMID: 11438660, PMCID: PMC87230, DOI: 10.1128/mcb.21.15.5041-5049.2001.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid MotifsAmino Acid SequenceAnimalsApoptosis Regulatory ProteinsBlotting, WesternCell Cycle ProteinsCell DivisionCHO CellsCircular DichroismCricetinaeGenetic VectorsGlutathione TransferaseLuciferasesMolecular Sequence DataMutationPeptide BiosynthesisPlasmidsPrecipitin TestsProtein BindingProtein BiosynthesisProtein Structure, TertiaryRecombinant Fusion ProteinsRepressor ProteinsSequence Homology, Amino AcidSin3 Histone Deacetylase and Corepressor ComplexSp1 Transcription FactorTranscription, GeneticTransforming Growth Factor betaZinc FingersConceptsSp1-like proteinsRepress transcriptionDeacetylase complexRepression motifTranscriptional repressionSin3 histone deacetylase complexBind GC-rich sequencesMechanism of transcriptional repressionSp1-like transcription factorsMSin3A-histone deacetylase complexGC-rich sequencesMammalian cell homeostasisCorepressor mSin3ARepression domainTranscriptional repressorA-helicesMSin3ATranscription factorsTIEG2Antiproliferative functionCell homeostasisMotifTranscriptionRepressionProtein