2021
Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach
McFall T, Stites E. Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach. Cell Reports 2021, 37: 110096. PMID: 34910921, PMCID: PMC8867612, DOI: 10.1016/j.celrep.2021.110096.Peer-Reviewed Original ResearchConceptsSensitivity to EGFR inhibitionSubsets of mutationsRas mutationsKRAS G13DCancer cell biologyEGFR inhibitionEpidermal growth factor receptor (EGFR)-targeted therapyTumor suppressor neurofibrominGene-basedBiophysical biomarkersInhibitor sensitivityCell biologyMutationsPersonalized medicineBiomarker strategiesKRAS mutantRasCancer treatmentKRASNF1BiomarkersBiophysical characteristicsG13DMutantsInhibitionCooperation between oncogenic Ras and wild-type p53 stimulates STAT non-cell autonomously to promote tumor radioresistance
Dong YL, Vadla GP, Lu J, Ahmad V, Klein TJ, Liu LF, Glazer PM, Xu T, Chabu CY. Cooperation between oncogenic Ras and wild-type p53 stimulates STAT non-cell autonomously to promote tumor radioresistance. Communications Biology 2021, 4: 374. PMID: 33742110, PMCID: PMC7979758, DOI: 10.1038/s42003-021-01898-5.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsAnimals, Genetically ModifiedCell ProliferationCytokinesDrosophila melanogasterDrosophila ProteinsFemaleGene Expression Regulation, NeoplasticGenes, rasHumansJanus KinasesLung NeoplasmsMaleMice, NudeMice, TransgenicParacrine CommunicationRadiation ToleranceSignal TransductionSTAT Transcription FactorsTumor BurdenTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsTumor microenvironmentTumor radioresistanceRas clonesOncogenic Ras mutationsClinical outcomesRA tissuesCancer patientsJAK/STATRadiation therapyRobust tumorOncogenic RasTherapy outcomeTumor resistanceTumor tissueRas mutationsTumor cellsJAK/OutcomesRadioresistanceCellular responsesTissueCell-cell interactionsPatientsCytokinesRadiotherapy
2019
A systems mechanism for KRAS mutant allele–specific responses to targeted therapy
McFall T, Diedrich J, Mengistu M, Littlechild S, Paskvan K, Sisk-Hackworth L, Moresco J, Shaw A, Stites E. A systems mechanism for KRAS mutant allele–specific responses to targeted therapy. Science Signaling 2019, 12 PMID: 31551296, PMCID: PMC6864030, DOI: 10.1126/scisignal.aaw8288.Peer-Reviewed Original ResearchConceptsEpidermal growth factor receptorWild-type Ras activationColorectal cancerSensitivity to EGFR inhibitionEpidermal growth factor receptor inhibitionKRAS mutantEGFR-independent mannerAllele-specific responsesRas activationGrowth factor receptorTumor suppressor neurofibrominPatient tumorsAntibody cetuximabTargeted therapyMechanisms of EGFR signalingCRC patientsEGFR inhibitionCancer treatment decisionsRas mutationsFactor receptorKRASTherapeutic strategiesTreatment decisionsEGFR SignalingPatients
2017
Role of molecular markers to predict distant metastasis in papillary thyroid carcinoma: Promising value of TERT promoter mutations and insignificant role of BRAF mutations—a meta-analysis
Vuong H, Altibi A, Duong U, Ngo H, Pham T, Tran H, Oishi N, Mochizuki K, Nakazawa T, Hassell L, Katoh R, Kondo T. Role of molecular markers to predict distant metastasis in papillary thyroid carcinoma: Promising value of TERT promoter mutations and insignificant role of BRAF mutations—a meta-analysis. Tumor Biology 2017, 39: 1010428317713913. PMID: 29037127, DOI: 10.1177/1010428317713913.Peer-Reviewed Original ResearchConceptsPapillary thyroid cancerTERT promoter mutationsDistant metastasisThyroid cancerPromoter mutationsRET/PTC rearrangementsBRAF mutationsPresence of distant metastasesAssessment of patient prognosisTumor risk stratificationAssociated with distant metastasisPapillary thyroid carcinomaMeta-analysisPredicting distant metastasisAssociation of BRAFRandom-effects modelThyroid carcinomaTERT promoterRisk stratificationPatient prognosisRas mutationsAdverse outcomesMetastasisIncreased riskBRAF
2016
The changing characteristics and molecular profiles of papillary thyroid carcinoma over time - a systematic review
Vuong H, Altibi A, Abdelhamid A, Ngoc P, Quan V, Tantawi M, Elfil M, Le Huy Vu T, Elgebaly A, Oishi N, Nakazawa T, Hirayama K, Katoh R, Huy N, Kondo T. The changing characteristics and molecular profiles of papillary thyroid carcinoma over time - a systematic review. Oncotarget 2016, 5: 10637-10649. PMID: 27793009, PMCID: PMC5354688, DOI: 10.18632/oncotarget.12885.Peer-Reviewed Original ResearchMeSH KeywordsAdultBiomarkers, TumorCarcinoma, PapillaryChi-Square DistributionFemaleGene RearrangementGenes, rasGenetic Predisposition to DiseaseHumansMaleMiddle AgedMutationPhenotypeProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-retRisk FactorsThyroid Cancer, PapillaryThyroid NeoplasmsTime FactorsTranscriptomeConceptsPapillary thyroid carcinomaMolecular profilingThyroid carcinomaClinicopathological featuresGenetic alterationsRisk factors of thyroid cancerPapillary thyroid carcinoma patientsSystematic reviewSurgical time periodStudent's t-testTumorigenesis of papillary thyroid carcinomaRET/PTC rearrangementsModification of patientsPearson chi-squareTeam of reviewersClinicopathological characteristicsPTC patientsBRAF mutationsThyroid cancerRas mutationsScreened titlesRisk factorsInclusion criteriaElectronic databasesPotential articles
2013
Genotype-Selective Combination Therapies for Melanoma Identified by High-Throughput Drug Screening
Held MA, Langdon CG, Platt JT, Graham-Steed T, Liu Z, Chakraborty A, Bacchiocchi A, Koo A, Haskins JW, Bosenberg MW, Stern DF. Genotype-Selective Combination Therapies for Melanoma Identified by High-Throughput Drug Screening. Cancer Discovery 2013, 3: 52-67. PMID: 23239741, PMCID: PMC3546137, DOI: 10.1158/2159-8290.cd-12-0408.Peer-Reviewed Original ResearchConceptsMutant BRAF melanomaCyclin-dependent kinase inhibitorBRAF melanomaSmall molecule inhibitorsHigh-throughput drug screeningDrug screeningEGF receptorCombination therapyDrug combinationsMelanoma culturesContext of genotypePairwise combinationsResistance phenotypeCombinatorial drug screeningUnique treatment regimensCombination of statinsVivo xenograftsKinase inhibitorsMutant BRAFMutationsEfficacious drug combinationsPartial responseTreatment regimensRas mutationsBRAF mutations
2011
High-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade
Kießling M, Oberholzer PA, Mondal C, Karpova MB, Zipser MC, Lin WM, Girardi M, MacConaill LE, Kehoe SM, Hatton C, French LE, Garraway LA, Polier G, Süss D, Klemke CD, Krammer PH, Gülow K, Dummer R. High-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade. Blood 2011, 117: 2433-2440. PMID: 21209378, PMCID: PMC3952811, DOI: 10.1182/blood-2010-09-305128.Peer-Reviewed Original ResearchMeSH KeywordsBiopsyHigh-Throughput Screening AssaysHumansLymphoma, T-Cell, CutaneousMitogen-Activated Protein Kinase KinasesMutationMycosis FungoidesNeoplasm StagingProtein Kinase InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)raf Kinasesras ProteinsSezary SyndromeSignal TransductionConceptsCutaneous T-cell lymphomaStage IV patientsHUT78 cellsIV patientsPleomorphic cutaneous T-cell lymphomaHigh-throughput mutation profilingMEK inhibitorsCTCL cell line Hut78T-cell lymphomaRAS/RAF/MEKCTCL cell linesOncogenic mutationsCommon oncogenic mutationsCTCL patientsOverall survivalSézary syndromeMycosis fungoidesBiopsy specimensPatients profitPreclinical resultsMEK inhibitor U0126NRAS mutationsLymphoid cellsCTCL samplesRas mutations
2005
RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia
Wiemels JL, Zhang Y, Chang J, Zheng S, Metayer C, Zhang L, Smith MT, Ma X, Selvin S, Buffler PA, Wiencke JK. RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia. Leukemia 2005, 19: 415-419. PMID: 15674422, DOI: 10.1038/sj.leu.2403641.Peer-Reviewed Original ResearchConceptsRas mutationsMaternal ageLeukemia casesPediatric acute lymphoblastic leukemiaAcute lymphoblastic leukemia casesDiagnostic bone marrow samplesIncident leukemia casesPaternal preconception smokingNorthern California Childhood Leukemia StudyAcute lymphoblastic leukemiaLymphoblastic leukemia casesBone marrow samplesKRAS codon 12California Childhood Leukemia StudyRAS gene mutationsChildhood Leukemia StudyEtiology of subtypesPreconception smokingCase seriesLymphoblastic leukemiaLeukemia patientsMultivariable modelMarrow samplesHigh hyperdiploidyChildhood leukemia
2003
ras mutations are associated with aggressive tumor phenotypes and poor prognosis in thyroid cancer.
Garcia-Rostan G, Zhao H, Camp RL, Pollan M, Herrero A, Pardo J, Wu R, Carcangiu ML, Costa J, Tallini G. ras mutations are associated with aggressive tumor phenotypes and poor prognosis in thyroid cancer. Journal Of Clinical Oncology 2003, 21: 3226-35. PMID: 12947056, DOI: 10.1200/jco.2003.10.130.Peer-Reviewed Original ResearchConceptsThyroid carcinomaResult of diseasePoor prognosisRas mutationsTumor differentiationK-ras codon 13 mutationDifferentiated thyroid carcinomaCodon 13 mutationsAggressive cancer behaviorAggressive tumor phenotypeFollicular cell derivationN-RAS mutationsClinicopathologic featuresIndependent predictorsUndifferentiated carcinomaThyroid cancerPoor survivalUndifferentiated tumorsPatientsCarcinomaActivating mutationsCancer behaviorSignificant associationTumorsRas tumors
1999
Ras mutations are uncommon in sporadic thyroid cancer in children and young adults
Fenton C, Anderson J, Lukes Y, Dinauer C, Tuttle RM, Francis GL. Ras mutations are uncommon in sporadic thyroid cancer in children and young adults. Journal Of Endocrinological Investigation 1999, 22: 781-789. PMID: 10614528, DOI: 10.1007/bf03343644.Peer-Reviewed Original ResearchConceptsMedullary thyroid cancerFollicular thyroid cancerChildhood thyroid cancerThyroid cancerPrevious radiation exposureRas mutationsRadiation exposureCodon 12Aggressive papillary thyroid cancerAdult thyroid cancerClass II diseaseSporadic thyroid cancerPapillary thyroid cancerArchival tissue blocksLung metastasesCancer 4Number of subjectsPatientsCancerLymphomaYoung adultsTissue blocksHuman cancersChildrenPrevious reports
1993
Prognostic significance of K-ras mutations in colorectal carcinoma
Benhattar J, Losi L, Chaubert P, Givel J, Costa J. Prognostic significance of K-ras mutations in colorectal carcinoma. Gastroenterology 1993, 104: 1044-1048. PMID: 8462792, DOI: 10.1016/0016-5085(93)90272-e.Peer-Reviewed Original ResearchConceptsK-ras mutationsPrognostic significanceColorectal carcinomaK-ras geneRecurrent diseaseCodon 12Good prognostic factorAdvanced colorectal carcinomaPossible prognostic significanceHuman colorectal carcinomaPolymerase chain reaction-based techniquesDukes' BPrognostic factorsColorectal cancerPrimary tumorOverall prevalenceHigh riskPatientsRas mutationsCarcinomaHuman tumorsTumorsDiseasePrevalenceGGT
1992
Stability of K-ras mutations throughout the natural history of human colorectal cancer
Losi L, Benhattar J, Costa J. Stability of K-ras mutations throughout the natural history of human colorectal cancer. European Journal Of Cancer 1992, 28: 1115-1120. PMID: 1627381, DOI: 10.1016/0959-8049(92)90468-h.Peer-Reviewed Original ResearchConceptsK-ras mutationsPrimary tumorRas mutationsNatural historyColorectal cancerTumor markersStable tumor markerHuman colorectal cancerDistant recurrenceRecurrent cancerRecurrent tumorsPolymerase chain reactionColorectal carcinomaCodon 12TumorsArchival tissueCancerChain reactionAllele-specific amplificationPatientsRecurrenceMarkersMutationsCarcinomaDisease
1990
Quantitation of the ras gene product in leukemic blast cells using enzymatic staining.
Gutheil J, Mane S, Bass K, Lee E, Needleman S. Quantitation of the ras gene product in leukemic blast cells using enzymatic staining. BioTechniques 1990, 9: 212-7. PMID: 2205250.Peer-Reviewed Original ResearchConceptsRas gene productGene productsRas speciesRas protein levelsProtein of interestGene product levelsQuantitation of proteinsSpecific ras mutationsUse of electrophoresisProtein levelsRas mutationsProteinP21 expressionHuman malignanciesSpeciesCellsLeukemic cellsMutationsEnzymatic stainingHigh specificityRadioactive reagentsExpressionElectrophoresisAssaysVivoRAS gene activation in acute myelogenous leukemia: Analysis by in vitro amplification and dna base sequence determination
Mane S, Meltzer S, Gutheil J, Kapil V, Lee E, Needleman S. RAS gene activation in acute myelogenous leukemia: Analysis by in vitro amplification and dna base sequence determination. Genes Chromosomes And Cancer 1990, 2: 71-77. PMID: 2278967, DOI: 10.1002/gcc.2870020113.Peer-Reviewed Original ResearchMeSH KeywordsBase SequenceCohort StudiesDNA Mutational AnalysisDNA, NeoplasmExonsGene Expression Regulation, NeoplasticGenes, rasHumansIatrogenic DiseaseLeukemia, Myeloid, AcuteMolecular Sequence DataPolymerase Chain ReactionProspective StudiesProto-Oncogene Proteins p21(ras)Transcriptional ActivationConceptsAcute myeloid leukemia patientsMaryland Cancer CenterMyeloid leukemia patientsAcute myelogenous leukemiaRAS gene activationProspective cohortCancer CenterLeukemia patientsPrecise prevalenceMyelogenous leukemiaNRAS mutationsRas activationRas mutationsGene point mutationsBiologic parametersLarger studyHuman cancersPatientsAMLProtooncogene activationExon mutationsActivationCell DNAMutationsPoint mutations
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