1990
Activation of c-Ki-ras in human gastrointestinal dysplasias determined by direct sequencing of polymerase chain reaction products.
Meltzer S, Mane S, Wood P, Resau J, Newkirk C, Terzakis J, Korelitz B, Weinstein W, Needleman S. Activation of c-Ki-ras in human gastrointestinal dysplasias determined by direct sequencing of polymerase chain reaction products. Cancer Research 1990, 50: 3627-30. PMID: 2187599.Peer-Reviewed Original ResearchConceptsC-Ki-rasUlcerative colitisBarrett's esophagusChain reaction productsPolymerase chain reaction productsSporadic colon cancerGastrointestinal lesionsPolymerase chain reactionEsophageal adenocarcinomaColonic specimensCodon 13Direct dideoxy sequencingColon cancerUncommon eventMalignant progressionCodon 12C-Ha-rasEsophagusPoint mutationsDysplasiaDisease statesChain reactionColitisDirect sequencingCancerRAS 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 mutationsHypereosinophilic syndrome with evolution to myeloproliferative disorder: temporal relationship to loss of Y chromosome and c-N-ras activation.
Needleman S, Mane S, Gutheil J, Kapil V, Heyman M, Testa J. Hypereosinophilic syndrome with evolution to myeloproliferative disorder: temporal relationship to loss of Y chromosome and c-N-ras activation. Hematopathology And Molecular Hematology 1990, 4: 149-55. PMID: 2258361.Peer-Reviewed Original ResearchMeSH KeywordsAdultBase SequenceDNA, NeoplasmDNA, Single-StrandedEosinophiliaGene Expression Regulation, NeoplasticGenes, rasHumansKaryotypingLeukemia, MyeloidLongitudinal StudiesMaleMolecular Sequence DataMyeloproliferative DisordersPolymerase Chain ReactionSex Chromosome AberrationsSyndromeTime FactorsY ChromosomeConceptsChronic myeloid leukemicY chromosome lossN-ras activationSubstitution of glycineRas activationChromosome lossY chromosomeMyeloid differentiationCodon 12 GGenetic lesionsTransversion mutationsC transversion mutationsMarrow failureMolecular biologic analysesBiologic analysisActivationChromosomesMyeloproliferative syndrome
1989
c-myc amplification coexistent with activating N-ras point mutation in the biphenotypic leukemic cell line RED-3.
Mallet M, Mane S, Meltzer S, Needleman S. c-myc amplification coexistent with activating N-ras point mutation in the biphenotypic leukemic cell line RED-3. Leukemia 1989, 3: 511-5. PMID: 2659902.Peer-Reviewed Original ResearchConceptsCell linesMYC activationAcute myelogenous leukemiaN-ras point mutationsActivating point mutationC-MycN-rasAML patientsAcute leukemiaHL-60AML cellsMyelogenous leukemiaAggressive acute leukemiasLineage infidelityHuman tumorsDerivative cell linesPoint mutationsPatientsLeukemiaActivationSmall proportionCellsRed 3Protooncogene cMalignancy