2022
Significance of KRAS mutation testing in biliary brushing cytology specimens: A 10‐year retrospective review
Sun T, Zuo T, Hui P, Cai G. Significance of KRAS mutation testing in biliary brushing cytology specimens: A 10‐year retrospective review. Cancer Cytopathology 2022, 130: 558-565. PMID: 35417072, DOI: 10.1002/cncy.22579.Peer-Reviewed Original ResearchConceptsExtrahepatic biliary stenosisKRAS mutation testingKRAS mutational analysisKRAS mutationsBiliary stenosisBiliary ductsInstitutional review board approvalResults of cytologyPancreatic duct adenocarcinomaBiliary brushing cytologyReview board approvalCytological diagnostic categoriesRetrospective reviewBiliary stricturesDuct adenocarcinomaAbsolute riskCytology examinationDuct brushingsBiliary brushingsBrushing cytologyMalignant conditionsCytological diagnosisBoard approvalClinical practiceCytology specimens
2019
EGFR mutation subtypes and response to immune checkpoint blockade treatment in non-small-cell lung cancer
Hastings K, Yu HA, Wei W, Sanchez-Vega F, DeVeaux M, Choi J, Rizvi H, Lisberg A, Truini A, Lydon CA, Liu Z, Henick BS, Wurtz A, Cai G, Plodkowski AJ, Long NM, Halpenny DF, Killam J, Oliva I, Schultz N, Riely GJ, Arcila ME, Ladanyi M, Zelterman D, Herbst RS, Goldberg SB, Awad MM, Garon EB, Gettinger S, Hellmann MD, Politi K. EGFR mutation subtypes and response to immune checkpoint blockade treatment in non-small-cell lung cancer. Annals Of Oncology 2019, 30: 1311-1320. PMID: 31086949, PMCID: PMC6683857, DOI: 10.1093/annonc/mdz141.Peer-Reviewed Original ResearchMeSH KeywordsAgedAllelesAntineoplastic Agents, ImmunologicalB7-H1 AntigenBiomarkers, TumorCarcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmErbB ReceptorsFemaleGenetic HeterogeneityHumansLungLung NeoplasmsMaleMiddle AgedMutationProgrammed Cell Death 1 ReceptorProgression-Free SurvivalRetrospective StudiesTobacco SmokingConceptsEGFR-mutant tumorsMemorial Sloan-Kettering Cancer CenterYale Cancer CenterImmune checkpoint inhibitorsPD-L1 expressionImmune checkpoint blockadeTumor mutation burdenCancer CenterLung tumorsCheckpoint blockadeEGFR mutant lung tumorsMutant tumorsCheckpoint inhibitorsLung cancerMutation burdenImmune checkpoint blockade treatmentLow tumor mutation burdenDana-Farber Cancer InstituteEGFR wild-type lung cancersCheckpoint blockade treatmentCell lung cancerEGFR mutation subtypesSimilar smoking historyCell death 1Lung cancer cases
2017
Paraoxonase 2 Facilitates Pancreatic Cancer Growth and Metastasis by Stimulating GLUT1-Mediated Glucose Transport
Nagarajan A, Dogra SK, Sun L, Gandotra N, Ho T, Cai G, Cline G, Kumar P, Cowles RA, Wajapeyee N. Paraoxonase 2 Facilitates Pancreatic Cancer Growth and Metastasis by Stimulating GLUT1-Mediated Glucose Transport. Molecular Cell 2017, 67: 685-701.e6. PMID: 28803777, PMCID: PMC5567863, DOI: 10.1016/j.molcel.2017.07.014.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsAntineoplastic AgentsApoptosis Regulatory ProteinsAryldialkylphosphataseCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementCell ProliferationEnergy MetabolismFemaleForkhead Box Protein O3Gene Expression Regulation, NeoplasticGlucoseGlucose Transporter Type 1HumansLiver NeoplasmsLung NeoplasmsMaleMice, NudeMutationPancreatic NeoplasmsProtein Kinase InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)RNA InterferenceSignal TransductionTime FactorsTranscription, GeneticTransfectionTumor BurdenTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsPDAC tumor growthGlucose transportCellular starvation responsesParaoxonase 2Glutamine metabolism pathwayNew metabolic regulatorPDAC tumor samplesShort hairpin RNATumor growthStarvation responseMetabolic genesTranscriptional targetsProtein kinaseTractable pathwayPancreatic cancer growthGenetic activationMetabolism pathwaysHairpin RNAMetabolic regulatorNew modulatorsHuman cancersPancreatic ductal adenocarcinomaMetabolic deregulationAMPKCancer growth
2014
Acquired Resistance of EGFR-Mutant Lung Adenocarcinomas to Afatinib plus Cetuximab Is Associated with Activation of mTORC1
Pirazzoli V, Nebhan C, Song X, Wurtz A, Walther Z, Cai G, Zhao Z, Jia P, de Stanchina E, Shapiro EM, Gale M, Yin R, Horn L, Carbone DP, Stephens PJ, Miller V, Gettinger S, Pao W, Politi K. Acquired Resistance of EGFR-Mutant Lung Adenocarcinomas to Afatinib plus Cetuximab Is Associated with Activation of mTORC1. Cell Reports 2014, 7: 999-1008. PMID: 24813888, PMCID: PMC4074596, DOI: 10.1016/j.celrep.2014.04.014.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAfatinibAnimalsAntibodies, Monoclonal, HumanizedAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCetuximabDrug Resistance, NeoplasmErbB ReceptorsHumansLung NeoplasmsMechanistic Target of Rapamycin Complex 1MiceMice, NudeMice, TransgenicMultiprotein ComplexesMutationQuinazolinesRandom AllocationTOR Serine-Threonine KinasesXenograft Model Antitumor AssaysConceptsTyrosine kinase inhibitorsFirst-generation tyrosine kinase inhibitorEGFR-mutant lung adenocarcinomaLung adenocarcinomaMechanisms of resistanceEGFR antibody cetuximabPotential therapeutic strategyBiopsy specimensAntibody cetuximabDrug combinationsMouse modelTherapeutic strategiesAfatinibAddition of rapamycinCetuximabDual inhibitionAcquired ResistanceKinase inhibitorsGenomic alterationsAdenocarcinomaPatientsActivationGenomic mechanismsDrugsMTORC1 activation
2013
Identification of EGFR mutation, KRAS mutation, and ALK gene rearrangement in cytological specimens of primary and metastatic lung adenocarcinoma
Cai G, Wong R, Chhieng D, Levy GH, Gettinger SN, Herbst RS, Puchalski JT, Homer RJ, Hui P. Identification of EGFR mutation, KRAS mutation, and ALK gene rearrangement in cytological specimens of primary and metastatic lung adenocarcinoma. Cancer Cytopathology 2013, 121: 500-507. PMID: 23495083, DOI: 10.1002/cncy.21288.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdultAgedAged, 80 and overAnaplastic Lymphoma KinaseBiomarkers, TumorBone NeoplasmsCytodiagnosisDNA, NeoplasmErbB ReceptorsFeasibility StudiesFemaleGene RearrangementHumansIn Situ Hybridization, FluorescenceLiver NeoplasmsLung NeoplasmsMaleMiddle AgedMutationNeoplasm Recurrence, LocalPrognosisProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Ras ProteinsReal-Time Polymerase Chain ReactionReceptor Protein-Tyrosine KinasesSoft Tissue NeoplasmsYoung AdultConceptsALK gene rearrangementMetastatic lung adenocarcinomaEGFR mutationsKRAS mutationsMetastatic tumorsEpidermal growth factor receptorLung adenocarcinomaCytological specimensGene rearrangementsMolecular testsMolecular alterationsKirsten rat sarcoma viral oncogene homolog (KRAS) mutationsALK gene rearrangement analysisAnaplastic lymphoma kinase (ALK) gene rearrangementEGFR T790M mutationRat sarcoma viral oncogene homolog mutationsCases of lungT790M mutationImportant therapeutic implicationsFine needle aspiratesGene rearrangement analysisCell block materialGrowth factor receptorRecurrent lungRecurrent adenocarcinoma
2012
Diagnostic value of K‐ras mutation analysis for pancreaticobiliary cytology specimens with indeterminate diagnosis
Cai G, Mahooti S, Lipata FM, Chhieng D, Hui P. Diagnostic value of K‐ras mutation analysis for pancreaticobiliary cytology specimens with indeterminate diagnosis. Cancer Cytopathology 2012, 120: 313-318. PMID: 22367918, DOI: 10.1002/cncy.21188.Peer-Reviewed Original Research