2023
GATA3 expression in primary lung carcinomas: correlation with histopathologic features and TTF-1, napsin A, and p40 expression
Wang M, Chen P, Cai G. GATA3 expression in primary lung carcinomas: correlation with histopathologic features and TTF-1, napsin A, and p40 expression. Human Pathology 2023, 135: 93-98. PMID: 36702357, DOI: 10.1016/j.humpath.2023.01.007.Peer-Reviewed Original ResearchConceptsLarge cell carcinomaPrimary lung carcinomaSarcomatoid carcinomaCell carcinomaNapsin ALung carcinomaGATA3 expressionTTF-1Non-small cell carcinomaNon-small cell lung carcinomaPrimary non-small cell lung carcinomasPrimary lung cancerSquamous cell carcinomaPanel of immunostainsCell lung carcinomaExpression of GATA3Whole-slide sectionsTMA casesAdenosquamous carcinomaTumor histologyHistopathologic featuresGATA3 stainingLung cancerP40 expressionTumor origin
2022
Evaluation of TRPS1 Expression in Pleural Effusion Cytology Specimens With Metastatic Breast Carcinoma
Wang M, Stendahl K, Cai G, Adeniran A, Harigopal M, Gilani SM. Evaluation of TRPS1 Expression in Pleural Effusion Cytology Specimens With Metastatic Breast Carcinoma. American Journal Of Clinical Pathology 2022, 158: 416-425. PMID: 35760555, DOI: 10.1093/ajcp/aqac066.Peer-Reviewed Original ResearchConceptsTrichorhinophalangeal syndrome type 1Breast originMetastatic carcinomaTRPS1 expressionBreast primaryBreast carcinomaPrimary siteMC casesMetastatic breast carcinomaSquamous cell carcinomaPleural effusion cytologySyndrome type 1Cell block materialStrong nuclear expressionEffusion cytology specimensCell carcinomaUrothelial carcinomaIHC panelMalignant melanomaLung adenocarcinomaIHC stainingPositive stainingCytology specimensCarcinomaEffusion cytology
2019
A Semiquantitative Scoring System May Allow Biopsy Diagnosis of Pulmonary Large Cell Neuroendocrine Carcinoma
Baine MK, Sinard JH, Cai G, Homer RJ. A Semiquantitative Scoring System May Allow Biopsy Diagnosis of Pulmonary Large Cell Neuroendocrine Carcinoma. American Journal Of Clinical Pathology 2019, 153: 165-174. PMID: 31593583, PMCID: PMC7571487, DOI: 10.1093/ajcp/aqz149.Peer-Reviewed Original ResearchLoss of thymidine kinase 1 inhibits lung cancer growth and metastatic attributes by reducing GDF15 expression
Malvi P, Janostiak R, Nagarajan A, Cai G, Wajapeyee N. Loss of thymidine kinase 1 inhibits lung cancer growth and metastatic attributes by reducing GDF15 expression. PLOS Genetics 2019, 15: e1008439. PMID: 31589613, PMCID: PMC6797230, DOI: 10.1371/journal.pgen.1008439.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAdultAgedAnimalsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationDatasets as TopicDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGrowth Differentiation Factor 15HumansLungLung NeoplasmsMaleMiceMiddle AgedNeoplasm Recurrence, LocalPrognosisSurvival AnalysisThymidine KinaseTranscription FactorsXenograft Model Antitumor AssaysConceptsShort hairpin RNALUAD cellsMetastatic attributesRho GTPase activityMAP kinase pathwayEctopic expressionGTPase activityTranscriptional overexpressionKinase pathwayKinase 1Cancer cell growthGenetic knockdownProfiling-based approachDifferentiation factor 15Hairpin RNALung adenocarcinoma patientsLung cancer growthCell growthLUAD therapyDownstream mediatorLUAD tumorsLUAD growthKey hallmarksReduced expressionDependent mannerEGFR 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
Impaired HLA Class I Antigen Processing and Presentation as a Mechanism of Acquired Resistance to Immune Checkpoint Inhibitors in Lung Cancer
Gettinger S, Choi J, Hastings K, Truini A, Datar I, Sowell R, Wurtz A, Dong W, Cai G, Melnick MA, Du VY, Schlessinger J, Goldberg SB, Chiang A, Sanmamed MF, Melero I, Agorreta J, Montuenga LM, Lifton R, Ferrone S, Kavathas P, Rimm DL, Kaech SM, Schalper K, Herbst RS, Politi K. Impaired HLA Class I Antigen Processing and Presentation as a Mechanism of Acquired Resistance to Immune Checkpoint Inhibitors in Lung Cancer. Cancer Discovery 2017, 7: cd-17-0593. PMID: 29025772, PMCID: PMC5718941, DOI: 10.1158/2159-8290.cd-17-0593.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsPatient-derived xenograftsHLA class ILung cancerClass ICell surface HLA class ILung cancer mouse modelPD-1 blockadeStandard treatment algorithmCancer mouse modelLung cancer samplesDefective antigen processingCheckpoint inhibitorsPD-1Treatment algorithmMouse modelAntagonistic antibodiesDiverse malignanciesAntigen processingCancer samplesB2MHomozygous lossTumorsCancerRecurrent mutationsParaoxonase 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
Evaluation of endobronchial ultrasound‐guided fine‐needle aspirations (EBUS‐FNA): Correlation with adequacy and histologic follow‐up
Karunamurthy A, Cai G, Dacic S, Khalbuss WE, Pantanowitz L, Monaco SE. Evaluation of endobronchial ultrasound‐guided fine‐needle aspirations (EBUS‐FNA): Correlation with adequacy and histologic follow‐up. Cancer Cytopathology 2013, 122: 23-32. PMID: 24127207, DOI: 10.1002/cncy.21350.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overBiopsy, NeedleCohort StudiesDatabases, FactualEndoscopic Ultrasound-Guided Fine Needle AspirationFalse Negative ReactionsFemaleHumansImmunohistochemistryLung NeoplasmsLymph NodesMaleMediastinal NeoplasmsMiddle AgedRetrospective StudiesSensitivity and SpecificityConceptsEndobronchial ultrasound-guided fine-needle aspirationUltrasound-guided fine-needle aspirationLymph nodesFine-needle aspirationDiagnostic yieldN1 lymph nodesN2 lymph nodesNegative cytologic diagnosisHilar lymph nodesMediastinal lymph nodesOverall diagnostic yieldChance of malignancyHigh diagnostic yieldNegative predictive valueFalse-negative diagnosesClinicopathologic findingsMediastinal lesionsLymphoid tissueInvasive modalitiesCytologic diagnosisPredictive valueUnsatisfactory casesGreater riskHistologicDiagnostic materialIdentification 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
2011
The cytomorphologic spectrum of salivary gland type tumors in the lung and mediastinum: A report of 16 patients
Monaco SE, Khalbuss WE, Ustinova E, Liang A, Cai G. The cytomorphologic spectrum of salivary gland type tumors in the lung and mediastinum: A report of 16 patients. Diagnostic Cytopathology 2011, 40: 1062-1070. PMID: 21591276, DOI: 10.1002/dc.21733.Peer-Reviewed Original ResearchConceptsSalivary gland-type tumorsMucoepidermoid carcinomaPrimary tumorType tumorsPolymorphous low-grade adenocarcinomaCommon histological subtypeAspiration cytology specimensDiagnosis of ACCSalivary duct carcinomaLow-grade adenocarcinomaMinor salivary glandsCytomorphologic spectrumDuct carcinomaHistological subtypesBasaloid tumorsCystic carcinomaCytomorphologic featuresSoft palateGrade adenocarcinomaDiagnostic pitfallsNasal cavityCytology casesCytology specimensMediastinumTumors