2023
TP53 Mutation-driven Stratified Mucin-producing Carcinoma Coexisting With Squamous Cell Carcinoma of the Vulva: A Case Study
Wadia R, McHenry A, Abi-Raad R, Hui P. TP53 Mutation-driven Stratified Mucin-producing Carcinoma Coexisting With Squamous Cell Carcinoma of the Vulva: A Case Study. International Journal Of Gynecological Pathology 2023, 42: 555-560. PMID: 37255422, DOI: 10.1097/pgp.0000000000000961.Peer-Reviewed Original ResearchConceptsSquamous cell carcinomaInvasive squamous cell carcinomaVulvar intraepithelial neoplasiaCell carcinomaIntraepithelial neoplasiaLichen sclerosusAssociated with high-risk human papillomavirus infectionHigh-risk human papillomavirus infectionDifferentiated vulvar intraepithelial neoplasiaPresence of lymphovascular invasionInguinal lymph node metastasisHuman papillomavirus infectionVulvar lichen sclerosusMucin-producing carcinomaLymph node metastasisIntraepithelial lesionsLymphovascular invasionTP53 mutationsNode metastasisPapillomavirus infectionNeoplastic componentsCarcinomaUnique caseTP53SclerosusKRAS mutation in primary ovarian serous borderline tumors correlates with tumor recurrence
McHenry A, Rottmann D, Buza N, Hui P. KRAS mutation in primary ovarian serous borderline tumors correlates with tumor recurrence. Virchows Archiv 2023, 483: 71-79. PMID: 37219599, DOI: 10.1007/s00428-023-03564-z.Peer-Reviewed Original ResearchConceptsOvarian serous borderline tumorsSerous borderline tumorsNon-invasive implantsDisease-free survivalKRAS mutationsTumor recurrenceExtraovarian implantsAdverse disease-free survivalWorse disease-free survivalHigher stage diseaseKRAS mutation testingHigher tumor stageWild-type KRASBRAF V600E mutationBRAF mutational analysisBorderline tumorsClinical outcomesHistological subtypesTumor stageBRAF mutationsUseful biomarkerInvasive implantsTumors correlatesV600E mutationMutational status
2022
Elimusertib (BAY1895344), a novel ATR inhibitor, demonstrates in vivo activity in ATRX mutated models of uterine leiomyosarcoma
Harold J, Bellone S, Manavella D, Mutlu L, McNamara B, Hartwich T, Zipponi M, Yang-Hartwich Y, Demirkiran C, Verzosa M, Choi J, Dong W, Buza N, Hui P, Altwerger G, Huang G, Andikyan V, Clark M, Ratner E, Azodi M, Schwartz P, Santin A. Elimusertib (BAY1895344), a novel ATR inhibitor, demonstrates in vivo activity in ATRX mutated models of uterine leiomyosarcoma. Gynecologic Oncology 2022, 168: 157-165. PMID: 36442427, PMCID: PMC9797429, DOI: 10.1016/j.ygyno.2022.11.014.Peer-Reviewed Original ResearchConceptsPatient-derived xenograftsUterine leiomyosarcomaVivo activityVehicle control treatmentMedian overall survivalTumor volume differencesOral scheduleWestern blot analysisOverall survivalOral gavageAggressive malignancyPDX modelsClinical trialsSCID miceTumor measurementsULMS patientsSignificant growth inhibitionNovel ATR inhibitorTumor samplesSignificant toxicityWestern blotKinase inhibitorsATRX mutationsGene mutationsControl vehicleCorrelative Assessment of p53 Immunostaining Patterns and TP53 Mutation Status by Next-Generation Sequencing in High-Grade Endometrial Carcinomas
Matsumoto N, Manrai P, Rottmann D, Wu X, Assem H, Hui P, Buza N. Correlative Assessment of p53 Immunostaining Patterns and TP53 Mutation Status by Next-Generation Sequencing in High-Grade Endometrial Carcinomas. International Journal Of Gynecological Pathology 2022, 42: 567-575. PMID: 36730675, DOI: 10.1097/pgp.0000000000000930.Peer-Reviewed Original ResearchConceptsHigh-grade endometrial carcinomasEndometrial carcinomaEndometrioid endometrial carcinomaTP53 mutation statusP53 immunohistochemistrySerous componentIHC staining patternNext-generation sequencing resultsNuclear overexpressionGrade 3 endometrioid endometrial carcinomaMutation statusTP53 mutationsCytoplasmic stainingStaining patternSerous endometrial carcinomaAberrant p53 expressionMixed endometrial carcinomasClinical prognosisSurrogate markerAberrant p53 proteinTherapeutic decisionsIHC patternsTP53 alterationsTumor histotypesP53 expressionSignificance 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
2021
A Timely Update of Immunohistochemistry and Molecular Classification in the Diagnosis and Risk Assessment of Endometrial Carcinomas.
Wang M, Hui P. A Timely Update of Immunohistochemistry and Molecular Classification in the Diagnosis and Risk Assessment of Endometrial Carcinomas. Archives Of Pathology & Laboratory Medicine 2021, 145: 1367-1378. PMID: 34673912, DOI: 10.5858/arpa.2021-0098-ra.Peer-Reviewed Original ResearchBiomarkers, TumorCarcinomaDNA Copy Number VariationsDNA Polymerase IIEndometrial NeoplasmsFemaleGene DosageHumansImmunohistochemistryMicrosatellite InstabilityMolecular Diagnostic TechniquesMutationPoly-ADP-Ribose Binding ProteinsPredictive Value of TestsPrognosisTerminology as TopicTumor Suppressor Protein p53
2020
Frequent loss of mutation-specific mismatch repair protein expression in nonneoplastic endometrium of Lynch syndrome patients
Wong S, Hui P, Buza N. Frequent loss of mutation-specific mismatch repair protein expression in nonneoplastic endometrium of Lynch syndrome patients. Modern Pathology 2020, 33: 1172-1181. PMID: 31932681, DOI: 10.1038/s41379-020-0455-x.Peer-Reviewed Original ResearchConceptsLynch syndrome patientsLynch syndromeMMR protein expressionSporadic endometrial carcinomasSyndrome patientsEndometrial cancerEndometrial glandsEndometrial carcinomaProtein expressionLynch syndrome-associated endometrial cancerGermline mutationsMismatch repair protein expressionMMR protein immunohistochemistryEndometrial cancer patientsNonneoplastic endometriumBenign endometrial tissuesMicrosatellite instability testingMMR protein lossGermline mutation analysisDNA mismatch repair genesRepair protein expressionMismatch repair genesBackground endometriumMMR immunohistochemistryProphylactic hysterectomy
2019
Whole-exome sequencing of cervical carcinomas identifies activating ERBB2 and PIK3CA mutations as targets for combination therapy
Zammataro L, Lopez S, Bellone S, Pettinella F, Bonazzoli E, Perrone E, Zhao S, Menderes G, Altwerger G, Han C, Zeybek B, Bianchi A, Manzano A, Manara P, Cocco E, Buza N, Hui P, Wong S, Ravaggi A, Bignotti E, Romani C, Todeschini P, Zanotti L, Odicino F, Pecorelli S, Donzelli C, Ardighieri L, Angioli R, Raspagliesi F, Scambia G, Choi J, Dong W, Bilguvar K, Alexandrov LB, Silasi DA, Huang GS, Ratner E, Azodi M, Schwartz PE, Pirazzoli V, Stiegler AL, Boggon TJ, Lifton RP, Schlessinger J, Santin AD. Whole-exome sequencing of cervical carcinomas identifies activating ERBB2 and PIK3CA mutations as targets for combination therapy. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 22730-22736. PMID: 31624127, PMCID: PMC6842590, DOI: 10.1073/pnas.1911385116.Peer-Reviewed Original ResearchConceptsPI3K/AKT/mTOR pathwaySquamous cell carcinomaWhole-exome sequencingAKT/mTOR pathwayPrimary cervical cancer cell linesPIK3CA inhibitorsRecurrent cervical cancer patientsMTOR pathwayCombination of copanlisibCervical cancer patientsPI3K/Akt/mTORCervical cancer xenograftsRegression of tumorsCervical cancer cell linesCervical tumor cell linesSingle nucleotide variantsWild-type tumorsRecurrent somatic missense mutationsAkt/mTORCell linesPan-HERCancer cell linesTypes 16/18Cervical cancerCancer patients
2018
Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors
Li C, Bonazzoli E, Bellone S, Choi J, Dong W, Menderes G, Altwerger G, Han C, Manzano A, Bianchi A, Pettinella F, Manara P, Lopez S, Yadav G, Riccio F, Zammataro L, Zeybek B, Yang-Hartwich Y, Buza N, Hui P, Wong S, Ravaggi A, Bignotti E, Romani C, Todeschini P, Zanotti L, Zizioli V, Odicino F, Pecorelli S, Ardighieri L, Silasi DA, Litkouhi B, Ratner E, Azodi M, Huang GS, Schwartz PE, Lifton RP, Schlessinger J, Santin AD. Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors. Proceedings Of The National Academy Of Sciences Of The United States Of America 2018, 116: 619-624. PMID: 30584090, PMCID: PMC6329978, DOI: 10.1073/pnas.1814027116.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsAzepinesBRCA1 ProteinBRCA2 ProteinCell Line, TumorClass I Phosphatidylinositol 3-KinasesFemaleHumansMiceMutationNeoplasm MetastasisNeoplasm Recurrence, LocalOvarian NeoplasmsProteinsProto-Oncogene Proteins c-mycTriazolesTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsOvarian cancerWhole-exome sequencingC-myc amplificationRecurrent tumorsPrimary tumorBET inhibitorsChemotherapy-resistant diseaseRecurrent ovarian cancerLethal gynecologic malignancyBilateral ovarian cancerChemotherapy-resistant tumorsPrimary metastatic tumorsMutational landscapeSomatic mutationsFresh-frozen tumorsGynecologic malignanciesMetastatic tumorsPrimary cell linesC-MYC gainPIK3CA amplificationTranscoelomic metastasisTherapeutic targetPatientsMetastatic abilityTumorsFOXL2 Mutation Analysis of Ovarian Sex Cord-Stromal Tumors
Buza N, Wong S, Hui P. FOXL2 Mutation Analysis of Ovarian Sex Cord-Stromal Tumors. International Journal Of Gynecological Pathology 2018, 37: 305-315. PMID: 28700438, DOI: 10.1097/pgp.0000000000000426.Peer-Reviewed Original ResearchConceptsSex cord-stromal tumorsAdult granulosa cell tumorGranulosa cell tumorsOvarian sex cord-stromal tumorsCell tumorsReticulin patternFOXL2 mutationStaining patternSertoli-Leydig cell tumorFOXL2 mutation statusAbundant pale cytoplasmSingle institutional cohortThird of casesWild-type tumorsFOXL2 mutation analysisNegative tumorsPositive tumorsTumor sizeReticulin stainingType tumorsPale cytoplasmNuclear atypiaMutation statusPositive casesTumors
2017
KRAS mutation of extraovarian implants of serous borderline tumor: prognostic indicator for adverse clinical outcome
Zuo T, Wong S, Buza N, Hui P. KRAS mutation of extraovarian implants of serous borderline tumor: prognostic indicator for adverse clinical outcome. Modern Pathology 2017, 31: 350-357. PMID: 29027536, DOI: 10.1038/modpathol.2017.121.Peer-Reviewed Original ResearchConceptsAtypical proliferative serous tumorNon-invasive implantsDisease-specific survivalSerous borderline tumorsHigh recurrence rateWorse disease-specific survivalStage IIIC diseaseKRAS mutationsInvasive implantsBRAF V600E mutationBorderline tumorsSerous tumorsRecurrence rateIIIC diseaseClinical outcomesHistological subtypesPrognostic indicatorExtraovarian implantsV600E mutationLow-grade serous carcinomaUnfavorable disease-specific survivalAdverse clinical outcomesHigher stage diseaseSignificant prognostic indicatorBRAF mutation frequencyPathologic Characteristics, Natural History, and Prognostic Implications of BRAFV600E Mutation in Pediatric Papillary Thyroid Carcinoma
Hardee S, Prasad ML, Hui P, Dinauer CA, Morotti RA. Pathologic Characteristics, Natural History, and Prognostic Implications of BRAFV600E Mutation in Pediatric Papillary Thyroid Carcinoma. Pediatric And Developmental Pathology 2017, 20: 206-212. PMID: 28521635, DOI: 10.1177/1093526616689628.Peer-Reviewed Original ResearchConceptsPapillary thyroid cancerPediatric papillary thyroid cancerPrognostic implicationsPediatric papillary thyroid carcinomaNegative casesBRAF-negative casesBRAF-negative patientsBRAF-positive casesTertiary medical centerAggressive clinical coursePapillary thyroid carcinomaSurgical pathology diagnosisCommon genetic aberrationsNegative patientsAggressive courseClinical coursePathologic characteristicsCase seriesClinical outcomesRetrospective reviewAggressive featuresPediatric casesRecurrence rateRetrospective studySingle institution
2016
Polymerase ε (POLE) ultra-mutation in uterine tumors correlates with T lymphocyte infiltration and increased resistance to platinum-based chemotherapy in vitro
Bellone S, Bignotti E, Lonardi S, Ferrari F, Centritto F, Masserdotti A, Pettinella F, Black J, Menderes G, Altwerger G, Hui P, Lopez S, de Haydu C, Bonazzoli E, Predolini F, Zammataro L, Cocco E, Ferrari F, Ravaggi A, Romani C, Facchetti F, Sartori E, Odicino FE, Silasi DA, Litkouhi B, Ratner E, Azodi M, Schwartz PE, Santin AD. Polymerase ε (POLE) ultra-mutation in uterine tumors correlates with T lymphocyte infiltration and increased resistance to platinum-based chemotherapy in vitro. Gynecologic Oncology 2016, 144: 146-152. PMID: 27894751, PMCID: PMC5183545, DOI: 10.1016/j.ygyno.2016.11.023.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic AgentsCarboplatinCarcinomaCD4 Lymphocyte CountCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell SurvivalDisease-Free SurvivalDNA Polymerase IIDrug Resistance, NeoplasmEndometrial NeoplasmsFemaleHumansMicrosatellite InstabilityMiddle AgedMutationPoly-ADP-Ribose Binding ProteinsTumor Cells, CulturedConceptsBetter prognosisTumor cell linesInfiltration of CD4Number of CD4Platinum-based chemotherapyT lymphocyte infiltrationPD-1 receptorCell linesLow metastatic capabilityPOLE-mutated tumorsWild-type ECsEC cell linesLymphocyte infiltrationFavorable prognosisPD-1EC patientsType tumorsEnhanced immunogenicityT lymphocytesMolecular subtypesTumors correlatesChemotherapyMetastatic capabilityPrognosisTumorsMutational landscape of uterine and ovarian carcinosarcomas implicates histone genes in epithelial–mesenchymal transition
Zhao S, Bellone S, Lopez S, Thakral D, Schwab C, English DP, Black J, Cocco E, Choi J, Zammataro L, Predolini F, Bonazzoli E, Bi M, Buza N, Hui P, Wong S, Abu-Khalaf M, Ravaggi A, Bignotti E, Bandiera E, Romani C, Todeschini P, Tassi R, Zanotti L, Odicino F, Pecorelli S, Donzelli C, Ardighieri L, Facchetti F, Falchetti M, Silasi DA, Ratner E, Azodi M, Schwartz PE, Mane S, Angioli R, Terranova C, Quick CM, Edraki B, Bilgüvar K, Lee M, Choi M, Stiegler AL, Boggon TJ, Schlessinger J, Lifton RP, Santin AD. Mutational landscape of uterine and ovarian carcinosarcomas implicates histone genes in epithelial–mesenchymal transition. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: 12238-12243. PMID: 27791010, PMCID: PMC5087050, DOI: 10.1073/pnas.1614120113.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overCarcinosarcomaClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistonesHumansMiddle AgedMutationOvarian NeoplasmsPTEN PhosphohydrolaseTelomeraseTumor Suppressor Protein p53Uterine NeoplasmsConceptsEpithelial-mesenchymal transitionWhole-exome sequencingHistone gene clusterMutational landscapeStable transgenic expressionExcess of mutationsMultiregion whole-exome sequencingHistone genesEvolutionary historyPhylogenetic relationshipsGene clusterHistone H2AChromosome segmentsSeparate lineagesCancer genesGenetic landscapeUterine serous carcinoma cell linesTransgenic expressionGenesCarcinoma cell linesGene TP53Frequent amplificationFrequent deletionsChromosome 6pInvasive propertiesSYD985, a Novel Duocarmycin-Based HER2-Targeting Antibody–Drug Conjugate, Shows Antitumor Activity in Uterine Serous Carcinoma with HER2/Neu Expression
Black J, Menderes G, Bellone S, Schwab CL, Bonazzoli E, Ferrari F, Predolini F, De Haydu C, Cocco E, Buza N, Hui P, Wong S, Lopez S, Ratner E, Silasi DA, Azodi M, Litkouhi B, Schwartz PE, Goedings P, Beusker PH, van der Lee MM, Timmers CM, Dokter WH, Santin AD. SYD985, a Novel Duocarmycin-Based HER2-Targeting Antibody–Drug Conjugate, Shows Antitumor Activity in Uterine Serous Carcinoma with HER2/Neu Expression. Molecular Cancer Therapeutics 2016, 15: 1900-1909. PMID: 27256376, DOI: 10.1158/1535-7163.mct-16-0163.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsAntibody-Dependent Cell CytotoxicityAntineoplastic AgentsBystander EffectCathepsin BCell Line, TumorCell SurvivalClass I Phosphatidylinositol 3-KinasesCystadenocarcinoma, SerousDisease Models, AnimalDuocarmycinsFemaleGene ExpressionHumansImmunoconjugatesIndolesMiceMiddle AgedMutationPhosphatidylinositol 3-KinasesPyrrolidinonesReceptor, ErbB-2Survival AnalysisUterine NeoplasmsXenograft Model Antitumor AssaysConceptsUterine serous carcinomaAntibody-dependent cellular cytotoxicityHER2/neu expressionAntibody-drug conjugatesT-DM1Neu expressionHER2-targeting antibody-drug conjugateNovel antibody-drug conjugateNovel HER2-targeting antibody-drug conjugatePrimary USC cell linesHigh HER2 expressionHER2/neu oncogeneHER2/neuMouse xenograft modelUSC cell linesFlow cytometry assayEndometrial cancerSerous carcinomaHER2 expressionTrastuzumab emtansineClinical studiesCellular cytotoxicitySYD985Aggressive formExpress HER2Dual CCNE1/PIK3CA targeting is synergistic in CCNE1-amplified/PIK3CA-mutated uterine serous carcinomas in vitro and in vivo
Cocco E, Lopez S, Black J, Bellone S, Bonazzoli E, Predolini F, Ferrari F, Schwab CL, Menderes G, Zammataro L, Buza N, Hui P, Wong S, Zhao S, Bai Y, Rimm DL, Ratner E, Litkouhi B, Silasi DA, Azodi M, Schwartz PE, Santin AD. Dual CCNE1/PIK3CA targeting is synergistic in CCNE1-amplified/PIK3CA-mutated uterine serous carcinomas in vitro and in vivo. British Journal Of Cancer 2016, 115: 303-311. PMID: 27351214, PMCID: PMC4973158, DOI: 10.1038/bjc.2016.198.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCell Line, TumorClass I Phosphatidylinositol 3-KinasesCyclin EDNA Copy Number VariationsFemaleGene Knockdown TechniquesHeterograftsHumansIn Situ Hybridization, FluorescenceIn Vitro TechniquesMiceMutationOncogene ProteinsPhosphatidylinositol 3-KinasesRNA, MessengerTissue Array AnalysisUterine NeoplasmsConceptsUterine serous carcinomaSerous carcinomaTumor growthCyclin E1 (CCNE1) gene amplificationRecurrent uterine serous carcinomaPrimary USC cell linesNovel therapeutic optionsSingle-agent treatmentIdeal therapeutic targetUSC cell linesCyclin E1 expressionUSC patientsUSC xenograftsInhibited cell growthCell cycle analysisAggressive variantTherapeutic optionsCCNE1 amplificationEndometrial tumorsCYC065Therapeutic targetClinical optionPIK3CA driver mutationsDriver mutationsXenografts
2015
Diagnostic application of KRAS mutation testing in uterine microglandular proliferations
Hong W, Abi-Raad R, Alomari AK, Hui P, Buza N. Diagnostic application of KRAS mutation testing in uterine microglandular proliferations. Human Pathology 2015, 46: 1000-1005. PMID: 25997988, DOI: 10.1016/j.humpath.2015.03.010.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdultAgedAged, 80 and overBiopsyCell ProliferationCervix UteriDiagnosis, DifferentialDNA Mutational AnalysisEndometrial HyperplasiaEndometrial NeoplasmsFemaleHumansMiddle AgedMutationPredictive Value of TestsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Ras ProteinsConceptsKRAS mutation analysisEndometrial adenocarcinomaMicroglandular hyperplasiaMicroglandular patternKRAS mutationsCareful morphological assessmentEndometrial mucinous carcinomaKRAS mutation testingCases of EMAMutation analysisFrequent KRAS mutationsElectronic medical recordsDifferential diagnostic toolHigh mitotic activityEndometrial biopsyImmunohistochemical workupUterine cervixMucinous carcinomaClinical historyDiagnostic challengeDiagnostic dilemmaGlandular proliferationMucinous lesionsMedical recordsEAC cases
2014
KRAS mutation testing in clinical practice
Perincheri S, Hui P. KRAS mutation testing in clinical practice. Expert Review Of Molecular Diagnostics 2014, 15: 375-384. PMID: 25487540, DOI: 10.1586/14737159.2015.986102.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsKRAS mutation testingKRAS mutationsMetastatic colorectal carcinomaLung cancer patientsMutations of KRASCommon human malignanciesMutation testingCombinatorial therapeutic strategiesCancer patientsColorectal carcinomaThyroid cancerClinical aggressivenessClinical OncologyTherapeutic strategiesClinical practiceMolecular testingCytological specimensHuman malignanciesPrecision medicinePatientsCancerEssential biomarkersDownstream effectorsCurrent practiceMutations
2013
Frequent KRAS mutation in complex mucinous epithelial lesions of the endometrium
Alomari A, Abi-Raad R, Buza N, Hui P. Frequent KRAS mutation in complex mucinous epithelial lesions of the endometrium. Modern Pathology 2013, 27: 675-680. PMID: 24186144, DOI: 10.1038/modpathol.2013.186.Peer-Reviewed Original ResearchConceptsPositive predictive valueMucinous lesionsKRAS mutationsMucinous changeMucinous adenocarcinomaEndometrial mucinous carcinomaHigh positive predictive valueComplex atypical hyperplasiaRisk stratification algorithmAtypical complex hyperplasiaImportant prognostic indicatorFrequent KRAS mutationsKRAS mutation analysisComplex hyperplasiaHysterectomy specimensClinical progressionEndometrial lesionsMucinous carcinomaAtypical hyperplasiaPrognostic indicatorMucinous differentiationEpithelial lesionsCurettage casesStratification algorithmPredictive valueTall Cell Variant of Papillary Thyroid Microcarcinoma: Clinicopathologic Features with BRAFV600E Mutational Analysis
Bernstein J, Virk RK, Hui P, Prasad A, Westra WH, Tallini G, Adeniran AJ, Udelsman R, Sasaki CT, Roman SA, Sosa JA, Prasad ML. Tall Cell Variant of Papillary Thyroid Microcarcinoma: Clinicopathologic Features with BRAFV600E Mutational Analysis. Thyroid 2013, 23: 1525-1531. PMID: 23682579, DOI: 10.1089/thy.2013.0154.Peer-Reviewed Original ResearchConceptsTall cell variantPapillary thyroid microcarcinomaPapillary microcarcinomaCell variantLymphovascular invasionNode metastasisThyroid microcarcinomaAdvanced stageCentral compartment lymph node metastasisLateral cervical node metastasesStage III/IVACentral compartment lymph nodesLateral cervical nodesMultifocal papillary carcinomaLymph node dissectionCervical node metastasisLymph node metastasisPapillary thyroid carcinomaNode dissectionTotal thyroidectomyCervical nodesLymph nodesClinicopathologic featuresMultifocal tumorsAggressive features