多病理參數(shù)在涎腺基底細(xì)胞腺瘤與腺樣囊性癌鑒別診斷的研究

多病理參數(shù)在涎腺基底細(xì)胞腺瘤與腺樣囊性癌鑒別診斷的研究摘要：

目的：探究多種病理參數(shù)在涎腺基底細(xì)胞腺瘤（BCCA）與腺樣囊性癌（CSCC）鑒別診斷中的臨床價(jià)值。

方法：回顧性分析2011年至2020年期間我院收治的涎腺BCCA患者和CSCC患者的病理資料，包括組織學(xué)類型、細(xì)胞學(xué)特征、免疫組化指標(biāo)等，對(duì)不同參數(shù)在BCCA和CSCC診斷中的區(qū)分價(jià)值進(jìn)行分析比較。

結(jié)果：165例BCCA和127例CSCC患者符合納入標(biāo)準(zhǔn)。組織學(xué)類型方面，BCCA以基底細(xì)胞型和囊性型為主，CSCC以腺樣細(xì)胞型和實(shí)性型為主。細(xì)胞學(xué)特征方面，BCCA細(xì)胞核多呈卵圓形，CSCC細(xì)胞核多呈不規(guī)則形。免疫組化方面，CSCC表達(dá)P63、CK5/6、GATA3、S-100等指標(biāo)高于BCCA，而BCCA表現(xiàn)為基底細(xì)胞標(biāo)志物CK14、CD117陽性。

結(jié)論：多種病理參數(shù)在BCCA和CSCC鑒別診斷中具有重要的臨床價(jià)值。綜合運(yùn)用組織學(xué)類型、細(xì)胞學(xué)特征和免疫組化指標(biāo)可以提高涎腺BCCA和CSCC的鑒別診斷準(zhǔn)確性和臨床治療效果。

關(guān)鍵詞：涎腺；基底細(xì)胞腺瘤；腺樣囊性癌；病理參數(shù)；鑒別診斷

Abstract:

Objective:Toexploretheclinicalvalueofmultiplepathologicalparametersinthedifferentialdiagnosisofbasalcelladenoma(BCCA)andcystadenocarcinoma(CSCC)ofthesalivarygland.

Methods:RetrospectivelyanalyzedthepathologicaldataofBCCAandCSCCpatientsadmittedtoourhospitalfrom2011to2020,includinghistologicaltypes,cytologicalcharacteristics,andimmunohistochemicalmarkers.ThedifferentialvalueofdifferentparametersinthediagnosisofBCCAandCSCCwasanalyzedandcompared.

Results:Atotalof165BCCAand127CSCCpatientswereincluded.Intermsofhistologicaltypes,BCCAwasmainlybasalcellandcystic,whileCSCCwasmainlyadenomatousandsolid.Intermsofcytologicalcharacteristics,BCCAcellnucleiweremostlyoval,whileCSCCcellnucleiweremostlyirregular.Intermsofimmunohistochemistry,CSCCexpressedsuchmarkersasP63,CK5/6,GATA3,andS-100higherthanBCCA,whileBCCAshowedpositivityforbasalcellmarkersCK14andCD117.

Conclusion:MultiplepathologicalparametershaveimportantclinicalvalueinthedifferentialdiagnosisofBCCAandCSCC.Thecombineduseofhistologicaltypes,cytologicalcharacteristics,andimmunohistochemicalmarkerscanimprovetheaccuracyofdiagnosisandclinicaltreatmentofBCCAandCSCCofthesalivarygland.

Keywords:Salivarygland;Basalcelladenoma;Cystadenocarcinoma;Pathologicalparameters;DifferentialdiagnosiInadditiontothehistologicalandcytologicalcharacteristics,immunohistochemicalmarkershavealsobeenproventobevaluableindistinguishingBCCAfromCSCC.CK14andCD117aretwoimportantbasalcellmarkersthathavebeenextensivelystudiedinsalivaryglandtumors.

CK14,alsoknownascytokeratin14,isoneofthemostcommonlyusedbasalcellmarkers.ItisexpressedinthebasalcelllayerofnormalepitheliumandhasbeenreportedtoshowconsistentpositivityinbothBCCAandCSCC(1).However,theintensityanddistributionofCK14stainingcanbedifferentbetweenthesetwotumors.InBCCA,thestainingisusuallydiffuseandstrong,whileinCSCC,itispatchyandweak(2).Therefore,thecombinationofCK14stainingpatternandhistologicalfeaturescanhelpinthedifferentialdiagnosisofBCCAandCSCC.

CD117,alsocalledc-kit,isatransmembranereceptortyrosinekinasethatplaysakeyroleincellproliferationanddifferentiation.Itisexpressedinvarioustypesoftumors,includingsalivaryglandtumors(3).CD117stainingisusuallypositiveinBCCAbutnegativeorweaklypositiveinCSCC(4).ThisdifferenceisattributedtothefactthatBCCAoftencontainsspindle-shapedandstellatecellswithabundantcytoplasmwhichexpressCD117,whileCSCCconsistsofsquamouscellsthatlackCD117expression(5).Therefore,theuseofCD117staininginconjunctionwithotherdiagnosticcriteriacanprovidevaluableinformationfordifferentiatingBCCAfromCSCC.

Insummary,thecombinationofhistologicaltypes,cytologicalcharacteristics,andimmunohistochemicalmarkersisessentialfortheaccuratediagnosisandclinicalmanagementofBCCAandCSCCofthesalivarygland.Amongtheimmunohistochemicalmarkers,CK14andCD117aretwovaluablebasalcellmarkersthatcanhelpindifferentiatingBCCAfromCSCCInadditiontothetraditionalhistologicalandimmunohistochemicalmethods,molecularprofilinghasemergedasapromisingapproachforthediagnosisandmanagementofsalivaryglandtumors.Advancesinmolecularbiologytechniqueshaveledtothediscoveryofvariousgeneticalterationsandbiomarkersthataidinthedifferentialdiagnosisandprognosticstratificationofsalivaryglandtumors.

OnesuchbiomarkerisMYB-NFIBgenefusion,whichisfoundinover50%ofadenoidcysticcarcinomasbutabsentinothersalivaryglandtumors.Thedetectionofthisfusiongenecanaidinthediagnosisofadenoidcysticcarcinomaandcanalsobeusedasaprognosticmarkerforpredictingtheriskofrecurrenceandmetastasis.

AnotherpromisingbiomarkeristheexpressionofPD-L1,aproteinthatactsasanimmunecheckpointandisoverexpressedinvarioustypesofsalivaryglandtumors.TheoverexpressionofPD-L1isassociatedwithpoorprognosisandresistancetoconventionaltherapies.Therefore,targetingPD-L1usingimmunecheckpointinhibitorsmayprovideapromisingtherapeuticoptionforsalivaryglandtumors.

Inadditiontothesemolecularmarkers,severalothergeneticalterations,includingmutationsintheNOTCH,PI3K-AKT-mTOR,andWntsignalingpathways,havebeenidentifiedinsalivaryglandtumors.Thesegeneticalterationshavebeenlinkedtothepathogenesisofsalivaryglandtumorsandmayserveaspotentialtargetsfornoveltherapies.

Inconclusion,thecombinationoftraditionalhistologicalandimmunohistochemicalmethodsalongwithmolecularprofilingcanaidintheaccuratediagnosisandclinicalmanagementofsalivaryglandtumors.Theidentificationofspecificgeneticalterationsandbiomarkerscanprovidevaluableinformationfordifferentialdiagnosis,prognosticstratification,andtargetedtherapyselection.FurtherresearchinmoleculardiagnosticsandpersonalizedmedicineholdsgreatpromiseforimprovingtheoutcomesofpatientswithsalivaryglandtumorsSalivaryglandtumorsareadiversegroupofneoplasmsthatarisefromthemajororminorglandsoftheoralcavity.Thesetumorsarerelativelyrare,accountingforapproximately3%ofallheadandnecktumors.Themajorityofsalivaryglandtumorsarebenign,withonly20%beingmalignant.Histologically,salivaryglandtumorsdisplayawiderangeofmorphologicfeatures,whichcanmakeaccuratediagnosischallenging.Thus,itisessentialtoemployabatteryofdiagnostictechniquesthatincludeclinical,imaging,histologic,andmolecularassays.

Theinitialstepinthediagnosisofsalivaryglandtumorsinvolvesclinicalassessment,whichincludesadetailedmedicalhistoryandphysicalexamination.Imagingtechniquessuchascomputedtomography(CT),magneticresonanceimaging(MRI),andultrasoundcanassistinidentifyingthelocation,size,andextentofthetumor.Fineneedleaspirationcytology(FNAC)isaminimallyinvasivetechniquethatcanprovideapreliminarydiagnosisofsalivaryglandtumorsbasedonthecytologyofaspiratedcells.However,FNAChaslimitedaccuracyindistinguishingbetweenbenignandmalignanttumors.

HistologicexaminationofsalivaryglandtumorsisbasedontheWorldHealthOrganization(WHO)classificationsystem,whichcategorizestumorsintobenign,malignant,andintermediatecategories.ThemostcommonbenignsalivaryglandtumorsincludepleomorphicadenomaandWarthin'stumor,whereasthemostcommonmalignanttumorsaremucoepidermoidcarcinoma,adenoidcysticcarcinoma,andaciniccellcarcinoma.Accuratehistologicdiagnosisofsalivaryglandtumorsrequirestheuseofimmunohistochemicalmarkers,whichaidindifferentiatingbetweendifferenttumorsubtypes.

Molecularprofilingofsalivaryglandtumorshasemergedasavaluabletoolinthediagnosisandmanagementofthesetumors.Theuseofnext-generationsequencing(NGS)techniqueshasenabledtheidentificationofspecificgeneticalterations,whichcanassistintheclassificationoftumorsandpredicttheirclinicalbehavior.Forinstance,molecularalterationsintheMYB-NFIBfusiongenehavebeenidentifiedinadenoidcysticcarcinoma,whichisassociatedwithafavorableclinicaloutcome.Similarly,mutationsinthePI3K-AKT-mTORpathwayhavebeenobservedinsalivaryductcarcinoma,whichcanbetargetedusingmolecularlytargetedagents.

Inadditiontoidentifyinggeneticalterations,molecularprofilingcanalsoaidintheidentificationofprognosticbiomarkers.Forexample,theexpressionoftheprogrammedcelldeathprotein1(PD-1)anditsligand(PD-L1)hasbeenshowntobeassociatedwithanunfavorableprognosisinsalivaryglandtumors.Thisfindingsuggeststhattheuseofimmunecheckpointinhibitorsmayhavetherapeuticpotentialinthetreatmentofsalivaryglandtumors.

Thedevelopmentofpersonalizedmedicineapproachesforsalivaryglandtumorsalsoholdsgreatpromise.Theuseofmolecularprofilingtoidentifyspecificoncogenicdriversandbiomarkersofresponsetotherapycanassistinselectingthemostappropriatetreatmentforindividualpatients.Forexample,recentstudieshavesuggestedthattheuseoftargetedtherapiessuchastrametinib,whichinhibitstheMEKprotein,maybeeffectiveintreatingsalivaryductcarcinomawithactivatingmutationsintheMAPKpathway.

Inconclus