简介：Epithelialovariancancerrepresentsthemostlethalgynecologicalmalignancyinthedevelopedworld,andcanbedividedintofivemainhistologicalsubtypes:highgradeserous,endometrioid,clearcell,mucinousandlowgradeserous.Thesesubtypesrepresentdistinctdiseaseentities,bothclinicallyandatthemolecularlevel.Molecularanalysishasrevealedsignificantgeneticheterogeneityinovariancancer,particularlywithinthehighgradeseroussubtype.Assuch,thissubtypehasbeenthefocusofmuchresearchefforttodate,revealingmolecularsubgroupsatboththegenomicandtranscriptomiclevelthathaveclinicalimplications.However,stratificationofovariancancerpatientsbasedontheunderlyingbiologyoftheirdiseaseremainsinitsinfancy.Here,wesummarizethemolecularchangesthatcharacterizethefivemainovariancancersubtypes,highlightpotentialopportunitiesfortargetedtherapeuticinterventionandoutlineprioritiesforfutureresearch.

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简介：Objective:Secretorybreastcarcinoma(SBC)isararetypeofbreastmalignancy,accountingforlessthan0.02%ofallinfiltratingbreastmalignancies.ThepureSBC,atypeofSBCwithoutanothertypeofbreastmalignantneoplasm,isparticularlyrare.ThisstudyaimedtoinvestigatetheclinicopathologicandmolecularfeaturesofpureSBC.Methods:Themainpathologicalparameterssuchasestrogenreceptor(ER),progesteronereceptor(PR),andhumanepithelialgrowthfactorreceptor2(C-erbB-2)weredetectedbyimmunohistochemistry(IHC),andtheclinicopathologicandprognosticdifferencewerecomparedwithinvasiveductalcarcinoma(IDC).Fluorescentinsituhybridization(FISH)andreversetranscriptionpolymerasechainreaction(RT-PCR)wasperformedtoidentifytheETV6-NTRK3rearrangementofSBC.Results:WefoundthatthepositivityratesofER,PR,C-erbB-2,p53,andS-100were47.7%(21/44),52.3%(23/44),36.4%(16/44),27.3%(12/44),and95.5%(42/44),respectively,whichwerehigherthanthosereportedinpreviousstudies.Specialperiodicacid-Schiffanalysiswasperformedin36patients,andthevalueoftheKi-67indexrangedfrom1%to50%(meanvalue:10%).Interestingly,mostpatientswithpureSBCharboredanETV6-NTRK3rearrangementwithan88.6%(39/44)expressionrate.ComparedwithIDC,thetumorsizeofmostpatientswithSBCwaslargerthan2cm(P=0.024).Ultrasoundshowedbenignlesions,andthetotalmisdiagnosisratewashigher(P=0.020).Althoughthepathologicalclassificationwasmostlytriple-negativebreastcancers(P=0.036),therewaslessmetastasis(P=0.029),andtheoverallprognosiswasbetterthanthatoftheIDCgroup.Conclusions:Althoughaxillarylymphnodemetastasis,localrecurrence,ordistantmetastasismayoccur,SBCisalsoconsideredanindolentneoplasmwithagoodprognosis.Oncediagnosed,surgicaltreatmentshouldbeperformedassoonaspossible,followedbyappropriateadjuvantchemotherapy,irradiation,andendocrinetherapies.

简介：Theimplementationofmolecularprofilingtechnologiesinoncologydeepensourknowledgeforthemolecularlandscapesofcancerdiagnoses,identifyingaberrationsthatcouldbelinkedwithspecifictherapeuticvulnerabilities.Inparticular,thereisanincreasinglistofmolecularlytargetedanticanceragentsundergoingclinicaldevelopmentthataimtoblockspecificmolecularaberrations.Thisleadstoaparadigmshift,withanincreasinglistofspecificaberrationsdictatingthetreatmentofpatientswithcancer.Thisparadigmshiftimpactsthefieldofclinicaltrials,sincetheclassicalapproachofhavingclinico-pathologicaldiseasecharacteristicsdictatingthepatients'enrolmentinoncologytrialsshiftstowardstheimplementationofmolecularprofilingasprescreeningstep.Inordertofacilitatethesuccessfulclinicaldevelopmentofthesenewanticancerdrugswithinspecificmolecularnichesofcancerdiagnoses,therehavebeendevelopednew,innovativetrialdesignsthatcouldbeclassifiedasfollows:i)longitudinalcohortstudiesthatimplement(ornot)'nested'downstreamtrials,2)studiesthatassesstheclinicalutilityofmolecularprofiling,3)'master'protocoltrials,iv)'basket'trials,v)trialsfollowinganadaptivedesign.Inthepresentarticle,wereviewtheseinnovativestudydesigns,providingrepresentativeexamplesfromeachcategoryandwediscussthechallengesthatstillneedtobeaddressedinthiseraofnewgenerationoncologytrialsimplementingmolecularprofiling.Emphasisisputonthefieldofbreastcancerclinicaltrials.

简介：Acutemyeloidleukemia(AML)isaclonaldisordercharacterizedbytheaccumulationofcomplexgenomicalterationsthatdefinethediseasepathophysiologyandoveralloutcome.RecentadvancesinsequencingtechnologieshavedescribedthemolecularlandscapeofAMLandidentifiedseveralsomaticalterationsthatimpactoverallsurvival.Despitealltheseadvancement,severalchallengesremainintranslatingthisinformationintoeffectivetherapy.HereinwewillreviewthemolecularlandscapeofAMLanddiscusstheimpactofthemostcommonsomaticmutationsondiseasebiologyandoutcome.

简介：Objective:Ki-67playsanimportantfunctionincelldivision,butitsexactroleisstillunknown.Moreover,fewworksregardingitsoverallfunctionwerepublished.ThepresentstudyevaluatedtheclinicalsignificanceofKi-67indexasaprognosticmarkerandpredictorofrecurrenceindifferentmolecularsubtypesofbreastcancer.TherelationshipofKi-67indexwithdifferentclinicopathologicalfactorswasalsoanalyzed.Methods:Ki-67indexwasmeasuredin107casesofprimarybreastcancerfrom2010-2012.Thesepatientswereevaluatedforestrogenreceptor,progesteronereceptor,andHER2.Ki-67wasdividedaccordingtopercentagelevels:<15%and>15%.Followuprangedfrom32monthsupto6years.Results:Approximately44,23,15,and25casesweregroupedasluminalA,luminalB,HER2subtype,andtriple-negative(TN),respectively.NoluminalApatientsshowedKi-67levelhigherthan15%,andtheirrecurrencewas20%.InluminalBgroup,Ki-67levelhigherthan15%wasobservedin69%ofpatients,andrecurrencewas39%.InHER2subtype,Ki-67washigherthan15%in34%ofcases,andrecurrencewas40%.Intriple-negativecases,Ki-67washigherthan15%in60%ofcases,andrecurrencewasdetectedin32%ofpatients.PatientswithKi-67lessthan15%displayedbetteroverallsurvivalthanthosewithKi-67higherthan15%(P=0.01).PatientswithKi-67higherthan15%exhibitedhigherincidenceofmetastasisandrecurrencethanthosewithKi-67lessthan15%(P=0.000).Conclusions:Ki-67maybeconsideredasavaluablebiomarkerinbreastcancerpatients.

简介：变形乳癌(MBC)被肿瘤生长，增长和变形前进的联合描绘并且典型地与辩解的目的被管理。标准全身的治疗的利益是相对有限的，疾病被认为医不好建议需要调查变形过程的各种各样的阶段的生物司机以便改进分子地驾驶的治疗的选择。察觉，枚举和传播肿瘤房间(CTC)的分子的分析提供一个吸引人的机会推进这知识。食物和药变清管理的CellSearch系统枚举的CTC在MBC病人是没有前进的幸存(PFS)和全面幸存(OS)的一个独立预示的因素。几份出版报纸为介绍了在血的7.5mL的基础CTC计数5的MBC病人表明了差的预后。因此，CTC的枚举在为MBC的治疗期间向一个工具提供比用常规放射学的测试的解剖评价的标准预定早预言疾病的前进的能力。在词法的变形过程癌症房间展览和phenotypic粘性经历epithelialmesenchymal转变(EMT)期间。这重要现象与被联系在上皮的标记的规定下面(例如，EpCAM)与在当前的CTC丰富方法的适用性的潜在的限制。在很多调查翻译的如此的观察瞄准了改进我们的能力枚举并且表现CTC的分子的描述。理论上，CTC的phenotypic分析能代表能对变形疾病识别一个新潜在的目标并且推进发展并且个性化的治疗监视的胸肿瘤的液体活体检视。

简介：Gastrointestinal(GI)cancerisoneofthemostcommoncausesofcancer-relateddeathsworldwide.Tumormarkersarevaluableindetectingpost-surgicalrecurrenceorinmonitoringresponsetochemotherapy.PyruvatekinaseisoformM2(PKM2),aglycolyticenzymecatalyzingconversionofphosphoenolpyruvate(PEP)topyruvate,confersagrowthadvantagetothetumorcellsandenablesthemtoadapttothetumormicroenvironment.Inthisreview,wehavesummarizedcurrentresearchontheexpressionandregulationofPKM2intumorcells,anditspotentialroleinGIcarcinogenesisandprogression.Furthermore,wehavealsodiscussedthepotentialofPKM2asadiagnosticandscreeningmarker,andatherapeutictargetinGIcancer.

简介：Precisionmedicineandpersonalizedtherapyarereceivingincreasedattention,andmolecular-subtypeclassificationhasbecomecrucialinplanningtherapeuticschedulesinclinicalpracticeforpatientswithbreastcancer.Humanepidermalgrowthfactorreceptor2(HER2)isassociatedwithhigh-gradebreasttumors,highratesoflymph-nodeinvolvement,highriskofrecurrence,andhighresistancetogeneralchemotherapy.AnalysisofHER2expressionishighlyimportantfordoctorstoidentifypatientswhocanbenefitfromtrastuzumabtherapyandmonitortheresponseandefficacyoftreatment.Inrecentyears,significanteffortshavebeendevotedtoachievingspecificandnoninvasiveHER2-positivebreastcancerimaginginvivo.Inthiswork,wereviewedexistingliteratureonHER2imaginginthepastdecadeandsummarizedthestudiesfromdifferentpointsofview,suchasimagingmodalitiesandHER2-specificprobes.WeaimedtoimprovetheunderstandingonthetranslationalprocessinmolecularimagingforHER2breastcancer.

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简介：TheroleofthetranscriptionfactorNF-κBinshapingthecancermicroenvironmentisbecomingincreasinglyclear.InflammationalterstheactivityofenzymesthatmodulateNF-κBfunction,andcausesextensivechangesingenomicchromatinthatultimatelydrasticallyaltercell-specificgeneexpression.NF-κBregulatestheexpressionofcytokinesandadhesionfactorsthatcontrolinteractionsamongadjacentcells.Assuch,NF-κBfinetunestissuecellularcomposition,aswellastissues'interactionswiththeimmunesystem.Therefore,NF-κBchangesthecellresponsetohormonesandtocontactwithneighboringcells.ActivatingNF-κBconferstranscriptionalandphenotypicplasticitytoacellandtherebyenablesprofoundlocalchangesintissuefunctionandcomposition.ResearchsuggeststhattheregulationofNF-κBtargetgenesisspecificallyalteredincancer.SuchalterationsoccurnotonlyduetomutationsofNF-κBregulatoryproteins,butalsobecauseofchangesintheactivityofspecificproteostaticmodulesandmetabolicpathways.ThisarticledescribesthemolecularmodeofNF-κBregulationwithafewcharacteristicexamplesoftargetgenes.