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简介：Ovariancanceristhesecondmostlethalgynecologicalcancerworldwideandwhilemostpatientsrespondtoinitialtherapy,theyoftenrelapsewithresistantdisease.Humanepidermalgrowthfactorreceptors(especiallyHER1/EGFRandHER2/ERBB2)areinvolvedindiseaseprogression;hence,strategiestoinhibittheiractioncouldproveadvantageousinovariancancerpatients,especiallyinpatientsresistanttofirstlinetherapy.Monoclonalantibodiesandtyrosinekinaseinhibitorsaretwoclassesofdrugsthatactonthesereceptors.Theyhavedemonstratedvaluableantitumoractivityinmultiplecancersandtheirpossibleuseinovariancancercontinuestobestudied.Inthisreview,wediscussthehumanepidermalgrowthfactorreceptorfamily;reviewemergingclinicalstudiesonmonoclonalantibodiesandtyrosinekinaseinhibitorstargetingthesereceptorsinovariancancerpatients;andproposefutureresearchpossibilitiesinthisarea.

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简介：作为一个内部应用的反煽动性的代理人，Escin广泛地在从损伤或操作导致诊所的发炎和浮肿的治疗被使用了。然而，它皮肤的发炎和浮肿上的外部使用的效果仍然保持未经勘探。在现在的学习，反煽动性并且escin的外部使用的anti-edematous效果在老鼠，在老鼠胀大的导致paraxylene的耳朵，和棉花在导致carrageenan的爪浮肿和导致组织安的毛状的渗透被学习在老鼠的导致小团的granuloma。前列腺素E2(PGE2)上的escin胶化的外部使用的效果，肿瘤坏死因素--(TNF-)，并且interleukin-1(IL-1)被ELISA决定。反煽动性的机制被与西方的弄污和实时PCR分析检测glucocorticoid受体(GR)的表示探索，与原子factor-B(NF-B)的进一步的探索，p38激活mitogen的蛋白质kinase(P38MAPK)和使活跃之物protein-1(AP-1)表情。我们证明escin的外部使用证明在不同动物模型的尖锐、长期的发炎上的重要反煽动性的效果和它的反煽动性的效果可能与PGE2，TNF-，和IL-1的下面规定有关。结果也证明escin由支持GR的表示施加了它的反煽动性的效果，与是的可能的机制象NF-B和AP-1那样的GR相关的发信号的分子的表情的抑制。

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简介：Objective:Therecurrenceorprogressionunderendocrinetherapyinhormonereceptor-positive(HR+)advancedbreastcancer(ABC)remainedacriticalclinicalchallenge.Chidamideisanoralsubtype-selectivehistonedeacetylase(HDAC)inhibitorwithmultiplefunctionsintumorgrowthinhibitionandmicroenvironmentmodulationviaepigeneticreprogramming.Thepurposeofthisstudywastoevaluatethesafety,pharmacokinetics(PK),andpreliminaryefficacyofchidamideincombinationwithexemestaneinHR+ABCpatients.Methods:EligiblepatientswerepostmenopausalwomenwithHR+ABCrecurrentorprogressedtoatleastoneendocrinetherapy.Bloodsampleswereobtainedintherun-inperiodandthefirstdayofcombinationtreatmentforPKanalysis.Incombinationtreatment,patientsweregivenexemestane25mgdailyandchidamide30mgtwiceaweek(BIW)untilprogressionofdiseaseorintolerabletoxicities.Atreatmentcyclewasdefinedas4weeks.Safety,PKparameters,andpreliminaryefficacywereevaluated.Results:Atotalof20patientswereenrolledbetweenJulyandDecember,2015.Themediannumberoftreatmentscyclewas5.2(20.8weeks)with2patientsstillontreatmentatthedatacut-offdateofOctober,2017.Thetreatment-relatedadverseevents(AE)≥grade3inmorethan2patientswereneutropenia(35%),thrombocytopenia(30%),andleucopenia(20%).Theplasmaexposureofexemestanewasconsistentinthepresenceorabsenceofchidamide.Aslightincreaseinchidamideexposurewasnotedinthepresenceofexemestane,probablyduetotheinter-andintra-patientvariations.Thebestresponsein16evaluablepatientswasassessedbyResponseEvaluationCriteriainSolidTumors(RECIST),including4patientswithpartialresponse,10patientswithstabledisease.Themedianprogression-freesurvival(PFS)was7.6months.Conclusions:ThecombinationofchidamidewithexemestanewasgenerallywelltoleratedwithpromisingpreliminaryefficacyinHR+ABCpatients.Theoverallresultsfromthisstudyencouragefurtherpivotaltrialinthispatie