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

简介：Glioblastoma(GBM)isoneofthedeadliesttumorsandhasamediansurvivalof3monthsifleftuntreated.Despiteadvancesinrationallytargetedpharmacologicalapproaches,theclinicalcareofGBMremainspalliativeinintent.Sincethemajorityofalteredsignalingcascadesinvolvedincancerestablishmentandprogressioneventuallyaffectcellcycleprogression,analternativeapproachforcancertherapyistodevelopinnovativecompoundsthatblocktheactivityofcrucialmoleculesneededbytumorcellstocompletecelldivision.Inthiscontext,wereviewpromisingongoingandfuturestrategiesforGBMtherapeuticsaimedtowardsG2/Minhibitionsuchasanti-microtubuleagentsandtargetedtherapyagainstG2/Mregulatorslikecyclin-dependentkinases,Aurorainhibitors,PLK1,BUB,1,andBUBR1,andsurvivin.Moreover,wealsoincludeinvestigationalagentsinthepreclinicalandearlyclinicalsettings.Althoughseveraldrugswereshowntobegliotoxic,mostofthemhavenotyetenteredtherapeutictrials.TheuseofeithersingleexposureoracombinationwithnovelcompoundsmayleadtotreatmentalternativesforGBMpatientsinthenearfuture.

简介：Inordertoimprovethestabilityandcorrosioninhibitionperformanceofbioenzyme,lipaseandlsozymewereco-immobilizedonthemesoporousmolecularsieveMCM-41bytheadsorptionmethod.Thentheimmobilizedenzymeswerecombinedwithaminotrimethylenephosphonicacidandpolyasparticacidtopreventcorrosioncausedbycirculatingcoolingwater.Theweight-lossmethodandelectrochemicaltechniqueswereusedtoevaluatetheperformanceofcompositeinhibitors.Theco-immobilizedlysozymeandlipaseachievedgoodinhibitioneffects.Aftertheywerecombinedwithaminotrimethylenephosphonicacidandpolyasparticacid,thecorrosioninhibitionpropertieswerefurtherimproved.Theinhibitionefficiencywaspromotedto94.4%.Duringthecorrosioninhibitionprocess,theimmobilizedenzymesplayedanimportantrole.Theadditionofcorrosioninhibitorcouldinhibittheanodicdissolutionandcathodichydrogenevolutionprocessofcarbonsteelatthesametime.Theadsorptionofco-immobilizedlysozymeandlipasecompositeinhibitoronthesteelsurfacewasajointactioninvolvingphysicaladsorptionandchemicaladsorption.

简介：Chemokine12(CXCL12)，也作为stromal知道房间导出factor-1(SDF-1)和CXCchemokine亚科的一个成员，无所不在地在许多纸巾和房间类型被表示。它为transmembraneG联合蛋白质的受体CXCR4和CXCR7与ligand明确地交往。CXCL12/CXCR4轴参加一系列生理、生物化学、病理学的过程，例如发炎和白血球trafficking，导致癌症的骨头疼痛，和postsurgical伤害，并且也是在在肿瘤房间和他们的微型环境之间的cross-talking的一个关键因素。CXCR4的异常overexpression为肿瘤幸存，增长，angiogenesis，homing和转移是批评的。在这评论，我们在癌症，在临床的学习下面的CXCR4禁止者，和自然产品CXCR4对手总结了CXCL12/CXCR4的角色。在结论，发信号的CXCL12/CXCR4为肿瘤开发是重要的并且指向小径可能代表一条有效途径到在癌症治疗开发新奇治疗。