简介：AbstractBrain metastasis (BM) is the leading cause of mortality in lung cancer patients. The process of BM (from initial primary tumor development, migration and intravasation, dissemination and survival in the bloodstream, extravasation, to colonization and growth to metastases) is a complex process for which few tumor cells complete the entire process. Recent research on BM of lung cancer has recently stressed the essential role of tumor microenvironment (TME) in assisting tumor cells in the completion of each BM step. This review summarizes recent studies regarding the effects of TME on tumor cells in the entire process of BM derived from lung cancer. The identification of vulnerable targets in the TME and their prospects to provide novel therapeutic opportunities are also discussed.

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简介：表明小径的TGF尾从苍蝇被保存到人并且被显示了调整象房间增长，区别，活动性，粘附，组织，和规划房间死亡的如此的多样的过程。在vitro并且在vivo，实验建议TGF尾能利用这些改变的程序在有免疫力的房间功能的肿瘤微型环境，提高的侵略性质，和抑制上通过它的效果支持癌症转移。表明在TGF尾发信号和癌症前进之间的一个连接的最近的临床的证据作为一个治疗学的目标在这条发信号的小径正在培养兴趣。Anti-TGF尾治疗当前在现出症状之前的潜的研究正在被开发并且测试。当这条小径在多重homeostatic过程被含有并且也被知道有tumor-suppressor功能，然而，指向TGF尾带实质的风险。另外，临床、试验性的结果证明TGF尾甚至在一样的肿瘤类型以内在肿瘤前进有多样、经常冲突的角色。为临床的使用的TGF尾禁止者的发展将要求TGF尾在它在哪个行动发信号，它的后果，和上下文的更深的理解。

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简介：Non-smallcelllungcancer(NSCLC)ranksastheleadingcauseofcancer-relateddeathintheworld.Brainmetastasis(BM)isacommoncomplicationofNSCLC,with25%–40%ofpatientsdevelopingBMduringthecourseofthedisease.Asignificantstrategyoflocaldiseasecontrolinthecentralnervoussystemisradiationtherapy.Withthedevelopmentofprecisionmedicine,theconceptoftreatinglungcancerBMhasgraduallychanged.Inthiscase,weperformedasurgicalproceduretoobtainenoughtumortissueforthedetectionofthetargetgeneandotherrelatedexperimentsafterthepatientwasinformed.Finally,wefoundthatthepatienthadbothhepatocytegrowthfactorreceptor(MET)geneamplificationandkinesinlightchain1-anaplasticlymphomakinasefusion(KLC1-ALK)throughnext-generationsequencingandshowedsensitivitytothetargetedtherapyofcrizotinib.Thepatientexhibitedgoodresponse.Ourcasewassuccessfulandunderwenttargetedtherapywiththeguidanceofprecisediagnosis.

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简介：Tumormetastasisisthedominantcauseofdeathincancerpatients.However,themolecularandcellularmechanismsunderlyingtumormetastasisarestillelusive.Theidentificationofproteinmoleculeswiththeirexpressionscorrelatedtothemetastaticprocesswouldhelptounderstandthemetastaticmechanismsandthusfacilitatethedevelopmentofstrategiesforthetherapeuticinterventionsandclinicalmanagementofcancer.Proteomicsisasystematicresearchapproachaimingtoprovidetheglobalcharacterizationofproteinexpressionandfunctionundergivenconditions.Proteomictechnologyhasbeenwidelyusedinbiomarkerdiscoveryandpathogeneticstudiesincludingtumormetastasis.Thisarticleprovidesabriefreviewoftheapplicationofproteomicsinidentifyingmolecularfactorsintumormetastasisprocess.Thecombinationofproteomicswithotherexperimentalapproachesinbiochemistry,cellbiology,moleculargeneticsandchemistry,togetherwiththedevelopmentofnewtechnologiesandimprovementsinexistingmethodologieswillcontinuetoextenditsapplicationinstudyingcancermetastasis.

简介：OurpreviousstudyshowedthattwoMKN45variants,namelyMKN45Lm-andMKN45Lm+selectedbylamininadhesioninvitro,haddifferentabilitiesofinvasionandmetastasisinvivo(inoculatedinnudemice)andinvitro(inBoydenchamber),alsohaddifferentexpressionofcysteineproteinase.Inthepresentstudy,weinvestigatedthecellapoptosisofthisMKN45variantsbyTUNELandFACSmethods.Theresultswereshownsignificantdifferentofcellapoptosisinthiscellsublines.TheMKN45Lm-cellshadasmallsubdiploidypeak(3.5%)inDNAcontentanalyzedbyflowcytometry,

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简介：Traumaticbraininjury(TBI)istheleadingcauseofdeathanddisabilityofpersonsunder45yearsoldintheUnitedStates,affectingover1.5millionindividualseachyear.Ithadbeenthoughtthatrecoveryfromsuchinjuriesisseverelylimitedduetotheinabilityoftheadultbraintoreplacedamagedneurons.However,recentstudiesindicatethatthematuremammaliancentralnervoussystem(CNS)hasthepotentialtoreplenishdamagedneuronsbyproliferationandneuronaldifferentiationofadultneuralstem/progenitorcellsresidingintheneurogenicregionsinthebrain.Furthermore,increasingevidenceindicatesthattheseendogenousstem/progenitorcellsmayplayregenerativeandreparativerolesinresponsetoCNSinjuriesordiseases.Insupportofthisnotion,heightenedlevelsofcellproliferationandneurogenesishavebeenobservedinresponsetobraintraumaorinsultssuggestingthatthebrainhastheinherentpotentialtorestorepopulationsofdamagedordestroyedneurons.Thisreviewwilldiscussthepotentialfunctionsofadultneurogenesisandrecentdevelopmentofstrategiesaimingatharnessingthisneurogeniccapacityinordertorepopulateandrepairtheinjuredbrain.

简介：Althoughthyroidcarcinomaisarelativelycommonformofmalignancy,metastaticspreadtotheskullisrare.Here,wereportacaseofpapillarythyroidcarcinomawithfrontalandparietalmetastasis.A61-year-oldChinesewomanpresentedwithaoneyearhistoryofagrowingmassonthecenterofthefrontalandparietalbone,initiallythoughttobemeningioma.Biopsyoftheskullbasemassafterintracalvariumexcision,indicatedatumorofthyroidorigin.Onemonthlaterthepatientunderwentatotalthyroidectomy.Pathologicalexaminationconfirmedadiagnosisofpapillarythyroidcarcinomawithfrontalandparietalbonemetastasis.Basedonthisexperience,thekeytosuccessfulmanagementoftheskullmetastasisofthyroidcarcinomaispromptdiagnosisandappropriatetreatment.Skullmetastasisshouldbeconsideredattheoutsetoftheclinicalcourseofpapillarythyroidcancer.Tofacilitatethis,patientsshouldbemeticulouslyinvestigatedbyamultidisciplinaryteamtoimprovequalityoflife.

简介：在肿瘤开始的癌症干细胞(CSC)的重要性坚定地在白血病被建立了并且最近为许多稳固的肿瘤报导了。然而，特别地关于转移，在多级式的癌症前进的CSC的角色有不定义beenwell。癌症转移要求在远机关播种和specializedCSCs的成功的殖民。正常干细胞和CSC的生物学分享显著类似并且当适用于癌症的学习时，可以有重要含意转移。而且，重叠分子和小径的集合最近被识别了调整干细胞移植和癌症转移。这些分子组成两个都为移植CSC由主要肿瘤和养育的机关微型环境的形成便于转移前壁龛的开始的细胞的相互作用的一个复杂网络。在这评论，我们在这个动态领域里调查了最近的进展并且建议CSC在tumorigenesis和转移在假定一个中央角色的癌症前进的一个统一模型。更好作为变形串联的一个基本部件理解ofCSCs将对变形癌症导致新奇治疗学的策略。

简介：Objective:Tostudythecorrelationbetweenbrainedema,elevatedintracranialpressure(ICP)andcellapoptosisintraumaticbraininjury(TBI).Methods:Inthisstudy,totally42rabbitsin7groupswerestudied.Sixoftheanimalswereidentifiedasacontrolgroup,andtheremaining36animalswereequallydividedinto6TBIgroups.TBImodelswereproducedbythemodifiedmethodofFeeney.Aftertheimpact,ICPofeachsubjectwasrecordedcontinuouslybyanICPmonitoruntiltheanimalwassacrificedatscheduledtime.Theapoptoticbraincellsweredetectedbyanterminaldeoxynucleotide-transferase-mediateddUTP-digoxigeninnickendlabeling(TUNEL)assay.Cerebralwatercontent(CWC)wasmeasuredwithadryingmethodandcalculatedaccordingtotheElliottformula.Then,ananalysiswasconductedtodeterminethecorrelationbetweenthecountofapoptoticcellsandtheclinicalpathologicalchangesofthebrain.Results:Apoptoticcellcountbegantoincrease2haftertheimpact,andreacheditsmaximumabout3daysaftertheimpact.ThepeakvalueofCWCandICPappeared1dayand3daysaftertheimpact,respectively.ApoptoticcellcounthadapositivecorrelationwithCWCandICP.Conclusions:InTBI,occurrenceofbrainedemaandICPincreasemightleadtoapoptosisofbraincells.Anytherapywhichcanrelievebrainedemaand/ordecreaseICPwouldbeabletoreduceneuronapoptosis,therebytoattenuatethesecondarybraindamage.