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·研写TheIntroduction•–Whatdidyou·研写TheIntroduction•–Whatdidyou•Whatdidyou科研论文四部分,主要内容有哪些•Whatdoyourfindings •–Whydidyoudothe–Whatwasyourhypothesisor本课内·本课内·研写••••Introduction写作顺·研写inIntroduction写作顺·研写in·研写·研写Settingthe(策略性)长度——10-15%oftheIntroduction包括的内·研Introduction包括的内·研写GapinHypothesis/purposestatementStrategyfortestinghypothesisorachievingpurpose123,·研·研写·研写Gapin·研写Gapin•从已知到未知强调填补这个gap的重要“However,wedonotknowwhateffectthistreatmentwillhaveonpatientswithstageIV“Whetherthesefindingswilltranslatetotheclinicalsettingisnotknown.”“Paststudiesofthisissuehaveresultedinconflictingfindings.”“Sofar,onlyqualitativefindingshavebeen“However,littleisknownaboutthelong-termimpactoncellfunctionsofraisedlevelsofAlthoughseveralstudieshaveassociatedQRSexpressionwithcolorectaladenocarcinoma,thedirecteffectsofQRSonestablishedcolorectalcancershavenotbeendetermined.AnunderstandingofhowQRScontributestotumorigenicityincolorectalcancercellsmayenableitsuseasaprognosticfactororeventherapeutic•••••••·研写·研写出现的三地方——introduction,abstract,In“WehypothesizedthattheRb-E2F1pathwayisoneofthecriticaltumor-suppressor/oncogenepathwaysinvolvedinregulatingtelomeraseexpressionandactivityinglioblastoma.”In“WefoundthattheRb-E2Fpathwayisinvolvedinregulatingtelomeraseexpressionandactivityincancerandnormalcells...”实验方实验方·研写“WeidentifiedthesequencesdownstreamfromtheTATAboxinbasalHypothesisInthisstudy,wetestedthehypothesisthatvariationsinothermembersoffibulingenefamilyareinvolvedinthepathogenesisofmaculardegenerationbyexaminingthecodingsequencesofthegenesforfibulin1,2,4,5,and6inmorethan400patientswithage-relatedmaculardegeneration.·研写·研写Totestthishypothesis,weexaminedB-celllymphomasthatcarriedspecificchromosomaltranslocations.Ineachcase,avaryingproportionofthemicrovascularendothelialcellsofthelymphomaexhibitedthelymphoma-specificgeneticaberration,suggestingacloserelationshipbetweenthetwotypesofcells.·研写Known·研写Known(generalto1Includeonlyenoughbackgroundtomakethereasonforthestudy23Organizetheinformationlikeafunnel,fromgeneralto·研写Gap·研写Gapin••Untilnow,ithasnotbeenpossibletoHowever,wedonotknowwhateffectthistreatmentwillhaveon...Therehasbeensomedisagreement,however,inthefindingswiththismodel...Sofar,onlyqualitativefindingshavebeenBecauseoftherarityofthiscancer,ithasbeendifficulttodeterminesurvivalrateswithstatisticalcertainty...•••·研写·研写•••Thepurposeofourstudywastodetermine...Wehypothesizedthat...Ourhypothesiswas·研写·研写••WetestedourhypothesisbyTodothis,weused...andanalyzed...inaninsitu·研写·研写••Overall,ourfindingsthat…Inthisstudy,wefound·研写TheriskofcancercanbesignificantlyincreasedbydisruptionofgenomicintegrityresultedfromdysfunctionalDNAdamageresponsesignalingand/oraberrantactivityofthekeycomponentsintheDNArepairpathways.TheDNArepairmachineriesworkconstantlytoremovenumerousDNAlesionscausedbychemotherapeuticagentssuchascisplatin,whichcontributestodrugresistanceinmanycancers.Asresistancetostandardcisplatin-basedchemotherapybecomesafrequentphenomenon,cancertreatmenttargetingimportantcomponentsintheDNArepairpathwaysemergestobeanimminentandcompellingtask.RDM1(RAD52motif1,orRDmotif)isinvolvedincellularresponsetocisplatin,andshowssimilaritiestoRAD52,akeyregulatorinDNArecombinationandrepair,wheretheRDmotifofRDM1functionallyresemblestheN-terminalregionofRAD52[1-3].Importantly,RDM1–/–cellsexhibitedincreasedsensitivitytocisplatin[4].Moreinterestingly,ourinitialcomprehensivebioinformaticsexplorationinmultipleOncomineexpressiondatasetshasalsoidentifiedRDM1asoneofthesignificantlyup-regulatedproteinsinhumanlungadenocarcinoma.Despitethesediscoveries,however,todate,littleisknownregardingtheroleofRDM1inhumancancer.GiventhepotentialroleofRDM1intheDNArepairpathwaysthatconstituteanimportantaspectofcancerinitiationandprogression,weproposethatRDM1maydisplayoncogenicpropertiesanddrivetumorigenesis.·研写Lungcancerisaleadingcauseofcancerdeaths,andremainsoneoftherefractorycancertypes.Adenocarcinomaaccountsfor40%ofalllungcancers.Thefive-yearsurvivalrateoflungcanceristhelowestamongthemajorcancers,includingcolon,breast,andprostatecancers[5].Evenwithmajorclinicalinterventions,suchassurgery,radiationtherapy,chemotherapy,targetedcancertherapy,andimmunotherapy,thesurvivalratehasnotbeenimprovedsignificantly,andlingersatonly15%withinfiveyearsoftreatment[6].TheclinicalstagingoflungcancersfollowstheTNMclassificationsystem,wherethedeterminingfactorsinclude:thesizeoftheprimarytumor(T),theeffectsontheregionallymphnodes(N),andthedistantmetastaticstatus(M).Recentyearshavewitnessedsomesuccessintargetedtherapiesforparticularmutationsinlungadenocarcinoma,suchasthoseinEGFRandALK,andthesestrategieshavebeenapprovedforuseasfirst-linetreatmentinadenocarcinoma[7-9].Conceptually,investigationofthemutationallandscapeinlungadenocarcinomawillhelpidentifynewtargetswhichcanbeenlistedtothegrowingbiomarkerpanelthatmayassistwiththediagnosis.Asaresult,itisimperativetouncovermorenovelmolecules,whichwillbebeneficialtothetreatmentanddiagnosisoflungadenocarcinoma.·研写Inthisstudy,wefoundthatRDM1isup-regulatedinclinicallungadenocarcinomasamplesasrevealedbyIHCstaining.Significantly,up-regulationofRDM1iscorrelatedwithpoorclinicalcharacteristicsandriskfac
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