EML4-ALK融合基因在非小细胞肺癌中的研究进展

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Research progress on the EML4-ALK fusion gene in non-small cell lung cancer ： molecular mechanisms and targeted therapies

Sun Mengxue1， Wang Min2** ，Miao Qing1 1Shandong Universityof Traditional Chinese Medicine，Jinan 250o14；²Departmentof Respiratoryand Critical Care， theSecond Affiliated Hospital of Shandong University of Traditional Chinese Medicine，Jinan250001 ** Corresponding author：Wang Min，email；13012996221@ 163.com

[Abstract]LungcancerisamalignantneoplasmcharacterizedbyahighincidenceandfatalityrateglobalyNon-smallcel lung cancer（NSCLC） constitutes 85 % of lung cancer cases.The advancement of molecular biotechnology and tailored therapeutics has usheredNSCLCtreatmentintotheeraofprecisionmedicine.Thechinodermmicrotubulesociatedproteinlike4（EML4）-anaplasticlymphomakinase（ALK）fusiongeneisatargetforpersonalizedtherapyinNSCLC.ALKinhibitorsexibitsubstantialtrapeutic ficacy.Nonethes，urmountingugistancehasonsisentlposedasignificatbaerthatwarantsatention.entifngnovel therapeutictargetsandemployingcombinatiomedicationtherapisaecrucialforefingsubsequnttreatmentstrategiesadsssing overallprogosisIntemanagementofatientswithE4-LKgnefusioniisimperativetreglarlymoitortumorprsio whileadministeringtargetedtherapies，andtotimelymodifythetherapyregimenbasedonthepatient’sstatetoensurelong-tebene fits.ThisarticleelaboratesonrecentadvancementsinresearchconcerningthEML4-ALKfusiongene，focusingonitsclinicalpatho logicalattributestargetedphamacologicalinvestigations，mechanismsoftreatmentresistance，andprospectivenoveltargets.

[Key words]Non-smallcellung cancer；EML4-ALK fusiongene；Clinicopathologicalcharacteristics；Drugresistance mechanism； Therapeutic targets

肺癌的全球死亡率一直居于首位，也是我国恶性肿瘤发病和死亡的首要原因[]。（剩余19117字）