Tib neeg EML4-ALK Fusion Gene Mutation

Cov khoom siv no yog siv los soj ntsuam 12 yam kev hloov pauv ntawm EML4-ALK fusion gene hauv cov qauv ntawm tib neeg cov neeg mob ntsws cancer hauv vitro.Cov txiaj ntsig kev xeem no tsuas yog siv rau kev kho mob nkaus xwb thiab yuav tsum tsis txhob siv los ua ib lub hauv paus rau kev kho tus kheej ntawm cov neeg mob.Cov kws kho mob yuav tsum txiav txim siab tag nrho ntawm cov txiaj ntsig kev xeem raws li cov xwm txheej xws li tus neeg mob tus mob, cov tshuaj qhia tshuaj, cov lus teb rau kev kho mob, thiab lwm yam ntsuas ntsuas ntsuas.Mob ntsws cancer yog cov qog qog nqaij hlav ntau tshaj plaws thoob ntiaj teb, thiab 80% ~ 85% ntawm cov neeg mob tsis yog mob qog noj ntshav me me (NSCLC).Gene fusion ntawm echinoderm microtubule-associated protein-zoo li 4 (EML4) thiab anaplastic lymphoma kinase (ALK) yog lub hom phiaj tshiab hauv NSCLC, EML4 thiab ALK raws li nyob rau hauv tib neeg P21 thiab P23 bands ntawm chromosome 2 thiab sib cais los ntawm kwv yees li 12.7. lab puag khub.Yam tsawg kawg 20 fusion variants tau pom, ntawm cov 12 fusion mutants hauv Table 1 yog qhov ntau, qhov mutant 1 (E13; A20) yog qhov ntau tshaj plaws, ua raws li mutants 3a thiab 3b (E6; A20), suav txog txog 33% thiab 29% ntawm cov neeg mob nrog EML4-ALK fusion gene NSCLC, feem.ALK inhibitors sawv cev los ntawm Crizotinib yog cov tshuaj me me-molecule tsom rau tsim rau ALK noob fusion hloov pauv.Los ntawm inhibiting qhov kev ua ntawm ALK tyrosine kinase cheeb tsam, thaiv nws downstream txawv txav kev taw qhia txoj kev, yog li inhibiting kev loj hlob ntawm cov qog hlwb, kom ua tiav cov hom phiaj kho rau cov qog.Cov kev tshawb fawb soj ntsuam tau pom tias Crizotinib muaj qhov ua tau zoo ntawm ntau dua 61% hauv cov neeg mob uas muaj EML4-ALK fusion hloov pauv, thaum nws yuav luag tsis cuam tshuam rau cov neeg mob qus.Yog li, kev tshawb pom ntawm EML4-ALK fusion kev hloov pauv yog lub hauv paus thiab lub hauv paus rau kev taw qhia kev siv tshuaj Crizotinib.