NU ene — | srxcesea | soncesca Human BCR-ABL Gene T3151 Mutation Detec (Real-Time PCR assay) @® cenemutarion ano cme (Chronic myo leukemia (CML accounts for 15% ~ 209 ofa Iukemia More than 95% of CM patents have ch ‘usion genes. imatinib (IN) a stine druglor the treatment of CML With the progses ofthe dseae course, almost sn aeate phate and 1584 ~ 20% of (ML relapsed after IM treatment developed resistance o IM, and the occurence aff ‘elated to BCR-ABL gene mutation, Among them almost all patents with T3151 point mutation were resistant to exist “The guideline recommends tha frequent and long-term fterruption of TKI retment and poor mediation compliance to adverse clinical results. Patients with poor fisttine TKI tolerance shoulé replace TKI in time Patients with _BOR-ADLgene are resistant to Dasatinib and oti 2CR-Aal gare tslenThe tonslacoton a chromosomes and 22 zona » lod tothe sion of ABLond BCR genes. oe the ose kinase sce” BA ‘le SCR-ABL on generelecs cell pofeaton sero > Indefiitely to promate hanar formation 909432 aw i. oe Ve) % The necesiy of detecting T3151 mutationin BCR-ABL fusion locus : NS . > hp oy DNA hele Bose sequence <_ "T3151 mutation [caused by she substiuton of threonine (THR) at paston 315 of exon 6 of ABLI gene by isoleucine (1 ‘hanged from ACT t ATT. After mutation, He315 canot form hyérogen bond with IM. and the ational hyrocarbon -substtated le sde chain wil prac spatial interfrenc, which mot condicv to IM binding, eign drug resi ‘the detection result of T215 mutation of BCR-ABL gene san important index to guide the medication of CML patients,