@Article{, title={Association of T315I mutation with resistance to tyrosine kinaseinhibitor therapy in patients with CML attended theOncology-Hematology center in Al-Najaf city of Iraq}, author={Rahem Mahdy Rahema,*, Adel Abdulhussien Abuhmoodb, Luwaa Husseinc}, journal={Karbala International Journal of Modern Science مجلة كربلاء العالمية للعلوم الحديثة}, volume={3}, number={4}, pages={231-240}, year={2017}, abstract={Background:Notwithstanding the tremendous achievement of imatinib against BCR-ABL, development of primary or secondaryresistance, most often because of point mutations in the BCR-ABL tyrosine kinase domain, is pretty commonplace. Among thesemutations, the most frequent mutation, T315I mutation, is resistant to all presently registered BCR-ABLTyrosine Kinase Inhibitors(TKIs) with the notable exception of ponatinib.Aims:Evaluation the etiological association of T315I mutation with the failure or warning molecular responses of our chronicmyeloid leukemia (CML) patients to Tyrosine Kinase Inhibitors (TKIs) in keeping to national and international guideline formolecular monitoring.Patients, materials and methods:This was a retrospective observational case control study of CML patients who attended theOncology-Hematology center in Al-Najaf city, performed during a period from April 2015 to April 2016. Medical information hasbeen reviewed for treatment response and the outcomes of serial measurements of BCR-ABL transcripts levels through RT-qPCRare accrued. Iraqi guideline based on international European Leukemia Net (ELN) 2013 guiding principle had been employed toevaluate the molecular response to TKI. Venous blood samples have been taken for detection of T315I mutation in eligibleregistered patients.Results:A total of fifty patients eligible for the study have been included out of 72 registered patients, 24 (48%) patients have beenresistant while 26 (52%) were responding to TKIs treatment. T315I mutation turned into detected in 4/24 (16.7%) of resistantpatients. The proportion of patients with T315I mutation were higher than that of control group, with a significant risk association todevelop resistance to TKI therapy (odd ratio 2.3, C.I.¼1.654e3.198).

} }