RT Journal Article SR Electronic T1 Phe354Leu Polymorphism of LKB1 Is a Potential Prognostic Factor for Cytogenetically Normal Acute Myeloid Leukemia JF In Vivo JO In Vivo FD International Institute of Anticancer Research SP 841 OP 847 VO 31 IS 5 A1 MING-YU YANG A1 HUI-HUA HSIAO A1 YI-CHANG LIU A1 CHENG-MING HSU A1 SHENG-FUNG LIN A1 PAI-MEI LIN YR 2017 UL http://iv.iiarjournals.org/content/31/5/841.abstract AB Background/Aim: Liver kinase B1 (LKB1) is a major activator of the AMP-dependent kinase/mammalian target of rapamycin pathway. The prevalence and the specificity of LKB1 gene mutation in acute myeloid leukemia (AML) have not been well established. This study aimed to examine mutation of LKB1 in AML and its clinical and pathological implications. Patients and Methods: Eighty-five patients newly diagnosed with cytogenetically normal AML were analyzed using polymerase chain reaction followed by direct sequencing. Results: A silent mutation (837C>T) of LKB1 was detected in one patient and a pathogenic polymorphism Phe354Leu which diminishes LKB1 ability to maintain cell polarity was detected in six (7%) patients. The Phe354Leu polymorphism occurred concurrently with mutations of nucleophosmin 1 (NPM1), fms-related tyrosine kinase 3 (FLT3) and CCAAT/enhancer binding protein alpha (CEBPA), but not with metabolism-related genes, isocitrate dehydrogenase [nicotinamide adenine dinucleotide phosphate (+)]1 (IDH1) and IDH2. Patients with Phe354Leu polymorphism diagnosed at younger ages had a worse overall survival. Conclusion: LKB1 may be involved in the leukemogenesis and progression of cytogenetically normal AML.