Peiqi Liang1, Rong Hu2, Zhuogang Liu3, Miao Miao3, Huinan Jiang3, Chuan Li3. 1. Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China; Department of Hematology, Shengjing Hospital of China Medical University, Shenyang, China. 2. Department of Hematology, Shengjing Hospital of China Medical University, Shenyang, China. Electronic address: hur@sj-hospital.org. 3. Department of Hematology, Shengjing Hospital of China Medical University, Shenyang, China.
Abstract
BACKGROUND: N-acetyltransferase 10 (NAT10) is considered as an oncogene in many tumors. This study investigated the NAT10 expression in Chinese acute myeloid leukemia (AML) patients and evaluated the predictive significance of NAT10 with a single-center retrospective study. METHODS: The Oncomine was used to analyze NAT10 expression in AML. We also collected bone marrow samples of 48 newly diagnosed AML patients and 20 benign individuals in our center. NAT10 mRNA expression levels were detected by real-time qPCR. Clinical data was obtained from inpatient medical records. RESULTS: Two microarrays in Oncomine showed that NAT10 was upregulated in AML. Our data revealed that AML patients had higher NAT10 expression levels than the normal controls (P < 0.01). NPM1-mutant patients had higher NAT10 mRNA levels than NPM1-wt patients. NAT10 expression level was higher in nonremission group than in overall remission group (P < 0.05). High NAT10 expression indicated a poor progression-free survival and overall survival. CONCLUSIONS: The results support NAT10 as a potential prognostic and therapeutic biomarker for AML.
BACKGROUND:N-acetyltransferase 10 (NAT10) is considered as an oncogene in many tumors. This study investigated the NAT10 expression in Chinese acute myeloid leukemia (AML) patients and evaluated the predictive significance of NAT10 with a single-center retrospective study. METHODS: The Oncomine was used to analyze NAT10 expression in AML. We also collected bone marrow samples of 48 newly diagnosed AMLpatients and 20 benign individuals in our center. NAT10 mRNA expression levels were detected by real-time qPCR. Clinical data was obtained from inpatient medical records. RESULTS: Two microarrays in Oncomine showed that NAT10 was upregulated in AML. Our data revealed that AMLpatients had higher NAT10 expression levels than the normal controls (P < 0.01). NPM1-mutant patients had higher NAT10 mRNA levels than NPM1-wt patients. NAT10 expression level was higher in nonremission group than in overall remission group (P < 0.05). High NAT10 expression indicated a poor progression-free survival and overall survival. CONCLUSIONS: The results support NAT10 as a potential prognostic and therapeutic biomarker for AML.