Expression and prognosis analysis of family in acute myeloid leukemia.

Aging (Albany NY)

Department of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, People's Republic of China.

Published: March 2020

family members () encode proteins that represent crucial factors in the active DNA demethylation pathway. Evidence has proved that mutation is associated with leukemogenesis, drug response, and prognosis in acute myeloid leukemia (AML). However, few studies revealed the expression and its clinical significance in AML. We conducted a detailed expression and prognosis analysis of TETs expression in human AML cell lines and patients by using public databases. We observed that expression especially and was closely associated with AML among various human cancers. expression was significantly reduced in AML patients, whereas and expression was significantly increased. Kaplan-Meier analysis showed that only expression was associated with overall survival (OS) and disease-free survival (DFS) among both total AML as well as non-M3 AML, and was confirmed by another independent cohort. Moreover, Cox regression analysis revealed that expression may act as an independent prognostic factor for OS and DFS in total AML. Interestingly, patients that received hematopoietic stem cell transplantation (HSCT) did not show significantly longer OS and DFS than those who did not receive HSCT in high-expressed groups; whereas, in low-expressed groups, patients that accepted HSCT showed significantly longer OS and DFS than those who did not accept HSCT. By bioinformatics analysis, expression was found positively correlated with tumor suppressor gene including , , , and negatively correlated with oncogenes such as and . Our study demonstrated that showed significant expression differences in AML, and expression acted as a potential prognostic biomarker in AML, which may guide treatment choice between chemotherapy and HSCT.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7138570PMC
http://dx.doi.org/10.18632/aging.102928DOI Listing

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