Identification of the Thyrotropin-Releasing Hormone (TRH) as a Novel Biomarker in the Prognosis for Acute Myeloid Leukemia

被引:5
作者
Gao, Yan [1 ,2 ]
Zhou, Jia-Fan [3 ]
Mao, Jia-Ying [1 ,2 ]
Jiang, Lu [4 ]
Li, Xue-Ping [2 ,5 ]
机构
[1] Sun Yat Sen Univ, Dept Med Oncol, Canc Ctr, Guangzhou 510060, Peoples R China
[2] Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China
[3] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Nephrol, Guangzhou 510655, Peoples R China
[4] Shanghai Jiao Tong Univ, Ruijin Hosp, Natl Res Ctr Translat Med Shanghai, Shanghai Inst Hematol,Sch Med,State Key Lab Med G, Shanghai 200025, Peoples R China
[5] Sun Yat Sen Univ, Dept Hematol Oncol, Canc Ctr, Guangzhou 510060, Peoples R China
关键词
acute myeloid leukemia; biomarkers; TRH expression; prognosis; MOLECULAR SUBTYPES; EXPRESSION; CANCER;
D O I
10.3390/biom12101359
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Acute myeloid leukemia (AML) is a biologically and genetically heterogeneous hematological malignance with an unsatisfactory risk stratification system. Recently, through the novel single-cell RNA sequencing technology, we revealed heterogeneous leukemia myeloblasts in RUNX1-RUNX1T1 AML. Thyrotropin-releasing hormone (TRH), as biomarkers of CD34(+)CD117(bri) myeloblasts, were found to be prognostic in RUNX1-RUNX1T1 AML. However, the clinical and genetic features of TRH in AML patients are poorly understood. Here, with data from TCGA AML, TRH was found to be downregulated in patients older than 60 years old, with DNMT3A and NPM1 mutations, while overexpressed in patients with KIT mutations. This was further validated in three other cohorts of primary AML including Beat AML (n = 223), GSE6891 (n = 461), and GSE17855 (n = 237). Furthermore, we demonstrated that the expression of TRH in AML could be used to improve the ELN 2017 risk stratification system. In conclusion, our preliminary analysis revealed that TRH, a novel biomarker for AML patients, could be used to evaluate the survival of AML.
引用
收藏
页数:14
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