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- Title
C59T mutation in exon 2 of monocytic leukemia‑associated antigen‑34 gene indicates a high risk of recurrence of acute myeloid leukemia.
- Authors
BO LEI; YINXIA CHEN; AILI HE; JING LUO; PENGYU ZHANG; FULING ZHOU; JIE LIU; XIN MENG; WANGGANG ZHAN; JING WANG
- Abstract
Monocytic leukemia‑associated antigen‑34 (MLAA‑34) is a novel monocytic leukemia‑associated antigen and a candidate oncogene. The aim of the present study was to investigate the involvement of the MLAA‑34 gene in acute myeloid leukemia (AML). MLAA‑34 expression level, chromosome location, gene copy number and single nucleotide polymorphisms (SNPs) of 40 patients with AML and 5 healthy volunteers were analyzed by reverse transcription‑polymerase chain reaction, fluorescence in situ hybridization and DNA sequencing. The effects of MLAA‑34 mutation on overall survival (OS) and progression‑free survival (PFS) of patients with AML were also analyzed. MLAA‑34 was significantly upregulated in patients with AML when compared with volunteer controls, and this upregulation was associated with a C59T SNP site located in the second exon of MLAA‑34. MLAA‑34 was mapped to 13q14.2 and no translocation was observed in patients with AML. In addition, this SNP site is affinitive to the well‑known molecular markers of AML, including Fms‑like tyrosine kinase 3 and DNA methyltransferase 3A, as well as extramedullary lesions, periphery leukocyte numbers, remission and cytogenetic abnormalities of patients with AML. Patients with AML with MLAA‑34 C59T mutations had significantly shorter OS and PFS times compared with that of patients without C59T mutations. The present findings indicated that the MLAA‑34 C59T mutation was a high‑risk factor for recurrence of AML, and may be a candidate target for AML therapy.
- Subjects
ACUTE myeloid leukemia; MONOCYTIC leukemia; ANTIGENS; DISEASE relapse; SINGLE nucleotide polymorphisms; FLUORESCENCE in situ hybridization
- Publication
Oncology Letters, 2017, Vol 14, Issue 1, p55
- ISSN
1792-1074
- Publication type
Article
- DOI
10.3892/ol.2017.6110