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C59T mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia

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...

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Autores principales: Lei, Bo, Chen, Yinxia, He, Aili, Luo, Jing, Zhang, Pengyu, Zhou, Fuling, Liu, Jie, Meng, Xin, Wang, Jing, Zhang, Wanggang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494830/
https://www.ncbi.nlm.nih.gov/pubmed/28693135
http://dx.doi.org/10.3892/ol.2017.6110
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author Lei, Bo
Chen, Yinxia
He, Aili
Luo, Jing
Zhang, Pengyu
Zhou, Fuling
Liu, Jie
Meng, Xin
Wang, Jing
Zhang, Wanggang
author_facet Lei, Bo
Chen, Yinxia
He, Aili
Luo, Jing
Zhang, Pengyu
Zhou, Fuling
Liu, Jie
Meng, Xin
Wang, Jing
Zhang, Wanggang
author_sort Lei, Bo
collection PubMed
description 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.
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spelling pubmed-54948302017-07-07 C59T mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia Lei, Bo Chen, Yinxia He, Aili Luo, Jing Zhang, Pengyu Zhou, Fuling Liu, Jie Meng, Xin Wang, Jing Zhang, Wanggang Oncol Lett Articles 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. D.A. Spandidos 2017-07 2017-05-02 /pmc/articles/PMC5494830/ /pubmed/28693135 http://dx.doi.org/10.3892/ol.2017.6110 Text en Copyright: © Lei et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Lei, Bo
Chen, Yinxia
He, Aili
Luo, Jing
Zhang, Pengyu
Zhou, Fuling
Liu, Jie
Meng, Xin
Wang, Jing
Zhang, Wanggang
C59T mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia
title C59T mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia
title_full C59T mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia
title_fullStr C59T mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia
title_full_unstemmed C59T mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia
title_short C59T mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia
title_sort c59t mutation in exon 2 of monocytic leukemia-associated antigen-34 gene indicates a high risk of recurrence of acute myeloid leukemia
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494830/
https://www.ncbi.nlm.nih.gov/pubmed/28693135
http://dx.doi.org/10.3892/ol.2017.6110
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