Clinicopathological Implications of Mitochondrial Genome Alterations in Pediatric Acute Myeloid Leukemia
Annals of Laboratory Medicine
; : 101-110, 2016.
Article
在 En
| WPRIM
| ID: wpr-34962
Responsible library:
WPRO
ABSTRACT
BACKGROUND: To the best of our knowledge, the association between pediatric AML and mitochondrial aberrations has not been studied. We investigated various mitochondrial aberrations in pediatric AML and evaluated their impact on clinical outcomes. METHODS: Sequencing, mitochondrial DNA (mtDNA) copy number determination, mtDNA 4,977-bp large deletion assessments, and gene scan analyses were performed on the bone marrow mononuclear cells of 55 pediatric AML patients and on the peripheral blood mononuclear cells of 55 normal controls. Changes in the mitochondrial mass, mitochondrial membrane potential, and intracellular reactive oxygen species (ROS) levels were also examined. RESULTS: mtDNA copy numbers were about two-fold higher in pediatric AML cells than in controls (P<0.0001). Furthermore, a close relationship was found between mtDNA copy number tertiles and the risk of pediatric AML. Intracellular ROS levels, mitochondrial mass, and mitochondrial membrane potentials were all elevated in pediatric AML. The frequency of the mtDNA 4,977-bp large deletion was significantly higher (P< 0.01) in pediatric AML cells, and pediatric AML patients harboring high amount of mtDNA 4,977-bp deletions showed shorter overall survival and event-free survival rates, albeit without statistical significance. CONCLUSIONS: The present findings demonstrate an association between mitochondrial genome alterations and the risk of pediatric AML.
Key words
全文:
1
索引:
WPRIM
主要主题:
DNA, Mitochondrial
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Bone Marrow Cells
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Leukemia, Myeloid, Acute
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Case-Control Studies
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Odds Ratio
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Survival Rate
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Cohort Studies
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Sequence Analysis, DNA
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Reactive Oxygen Species
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Gene Deletion
研究类型:
Etiology_studies
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Incidence_studies
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Observational_studies
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Risk_factors_studies
限制:
Child
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Female
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Humans
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Male
语言:
En
期刊:
Annals of Laboratory Medicine
年:
2016
类型:
Article