Mitochondrial 10398A>G NADH-Dehydrogenase Subunit 3 of Complex I Is Frequently Altered in Intra-Axial Brain Tumors in Malaysia
Brain Tumor Research and Treatment
;
: 31-38, 2018.
Article
Dans Anglais
| WPRIM
| ID: wpr-713835
ABSTRACT
BACKGROUND:
Mitochondria are major cellular sources of reactive oxygen species (ROS) generation which can induce mitochondrial DNA damage and lead to carcinogenesis. The mitochondrial 10398A>G alteration in NADH-dehydrogenase subunit 3 (ND3) can severely impair complex I, a key component of ROS production in the mitochondrial electron transport chain. Alteration in ND3 10398A>G has been reported to be linked with diverse neurodegenerative disorders and cancers. The aim of this study was to find out the association of mitochondrial ND3 10398A>G alteration in brain tumor of Malaysian patients.METHODS:
Brain tumor tissues and corresponding blood specimens were obtained from 45 patients. The ND3 10398A>G alteration at target codon 114 was detected using the PCR-RFLP analysis and later was confirmed by DNA sequencing.RESULTS:
Twenty-six (57.8%) patients showed ND3 10398A>G mutation in their tumor specimens, in which 26.9% of these mutations were heterozygous mutations. ND3 10398A>G mutation was not significantly correlated with age, gender, and histological tumor grade, however was found more frequently in intra-axial than in extra-axial tumors (62.5% vs. 46.2%, p G mutations in a Malaysian brain tumor population. It can be concluded that mitochondrial ND3 10398A>G alteration is frequently present in brain tumors among Malaysian population and it shows an impact on the intra-axial tumors.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Encéphale
/
Tumeurs du cerveau
/
Codon
/
ADN mitochondrial
/
Analyse de séquence d'ADN
/
Espèces réactives de l'oxygène
/
Maladies neurodégénératives
/
Transport d'électrons
/
Carcinogenèse
/
Malaisie
Limites du sujet:
Humains
Pays comme sujet:
Asie
langue:
Anglais
Texte intégral:
Brain Tumor Research and Treatment
Année:
2018
Type:
Article
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