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Identification of novel genetic alterations in samples of malignant glioma patients.

ABSTRACT: Glioblastoma is the most frequent and malignant human brain tumor. High level of genomic instability detected in glioma cells implies that numerous genetic alterations accumulate during glioma pathogenesis. We investigated alterations in AP-PCR DNA profiles of 30 glioma patients, and detected specific changes in 11 genes not previously associated with this disease: LHFPL3, SGCG, HTR4, ITGB1, CPS1, PROS1, GP2, KCNG2, PDE4D, KIR3DL3, and INPP5A. Further correlations revealed that 8 genes might play important role in pathogenesis of glial tumors, while changes in GP2, KCNG2 and KIR3DL3 should be considered as passenger mutations, consequence of high level of genomic instability. Identified genes have a significant role in signal transduction or cell adhesion, which are important processes for cancer development and progression. According to our results, LHFPL3 might be characteristic of primary glioblastoma, SGCG, HTR4, ITGB1, CPS1, PROS1 and INPP5A were detected predominantly in anaplastic astrocytoma, suggesting their role in progression of secondary glioblastoma, while alterations of PDE4D seem to have important role in development of both glioblastoma subtypes. Some of the identified genes showed significant association with p53, p16, and EGFR, but there was no significant correlation between loss of PTEN and any of identified genes. In conclusion our study revealed genetic alterations that were not previously associated with glioma pathogenesis and could be potentially used as molecular markers of different glioblastoma subtypes.

SUBMITTER: Milinkovic V

PROVIDER: S-EPMC3864906 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Identification of novel genetic alterations in samples of malignant glioma patients.

Milinkovic Vedrana V Bankovic Jasna J Rakic Miodrag M Stankovic Tijana T Skender-Gazibara Milica M Ruzdijic Sabera S Tanic Nikola N

PloS one 20131216 12

Glioblastoma is the most frequent and malignant human brain tumor. High level of genomic instability detected in glioma cells implies that numerous genetic alterations accumulate during glioma pathogenesis. We investigated alterations in AP-PCR DNA profiles of 30 glioma patients, and detected specific changes in 11 genes not previously associated with this disease: LHFPL3, SGCG, HTR4, ITGB1, CPS1, PROS1, GP2, KCNG2, PDE4D, KIR3DL3, and INPP5A. Further correlations revealed that 8 genes might pla ...[more]

PMID: 24358143

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Project description:BackgroundMalignant glioma is the second leading cause of cancer-related death worldwide, and is known to exhibit a high degree of heterogeneity in its deregulation of different oncogenic pathways. The molecular subclasses of human glioma are not well known. Thus, it is crucial to identify vital oncogenic pathways in glioma with significant relationships to patient survival.MethodsIn this study, we devised a bioinformatics strategy to map patterns of oncogenic pathway activation in glioma, from the Gene Expression Omnibus (GEO). Bioinformatics analysis revealed that 749 genes were differentially expressed and classified into different glioma grades.ResultsUsing gene expression signatures, we identified three oncogenic pathways (MAPK signaling pathway, Wnt signaling pathway, and ErbB signaling pathway) deregulated in the majority of human glioma. Following gene microarray analysis, the gene expression profile in the differential grade glioma was further validated by bioinformatic analyses, with coexpression network construction. Furthermore, we found that cytochrome c oxidase subunit Vb (COX5B), the terminal enzyme of the electron transport chain, was the central gene in a coexpression network that transfers electrons from reduced cytochrome c to oxygen and, in the process, generates an electrochemical gradient across the mitochondrial inner membrane. The expression level of COX5B was then detected in 87 glioma tissues as well as adjacent normal tissues using immunohistochemistry. We found that COX5B was significantly upregulated in 67 of 87 (77.0%) glioma and glioblastoma tissues, compared with adjacent tissue (p<0.01). Furthermore, statistical analysis showed the COX5B expression level was significantly associated with clinical stage and lymph node status, while there were no correlations between COX5B expression and age or tumor size.ConclusionThese data indicate that COX5B may be implicated in glioma pathogenesis and as a biomarker for identification of the pathological grade of glioma.

Dataset Information

Identification of novel genetic alterations in samples of malignant glioma patients.

Publications

Identification of novel genetic alterations in samples of malignant glioma patients.

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