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Gene expression profiling of meningiomas: current status after a decade of microarray-based transcriptomic studies.

Aarhus M, Lund-Johansen M, Knappskog PM - Acta Neurochir (Wien) (2011)

Bottom Line: We identified 13 articles matching the inclusion criteria.All studies had been performed during the last decade.Due to lack of consensus on how microarray data are presented, possible general trends found across the studies are difficult to extract.

View Article: PubMed Central - PubMed

Affiliation: Centre for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway. mads.aarhus@me.com

ABSTRACT

Purpose: This article provides a review of the transcriptomic expression profiling studies that have been performed on meningiomas so far. We discuss some future prospects and challenges ahead in the field of gene expression profiling.

Methods: We performed a systematic search in the PubMed and EMBASE databases in May 2010 using the following search terms alone or in combination: "meningioma", "microarray analysis", "oligonucleotide array sequence analysis", or "gene expression profiling". Only original research articles in English that had used RNA hybridized to high-resolution microarray chips to generate gene expression profiles were included.

Results: We identified 13 articles matching the inclusion criteria. All studies had been performed during the last decade.

Conclusions: The main results of the studies can be grouped in three categories: (1) several groups have identified meningioma-specific genes and genes associated with the three WHO grades, and the main histological subtypes of grade I meningiomas; (2) one publication has shown that the general transcription profile of samples of all WHO grades differs in vivo and in vitro; (3) one report provides evidence that microarray technology can be used in an automated fashion to classify tumors. Due to lack of consensus on how microarray data are presented, possible general trends found across the studies are difficult to extract. This could obstruct the discovery of important genes and pathways universally involved in meningioma biology.

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Radiological appearances of meningiomas. a Magnetic resonance imaging (MRI) showing a large convexity meningioma with edema and displacement of the midline to the anatomical left. b MRI section illustrating a WHO grade I convexity meningioma invading the frontal bone. c Large meningioma arising in the cerebello-pontine angle compressing the brain stem. d Computerized tomography showing multiple meningiomas and postoperative changes in a patient with neurofibromatosis type 2
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Fig2: Radiological appearances of meningiomas. a Magnetic resonance imaging (MRI) showing a large convexity meningioma with edema and displacement of the midline to the anatomical left. b MRI section illustrating a WHO grade I convexity meningioma invading the frontal bone. c Large meningioma arising in the cerebello-pontine angle compressing the brain stem. d Computerized tomography showing multiple meningiomas and postoperative changes in a patient with neurofibromatosis type 2

Mentions: Meningiomas (Fig. 2), being the second most common intracranial neoplasm (20–30% of all cases) [4], have been extensively studied in the past. An important contribution to the understanding of the pathogenesis was the identification of the NF2 gene located on chromosome 22q12.2 [5–8]. Loss of one allele of this gene is causing the autosomal dominant syndrome neurofibromatosis type 2, in which bilateral vestibular schwannomas are pathognomonic, and multiple meningiomas often develop. From research on sporadic (non-NF2-related) meningiomas it has been found that loss of heterozygosity is found in 40–70% of cases and mutations in the remaining allele present in 60% [9–12]. Thus, a main mechanism of meningioma initiation follows the pattern of Knudsons two-hit hypothesis: first, a risk allele is deleted, and then a mutation in the remaining allele containing a tumor suppressor gene initiates neoplastic growth [13]. However, it follows that this mechanism is not uniformly causing meningiomas, and that other genes or pathways are contributing to the tumorigenesis. Hence, gene expression profiling studies have the potential to discover novel genes and signaling pathways with a role in meningioma biology.Fig. 2


Gene expression profiling of meningiomas: current status after a decade of microarray-based transcriptomic studies.

Aarhus M, Lund-Johansen M, Knappskog PM - Acta Neurochir (Wien) (2011)

Radiological appearances of meningiomas. a Magnetic resonance imaging (MRI) showing a large convexity meningioma with edema and displacement of the midline to the anatomical left. b MRI section illustrating a WHO grade I convexity meningioma invading the frontal bone. c Large meningioma arising in the cerebello-pontine angle compressing the brain stem. d Computerized tomography showing multiple meningiomas and postoperative changes in a patient with neurofibromatosis type 2
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3040823&req=5

Fig2: Radiological appearances of meningiomas. a Magnetic resonance imaging (MRI) showing a large convexity meningioma with edema and displacement of the midline to the anatomical left. b MRI section illustrating a WHO grade I convexity meningioma invading the frontal bone. c Large meningioma arising in the cerebello-pontine angle compressing the brain stem. d Computerized tomography showing multiple meningiomas and postoperative changes in a patient with neurofibromatosis type 2
Mentions: Meningiomas (Fig. 2), being the second most common intracranial neoplasm (20–30% of all cases) [4], have been extensively studied in the past. An important contribution to the understanding of the pathogenesis was the identification of the NF2 gene located on chromosome 22q12.2 [5–8]. Loss of one allele of this gene is causing the autosomal dominant syndrome neurofibromatosis type 2, in which bilateral vestibular schwannomas are pathognomonic, and multiple meningiomas often develop. From research on sporadic (non-NF2-related) meningiomas it has been found that loss of heterozygosity is found in 40–70% of cases and mutations in the remaining allele present in 60% [9–12]. Thus, a main mechanism of meningioma initiation follows the pattern of Knudsons two-hit hypothesis: first, a risk allele is deleted, and then a mutation in the remaining allele containing a tumor suppressor gene initiates neoplastic growth [13]. However, it follows that this mechanism is not uniformly causing meningiomas, and that other genes or pathways are contributing to the tumorigenesis. Hence, gene expression profiling studies have the potential to discover novel genes and signaling pathways with a role in meningioma biology.Fig. 2

Bottom Line: We identified 13 articles matching the inclusion criteria.All studies had been performed during the last decade.Due to lack of consensus on how microarray data are presented, possible general trends found across the studies are difficult to extract.

View Article: PubMed Central - PubMed

Affiliation: Centre for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway. mads.aarhus@me.com

ABSTRACT

Purpose: This article provides a review of the transcriptomic expression profiling studies that have been performed on meningiomas so far. We discuss some future prospects and challenges ahead in the field of gene expression profiling.

Methods: We performed a systematic search in the PubMed and EMBASE databases in May 2010 using the following search terms alone or in combination: "meningioma", "microarray analysis", "oligonucleotide array sequence analysis", or "gene expression profiling". Only original research articles in English that had used RNA hybridized to high-resolution microarray chips to generate gene expression profiles were included.

Results: We identified 13 articles matching the inclusion criteria. All studies had been performed during the last decade.

Conclusions: The main results of the studies can be grouped in three categories: (1) several groups have identified meningioma-specific genes and genes associated with the three WHO grades, and the main histological subtypes of grade I meningiomas; (2) one publication has shown that the general transcription profile of samples of all WHO grades differs in vivo and in vitro; (3) one report provides evidence that microarray technology can be used in an automated fashion to classify tumors. Due to lack of consensus on how microarray data are presented, possible general trends found across the studies are difficult to extract. This could obstruct the discovery of important genes and pathways universally involved in meningioma biology.

Show MeSH
Related in: MedlinePlus