Malignant progression in meningioma: documentation of a series and analysis of cytogenetic findings

Al‐Mefty, Ossama; Kadri, Paulo A S; Pravdenkova, Svetlana; Sawyer, Jeffrey R.; Stangeby, Colin; Husain, Muhammad

doi:10.3171/jns.2004.101.2.0210

Cited by 201 publications

(149 citation statements)

References 88 publications

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“…Based on that, a model of genetic progression was proposed for meningiomas, similar to other malignancies [25]. Subsequent data, however, suggested that genetic alterations present in recurrent, grade II-III meningiomas were already present in the initial tumor, failing to confirm the "progression" model [28,29]. Our observations support correlations between LOH data and histological analysis, are unable to support the "progression" model, and do not increase the prognostic power of LOH.…”

Section: Discussioncontrasting

confidence: 44%

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

Menghi¹,

Orzan²,

Eoli³

et al. 2011

The Oncologist

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Meningiomas are the most frequent intracranial tumors. Surgery can be curative, but recurrences are possible. We performed gene expression analyses and loss of heterozygosity (LOH) studies looking for new markers predicting the recurrence risk. We analyzed expression profiles of 23 meningiomas (10 grade I, 10 grade II, and 3 grade III) and validated the data using quantitative polymerase chain reaction (qPCR). We performed LOH analysis on 40 meningiomas, investigating chromosomal regions on 1p, 9p, 10q, 14q, and 22q. We found 233 and 268 probe sets to be significantly down-and upregulated, respectively, in grade II or III meningiomas. Genes downregulated in high-grade meningiomas were overrepresented on chromosomes 1, 6, 9, 10, and 14. Based on functional enrichment analysis, we selected LIM domain and actin binding 1 (LIMA1), tissue inhibitor of metalloproteinases 3 (TIMP3), cyclin-dependent kinases regulatory subunit 2 (CKS2), leptin receptor (LEPR), and baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) for validation using qPCR and confirmed their differential expression in the two groups of tumors. We calculated ⌬Ct values of CKS2 and LEPR and found that their differential expression (C-L index) was significantly higher in grade I than in grade II or III meningiomas (p < .0001). Interestingly, the C-L index of nine grade I meningiomas from patients who relapsed in <5 years was significantly lower than in grade I meningiomas from patients who did not relapse. These findings indicate that the C-L index may be relevant to define the progression risk in meningioma patients, helping guide their clinical management. A prospective analysis on a larger number of cases is warranted.

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Section: Discussioncontrasting

confidence: 44%

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

Menghi¹,

Orzan²,

Eoli³

et al. 2011

The Oncologist

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“…This risk should be considered when decisions are made to use radiation in routine imaging examinations, such as CT scanning, 10 or to administer higher doses of radiation for treatment of benign tumors during childhood, adolescence, and young adulthood. [2][3][4]17,42,78,81 Radiation-induced meningiomas are characterized by marked changes to the scalp, including alopecia, atrophy, and poor vascularization. Patients with RIMs frequently present with multiple tumors.…”

Section: Discussionmentioning

confidence: 99%

“…2,76 Histological features are distinctive compared with SM. Soffer et al 76 have noted high cellularity, nuclear pleomorphism, an increased mitotic rate, focal necrosis, bone invasion, and tumor infiltration of the brain in a series of 42 patients with low-dose RIM.…”

Section: Radiation-induced Meningiomamentioning

confidence: 99%

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Radiation-induced meningioma

Umansky¹,

Shoshan²,

Rosenthal³

et al. 2008

FOC

171

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✓ The long-term or delayed side effects of irradiation on neural tissue are now known to include the induction of new central nervous system neoplasms. However, during the first half of the 20th century, human neural tissue was generally considered relatively resistant to the carcinogenic and other ill effects of ionizing radiation. As a result, exposure to relatively high doses of x-rays from diagnostic examinations and therapeutic treatment was common. In the present article the authors review the literature relating to radiation-induced meningiomas (RIMs). Emphasis is placed on meningiomas resulting from childhood treatment for primary brain tumor or tinea capitis, exposure to dental x-rays, and exposure to atomic explosions in Hiroshima and Nagasaki. The incidence and natural history of RIMs following exposure to high- and low-dose radiation is presented, including latency, multiplicity, histopathological features, and recurrence rates. The authors review the typical presentation of patients with RIMs and discuss unique aspects of the surgical management of these tumors compared with sporadic meningioma, based on their clinical experience in treating these lesions.

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“…38 Additional possible explanations for the difficulty in predicting the behavior of meningiomas have included the observations that there are numerous histological similarities between tumors in each grade and that these tumors exist along a spectrum in which lowgrade meningiomas can progress to a higher grade. 2 There is no clear explanation, however, as to why the majority of recurrent meningiomas derive from benign histology even after apparently radical removal. 55 Other attempts to classify meningiomas have used genomic techniques to study their genesis and progres sion, 73 as well as to search for genetic mutations and variable gene expression mediated via epigenetic modi fications.…”

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confidence: 99%

A review of epigenetic and gene expression alterations associated with intracranial meningiomas

He¹,

Pham²,

Pease³

et al. 2013

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Object A more comprehensive understanding of the epigenetic abnormalities associated with meningioma tumorigenesis, growth, and invasion may provide useful targets for molecular classification and development of targeted therapies for meningiomas. Methods The authors performed a review of the current literature to identify the epigenetic modifications associated with the formation and/or progression of meningiomas. Results Several epigenomic alterations, mainly pertaining to DNA methylation, have been associated with meningiomas. Hypermethylation of TIMP3 inactivates its tumor suppression activity while CDKN2 (p14[ARF]) and TP73 gene hypermethylation and HIST1H1c upregulation interact with the p53 regulation of cell cycle control. Other factors such as HOX, IGF, WNK2, and TGF-β epigenetic modifications allow either upregulation or downregulation of critical pathways for meningioma development, progression, and recurrence. Conclusions Genome-wide methylation profiling demonstrated that global hypomethylation correlates with tumor grades and severity. Identification of additional epigenetic changes, such as histone modification and higher-order chromosomal structure, may allow for a more thorough understanding of tumorigenesis and enable future individualized treatment strategies for meningiomas.

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Malignant progression in meningioma: documentation of a series and analysis of cytogenetic findings

Cited by 201 publications

References 88 publications

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

Radiation-induced meningioma

A review of epigenetic and gene expression alterations associated with intracranial meningiomas

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