Association of loss of 1p and alterations of chromosome 14 in meningioma progression

López‐Ginés, Concha; Cerdá-Nicolás, Miguel; Gil-Benso, Rosario; Callaghan, Robert C.; Collado, María; Roldán, Pedro; Llombart‐Bosch, Antonio

doi:10.1016/s0165-4608(03)00279-6

Cited by 39 publications

(33 citation statements)

References 23 publications

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“…LOH studies were the first to show an association with clinical grade, with 1p and 14q losses having a prominent role [21][22][23][24] in association with high-grade meningiomas. LOH on 22q, where NF2 is located, is also diffuse in grade I meningiomas and does not appear to be linked to greater malignancy [25][26][27].…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

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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“…In grade III meningiomas, 9p21 deletions encompassing CDKN2A/CDKN2B are associated with poorer survival (16). Very few studies including successive, recurrent specimens from the same patient whose tumor had progressed to a more malignant histologic phenotype have been conducted (17)(18)(19)(20). They showed losses on chromosome 22q in samples of all grades, associated with 1p, 9q, 10q, and 14q losses, sometimes solely observed in high-grade tumors.…”

mentioning

confidence: 99%

Genomic Profiling Reveals Alternative Genetic Pathways of Meningioma Malignant Progression Dependent on the UnderlyingNF2Status

Goutagny

Yang

Zucman‐Rossi

et al. 2010

Clinical Cancer Research

103

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Purpose: Meningiomas are the most common central nervous system tumors in the population of age 35 and older. WHO defines three grades predictive of the risk of recurrence. Clinical data supporting histologic malignant progression of meningiomas are sparse and underlying molecular mechanisms are not clearly depicted.Experimental Design: We identified genetic alterations associated with histologic progression of 36 paired meningioma samples in 18 patients using 500K SNP genotyping arrays and NF2 gene sequencing.Results: The most frequent chromosome alterations observed in progressing meningioma samples are early alterations (i.e., present both in lower-and higher-grade samples of a single patient). In our series, NF2 gene inactivation was an early and frequent event in progressing meningioma samples (73%). Chromosome alterations acquired during progression from grade I to grade II meningioma were not recurrent. Progression to grade III was characterized by recurrent genomic alterations, the most frequent being CDKN2A/CDKN2B locus loss on 9p.Conclusion: Meningiomas displayed different patterns of genetic alterations during progression according to their NF2 status: NF2-mutated meningiomas showed higher chromosome instability during progression than NF2-nonmutated meningiomas, which had very few imbalanced chromosome segments. This pattern of alterations could thus be used as markers in clinical practice to identify tumors prone to progress among grade I meningiomas. Clin Cancer Res; 16(16); 4155-64. ©2010 AACR.

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“…From the clinical point of view, chromosome 14 loss has been associated with a shorter recurrence-free survival, independently of tumour histopathology, particularly when detected in all tumour cells in the sample (eg, in the ancestral tumour cell clone) in association with del(1p36). 3,9,10,25 Altogether, these results suggest the presence of one or more tumour suppressor genes in this chromosome. Despite this, few studies have been reported so far in which a more precise characterization of the genetic changes involving chromosome 14, aimed at a better understanding of the clinical behaviour of the tumour, have been analysed.…”

Section: Discussionmentioning

confidence: 66%

Array-based comparative genomic hybridization of mapped BAC DNA clones to screen for chromosome 14 copy number abnormalities in meningiomas

et al. 2008

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Association of loss of 1p and alterations of chromosome 14 in meningioma progression

Cited by 39 publications

References 23 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

Genomic Profiling Reveals Alternative Genetic Pathways of Meningioma Malignant Progression Dependent on the UnderlyingNF2Status

Array-based comparative genomic hybridization of mapped BAC DNA clones to screen for chromosome 14 copy number abnormalities in meningiomas

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