Multiplex ligation-dependent probe amplification (MLPA) screening in meningioma

Laboratorio de Oncogenética Molecular, Unidad de Investigación, Hospital Universitario La Paz, Paseo Castellana 261, 28046 Madrid, Spain
Cancer Genetics and Cytogenetics (Impact Factor: 1.93). 04/2007; 173(2):170-2. DOI: 10.1016/j.cancergencyto.2006.09.011
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Available from: Victor Martinez-Glez,
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    • "Information on probe sequences and ligation sites can be obtained at http:// The MLPA protocol was performed as described by the manufacturers, using 100 ng of DNA from control and tumor samples [42]. Data analysis was performed with MRC Coffalyser software (MRC-Holland). "
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    ABSTRACT: The molecular pathology of meningiomas and shwannomas involve the inactivation of the NF2 gene to generate grade I tumors. Genomic losses at 1p and 14q are observed in both neoplasms, although more frequently in meningiomas. The inactivation of unidentified genes located in these regions appears associated with tumor progression in meningiomas, but no clues to its molecular/clinical meaning are available in schwannomas. Recent microarray gene expression studies have demonstrated the existence of molecular subgroups in both entities. In the present study, we correlated the presence of genomic deletions at 1p, 14q, and 22q with the expression patterns of 96 tumor-related genes obtained by cDNA low-density microarrays in a series of 65 tumors including 42 meningiomas and 23 schwannomas. Two expression pattern groups were identified by cDNA mycroarray analysis when compared to the expression pattern in normal control RNA in both meningiomas and schwannomas, each one with patterns similar and different from the normal control. Meningioma and schwannoma subgroups differed in the expression of 38 and 16 genes, respectively. Using MLPA and microsatellites, we identified genomic losses at 1p, 14q, and 22q at nonrandom frequencies (12.5-69%) in meningiomas and schwannomas. Losses at 22q were almost equally frequent in both molecular expression subgroups in both neoplasms. However, deletions at 1p and 14q accumulated in meningiomas with a gene expression pattern different from the normal pattern, whereas the inverse situation occurred in schwannomas. Those anomalies characterized the schwannomas with expression pattern similar to the normal control. These findings suggest that deletions at 1p and 14q enhance the development of an abnormal tumor-related gene expression pattern in meningiomas, but this fact is not corroborated in schwannomas.
    Cancer genetics and cytogenetics 01/2010; 196(1):1-6. DOI:10.1016/j.cancergencyto.2009.08.003 · 1.93 Impact Factor
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    • "Information regarding the probe sequences and ligation sites can be found at MLPA analysis was performed as we described previously [16] [34]. In brief, we used 100 ng for each normal DNA control and tumor sample. "
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    ABSTRACT: Identification of the 1p/19q allelic status in gliomas, primarily those with a major oligodendroglial component, has become an excellent molecular complement to tumor histology in order to identify those cases sensitive to chemotherapy. In addition to loss of heterozygosity (LOH), fluorescence in situ hybridization (FISH), or comparative genomic hybridization (CGH), multiplex ligation-dependent probe amplification (MLPA) has been shown to be an alternative methodology to identify deletions of those chromosome arms. We used MLPA to explore the 1p and 19q allelic constitution in a series of 76 gliomas: 41 tumors with a major oligodendroglial component, 34 glioblastomas, and one low-grade astrocytoma. We compared the MLPA findings of the oligodendroglial cases with those previously obtained using LOH in the same samples. Thirty-eight of 41 oligodendrogliomas displayed identical findings by both LOH and MLPA, and losses at either 1p and/or 19q were identified in 12 of 35 (34%) astrocytic tumors. These findings agree with data previously reported comparing MLPA versus FISH or CGH in gliomas and suggest that MLPA can be used in the identification of the 1p/19q allelic deletions on these brain neoplasms.
    Cancer genetics and cytogenetics 05/2009; 190(2):93-6. DOI:10.1016/j.cancergencyto.2008.09.017 · 1.93 Impact Factor
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    • "Preliminary data on CpG island CITED4 promoter methylation status in glioblastomas showed the epigenetic change in 2/14 glioblastomas studied (unpublished data) and both cases also presented loss of heterozygosity at 1p. By means of multiplex ligationedependent probe amplification (MLPA) analysis performed as described [21], the series reported here displayed deletions at 1p in 7/24 tumors. Partial loss at 1p36, 1p34, and 1p13.2 presented in one case each, and two additional tumors displayed complete 1p loss and an intact 19q. "

    Cancer genetics and cytogenetics 10/2008; 185(2):114-6. DOI:10.1016/j.cancergencyto.2008.05.013 · 1.93 Impact Factor
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