Molecular biological determinations of meningioma progression and recurrence.
Meningiomas are tumors that arise from the coverings of the brain or spinal cord. 5% of the cases turn into malignant forms with aggressive clinical behavior and increased risk of tumor recurrence. One hundred and five patients with meningiomas were operated by open surgery. To investigate predictor...
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oai:doaj.org-article:4d86c685477e477ab16d412e4b262fde2021-11-18T08:23:57ZMolecular biological determinations of meningioma progression and recurrence.1932-620310.1371/journal.pone.0094987https://doaj.org/article/4d86c685477e477ab16d412e4b262fde2014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24722350/?tool=EBIhttps://doaj.org/toc/1932-6203Meningiomas are tumors that arise from the coverings of the brain or spinal cord. 5% of the cases turn into malignant forms with aggressive clinical behavior and increased risk of tumor recurrence. One hundred and five patients with meningiomas were operated by open surgery. To investigate predictors of meningioma recurrence in total 124 samples of 105 patients were investigated by iFISH. Dual-probe hybridization was performed to access chromosomal alterations of chromosomes 1p-, 9p- and 22q. Additionally, methylation of TIMP3 and p16 was analyzed with MS-PCR. Of the 105 investigated tumors 59.1% (62/105) were WHO grade I, 33.3% (35/105) were WHO grade II and 7.7% (8/105) were anaplastic meningiomas (grade III), respectively. The histopathological data correlates with the recurrence rate of the investigated meningiomas. Hypermethylation of TIMP3 was detected in 13.3% of all meningiomas: 10.9% in WHO grade I meningiomas, 25.0% in grade II and 14.3% in grade III meningiomas, respectively. No correlation of TIMP3 hypermethylation with tumor recurrence or WHO grade (p = 0.2) was observed. Interestingly, deletion of 1p36 emerged as a significant predictor of shorter overall survival (log rank test, p<0.001), whereas TIMP3 promoter methylation had no significant effect on overall survival (log rank test, p = 0.799). The results of the current study support the finding that the deletion of chromosome 1p is an independent marker of meningioma recurrence and progression (p = 0.0097). Therefore the measurement of genetic aberrations in meningiomas allows in a combined histological approach a more precise assessment of the prognosis of meningiomas than histopathology alone.Stefan LinslerDennis KraemerChristina DriessJoachim OertelKai KammersJörg RahnenführerRalf KetterSteffi UrbschatPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 4, p e94987 (2014) |
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Medicine R Science Q Stefan Linsler Dennis Kraemer Christina Driess Joachim Oertel Kai Kammers Jörg Rahnenführer Ralf Ketter Steffi Urbschat Molecular biological determinations of meningioma progression and recurrence. |
description |
Meningiomas are tumors that arise from the coverings of the brain or spinal cord. 5% of the cases turn into malignant forms with aggressive clinical behavior and increased risk of tumor recurrence. One hundred and five patients with meningiomas were operated by open surgery. To investigate predictors of meningioma recurrence in total 124 samples of 105 patients were investigated by iFISH. Dual-probe hybridization was performed to access chromosomal alterations of chromosomes 1p-, 9p- and 22q. Additionally, methylation of TIMP3 and p16 was analyzed with MS-PCR. Of the 105 investigated tumors 59.1% (62/105) were WHO grade I, 33.3% (35/105) were WHO grade II and 7.7% (8/105) were anaplastic meningiomas (grade III), respectively. The histopathological data correlates with the recurrence rate of the investigated meningiomas. Hypermethylation of TIMP3 was detected in 13.3% of all meningiomas: 10.9% in WHO grade I meningiomas, 25.0% in grade II and 14.3% in grade III meningiomas, respectively. No correlation of TIMP3 hypermethylation with tumor recurrence or WHO grade (p = 0.2) was observed. Interestingly, deletion of 1p36 emerged as a significant predictor of shorter overall survival (log rank test, p<0.001), whereas TIMP3 promoter methylation had no significant effect on overall survival (log rank test, p = 0.799). The results of the current study support the finding that the deletion of chromosome 1p is an independent marker of meningioma recurrence and progression (p = 0.0097). Therefore the measurement of genetic aberrations in meningiomas allows in a combined histological approach a more precise assessment of the prognosis of meningiomas than histopathology alone. |
format |
article |
author |
Stefan Linsler Dennis Kraemer Christina Driess Joachim Oertel Kai Kammers Jörg Rahnenführer Ralf Ketter Steffi Urbschat |
author_facet |
Stefan Linsler Dennis Kraemer Christina Driess Joachim Oertel Kai Kammers Jörg Rahnenführer Ralf Ketter Steffi Urbschat |
author_sort |
Stefan Linsler |
title |
Molecular biological determinations of meningioma progression and recurrence. |
title_short |
Molecular biological determinations of meningioma progression and recurrence. |
title_full |
Molecular biological determinations of meningioma progression and recurrence. |
title_fullStr |
Molecular biological determinations of meningioma progression and recurrence. |
title_full_unstemmed |
Molecular biological determinations of meningioma progression and recurrence. |
title_sort |
molecular biological determinations of meningioma progression and recurrence. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2014 |
url |
https://doaj.org/article/4d86c685477e477ab16d412e4b262fde |
work_keys_str_mv |
AT stefanlinsler molecularbiologicaldeterminationsofmeningiomaprogressionandrecurrence AT denniskraemer molecularbiologicaldeterminationsofmeningiomaprogressionandrecurrence AT christinadriess molecularbiologicaldeterminationsofmeningiomaprogressionandrecurrence AT joachimoertel molecularbiologicaldeterminationsofmeningiomaprogressionandrecurrence AT kaikammers molecularbiologicaldeterminationsofmeningiomaprogressionandrecurrence AT jorgrahnenfuhrer molecularbiologicaldeterminationsofmeningiomaprogressionandrecurrence AT ralfketter molecularbiologicaldeterminationsofmeningiomaprogressionandrecurrence AT steffiurbschat molecularbiologicaldeterminationsofmeningiomaprogressionandrecurrence |
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