All tumor tissues also showed amplification on chromosomes 5, 7, 9, and 16.CONCLUSION: Although further studies with larger cohorts are required to identify genes involved in MPE tumorigenesis and tovalidate our results, these findings provide a basis for advanced molecular biological and genetic studies of MPEs.
📌 3 Maddede Bu Makale
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Amaç & Hipotez:AIM: To identify the copy number variations that are specific to myxopapillary ependymomas (MPEs) of the cauda equina.MATERIAL and METHODS: The patient cohort included five patients who underwent resection of histologically confirmed MPEs.Tumor samples collected during surgery and stored in liquid nitrogen as well as corresponding blood samples collected wereanalyzed.
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Temel Bulgular & Veri:Genomic DNA from the venous blood and tumor samples was obtained using standard techniques and hybridized to aCytoscan 750K Array in accordance with the manufacturer’s introductions.RESULTS: As a novel finding, amplification on chromosome 14q32.33 was detected in all tumor and blood samples, except onetumor sample.
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Sonuç & Katkı:All tumor tissues also showed amplification on chromosomes 5, 7, 9, and 16.CONCLUSION: Although further studies with larger cohorts are required to identify genes involved in MPE tumorigenesis and tovalidate our results, these findings provide a basis for advanced molecular biological and genetic studies of MPEs.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri
Özet
AIM: To identify the copy number variations that are specific to myxopapillary ependymomas (MPEs) of the cauda equina.MATERIAL and METHODS: The patient cohort included five patients who underwent resection of histologically confirmed MPEs.Tumor samples collected during surgery and stored in liquid nitrogen as well as corresponding blood samples collected wereanalyzed. Genomic DNA from the venous blood and tumor samples was obtained using standard techniques and hybridized to aCytoscan 750K Array in accordance with the manufacturer’s introductions.RESULTS: As a novel finding, amplification on chromosome 14q32.33 was detected in all tumor and blood samples, except onetumor sample. All tumor tissues also showed amplification on chromosomes 5, 7, 9, and 16.CONCLUSION: Although further studies with larger cohorts are required to identify genes involved in MPE tumorigenesis and tovalidate our results, these findings provide a basis for advanced molecular biological and genetic studies of MPEs.
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Bu Makaleye Atıf Yap
ÖZEN, A., BAYRAKLI, F., SONMEZ, O., EYUBOGLU, I. P., ERDOĞAN, O., ERZİK, C., YAKICIER, M. C., BOZKURT, S. U. (2020). Analyses of Copy Number Variations in Myxopapillary Ependymomas of Cauda Equina. Turkish Neurosurgery, Cilt: 30 - Sayı: 3, 428–433. https://ajindex.com/articles/404281
Barton VN, Donson AM, Kleinschmidt-Demasters BK, Birks DK, Handler MH, Foreman NK: Unique molecular characteristics of pediatric myxopapillary ependymoma. Brain Pathol 20:560–570, 2010 2. Johnson RA, Wright KD, Poppleton H, Mohankumar KM, Finkelstein D, Pounds SB, Rand V, Leary SES, White E, Eden C, Hogg T, Northcott P, MacK S, Neale G, Wang YD, Coyle B, Atkinson J, Dewire M, Kranenburg TA, Gillespie Y, Allen JC, Merchant T, Boop FA, Sanford RA, Gajjar A, Ellison DW, Taylor MD, Grundy RG, Gilbertson RJ: Cross-species genomics matches driver mutations and cell compartments to model ependymoma. Nature 466:632–636, 2010 3. Lee CH, Chung CK, Kim CH: Genetic differences on intracranial versus spinal cord ependymal tumors: A metaanalysis of genetic researches. Eur Spine J 25:3942–3951, 2016 4. Leeper H, Felicella MM, Walbert T: Recent advances in the classification and treatment of ependymomas. Curr Treat Options Oncol 18(9):55, 2017 5. Louis DN, Perry A, Reifenberger G, Deimling A, FigarellaBranger D, Cavenee WK, Ohgaki H, Wiestler OD, Kleihues P, Ellison DW: The 2016 World Health Organization classification of tumors of the central nervous system: A summary. Acta Neuropathol 131:803–820, 2016 6. Mack SC, Witt H, Piro RM, Gu L, Zuyderduyn S, Stütz AM, Wang X, Gallo M, Garzia L, Zayne K, Zhang X, Ramaswamy V, Jäger N, Jones DTW, Sill M, Pugh TJ, Ryzhova M, Wani KM, Shih DJH, Head R, Remke M, Bailey SD, Zichner T, Faria CC, Barszczyk M, Stark S, Seker-Cin H, Hutter S, Johann P, Bender S, Hovestadt V, Tzaridis T, Dubuc AM, Northcott PA, Peacock J, Bertrand KC, Agnihotri S, Cavalli FMG, Clarke I, Nethery-Brokx K, Creasy CL, Verma SK, Koster J, Wu X, Yao Y, Milde T, Sin-Chan P, Zuccaro J, Lau L, Pereira S, CasteloBranco P, Hirst M, Marra MA, Roberts SS, Fults D, Massimi L, Cho YJ, Meter T, Grajkowska W, Lach B, Kulozik AE, Deimling A, Witt O, Scherer SW, Fan X, Muraszko KM, Kool M, Pomeroy SL, Gupta N, Phillips J, Huang A, Tabori U, Hawkins C, Malkin D, Kongkham PN, Weiss WA, Jabado N, Rutka JT, Bouffet E, Korbel JO, Lupien M, Aldape KD, Bader GD, Eils R, Lichter P, Dirks PB, Pfister SM, Korshunov A,Taylor MD: Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 506:445–450, 2014 7. Malgulwar PB, Nambirajan A, Pathak P, Faruq M, Rajeshwari M, Singh M, Suri V, Sarkar C, Sharma MC: C11orf95-RELA fusions and upregulated NF-KB signalling characterise a subset of aggressive supratentorial ependymomas that express L1CAM and nestin. J Neuro