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Tabernero, Maria Dolores; Maíllo, Angel; Nieto, Ana Belen; Diez-Tascón, Cristina; Lara, Mónica; Sousa, Pablo; Otero, Alvaro; Castrillo, Abel; Patino-Alonso, Maria del Carmen; Espinosa, Ana; Mackintosh, Carlos; Alava, Enrique de; Orfao, Alberto
Genes chromosomes & cancer, June 2012, Letnik: 51, Številka: 6Journal Article
Despite recent advances in the identification of the cytogenetic profiles of meningiomas, a significant group of tumors still show normal karyotypes or few chromosomal changes. The authors analyzed the cytogenetic profile of 50 meningiomas using fluorescence in situ hybridization and high‐density (500 K) single nucleotide polymorphism (SNP) arrays. Our results confirm that del(22q) (52%) and del(1p) (16%) (common deleted regions: 22q11.21‐22q13.3. and 1p31.2‐p36.33) are the most frequent alterations. Additionally, recurrent monosomy 14 (8%), del(6q) (10%), del(7p) (10%), and del(19q) (4%) were observed, while copy number patterns consistent with recurrent chromosomal gains, gene amplification, and copy number neutral loss of heterozygosity (cnLOH) were either absent or rare. Based on their overall SNP profiles, meningiomas could be classified into: (i) diploid cases, (ii) meningiomas with a single chromosomal change e.g., monosomy 22/del(22q) and (iii) tumors with ≥2 altered chromosomes. In summary, our results confirm and extend on previous observations showing that the most recurrent chromosomal abnormalities in meningiomas correspond to chromosome losses localized in chromosomes 1, 22 and less frequently in chromosomes 6, 7, 14, and 19, while chromosomal gains and cnLOH are restricted to a small proportion of cases. Finally, a set of cancer‐associated candidate genes associated with the TP53, MYC, CASP3, HDAC1, and TERT signaling pathways was identified, in cases with coexisting monosomy 14 and del(1p). © 2012 Wiley Periodicals, Inc.
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