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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Oncología > Oncología molecular > DA - CIMA - Oncología - Oncología molecular - Artículos de Revista >

Identified hidden genomic changes in mantle cell lymphoma using high-resolution single nucleotide polymorphism genomic array
Authors: Kawamata, N. (N.)
Ogawa, S. (Seishi)
Gueller, S. (S.)
Ross, S.H. (Samuel H.)
Huynh, T. (T.)
Chen, J. (J.)
Chang, A. (A.)
Nabavi-Nouis, S. (Shayan)
Megrabian, N. (Nairi)
Siebert, R. (Reiner)
Martinez-Climent, J.A. (José Ángel)
Koeffler, H.P. (H. Philip)
Keywords: DNA mutational analysis
Gene deletion
Gene duplication
Lymphoma, Mantle-cell
Issue Date: 2009
Publisher: Elsevier
Publisher version:
ISSN: 1873-2399
Citation: Kawamata N, Ogawa S, Gueller S, Ross SH, Huynh T, Chen J, et al. Identified hidden genomic changes in mantle cell lymphoma using high-resolution single nucleotide polymorphism genomic array. Exp Hematol 2009 Aug;37(8):937-946.
OBJECTIVE: Mantle cell lymphoma (MCL) is a lymphoma characterized by aberrant activation of CCND1/cyclin D1 followed by sequential genetic abnormalities. Genomic abnormalities in MCL have been extensively examined by classical cytogenetics and microarray-based comparative genomic hybridization techniques, pointing out a number of alterations in genomic regions that correlate with the neoplastic phenotype and survival. Recently, single nucleotide polymorphism genomic microarrays (SNP-chip) have been developed and used for analysis of cancer genomics. This technique allows detection of genomic changes with higher resolution, including loss of heterozygosity without changes of gene dosage, so-called acquired uniparental disomy (aUPD). MATERIALS AND METHODS: We have examined 33 samples of MCL (28 primary MCL and 5 cell lines) using the 250,000 SNP-chip from Affymetrix. RESULTS: Known alterations were confirmed by SNP arrays, including deletion of INK4A/ARF, duplication/amplification of MYC, deletion of ATM, and deletion of TP53. We also identified a duplication/amplification that occurred at 13q involving oncogenic microRNA, miR17-92. We found other genomic abnormalities, including duplication/amplification of cyclin D1, del(1p), del(6q), dup(3q) and dup(18q). Our SNP-chip analysis detected these abnormalities at high resolution, allowing us to narrow the size of the commonly deleted regions, including 1p and 6q. Our SNP-chip analysis detected a number of aUPD sites, including whole chromosome 9 aUPD and 9p aUPD. We also found an MCL case with 19p, leading to homozygous deletion of TNFSF genes. CONCLUSION: SNP-chip analysis detected in MCL very small genomic gains/losses, as well as aUPDs, which could not be detected by more conventional methods.
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