Reardon D A, Michalkiewicz E, Boyett J M, Sublett J E, Entrekin R E, Ragsdale S T, Valentine M B, Behm F G, Li H, Heideman R L, Kun L E, Shapiro D N, Look A T
Department of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Cancer Res. 1997 Sep 15;57(18):4042-7.
We analyzed 27 samples of primary medulloblastoma, using comparative genomic hybridization and a novel statistical approach to evaluate chromosomal regions for significant gain or loss of genomic DNA. An array of nonrandom changes was found in most samples. Two discrete regions of high-level DNA amplification of chromosome bands 5p15.3 and 11q22.3 were observed in 3 of 27 tumors. Nonrandom genomic losses were most frequent in regions on chromosomes 10q (41% of samples), 11 (41%), 16q (37%), 17p (37%), and 8p (33%). Regions of DNA gain most often involved chromosomes 17q (48%) and 7 (44%). These findings suggest a greater degree of genomic imbalance in medulloblastoma than has been recognized previously and highlight chromosomal loci likely to contain oncogenes or tumor suppressor genes that may contribute to the molecular pathogenesis of this tumor.
我们使用比较基因组杂交和一种新颖的统计方法,对27个原发性髓母细胞瘤样本进行分析,以评估染色体区域基因组DNA的显著增加或减少情况。在大多数样本中发现了一系列非随机变化。在27个肿瘤中的3个中观察到染色体带5p15.3和11q22.3的两个离散的高水平DNA扩增区域。非随机基因组缺失在染色体10q(41%的样本)、11(41%)、16q(37%)、17p(37%)和8p(33%)区域最为常见。DNA增加区域最常涉及染色体17q(48%)和7(44%)。这些发现表明,髓母细胞瘤中的基因组失衡程度比之前认识到的更大,并突出了可能包含致癌基因或肿瘤抑制基因的染色体位点,这些基因可能有助于该肿瘤的分子发病机制。