间变性
威尔姆斯瘤
癌症研究
生物
计算生物学
遗传学
作者
Richard D. Williams,Reem Al‐Saadi,Rachael Natrajan,Alan Mackay,Tasnim Chagtai,Suzanne E. Little,Sandra Hing,Kerry Fenwick,Alan Ashworth,Paul E. Grundy,James R. Anderson,Jeffrey S. Dome,Elizabeth J. Perlman,Chris Jones,Kathy Pritchard‐Jones
摘要
Abstract Anaplasia in Wilms tumor, a distinctive histology characterized by abnormal mitoses, is associated with poor patient outcome. While anaplastic tumors frequently harbour TP53 mutations, little is otherwise known about their molecular biology. We have used array comparative genomic hybridization (aCGH) and cDNA microarray expression profiling to compare anaplastic and favorable histology Wilms tumors to determine their common and differentiating features. In addition to changes on 17p, consistent with TP53 deletion, recurrent anaplasia‐specific genomic loss and under‐expression were noted in several other regions, most strikingly 4q and 14q. Further aberrations, including gain of 1q and loss of 16q were common to both histologies. Focal gain of MYCN , initially detected by high resolution aCGH profiling in 6/61 anaplastic samples, was confirmed in a significant proportion of both tumor types by a genomic quantitative PCR survey of over 400 tumors. Overall, these results are consistent with a model where anaplasia, rather than forming an entirely distinct molecular entity, arises from the general continuum of Wilms tumor by the acquisition of additional genomic changes at multiple loci. © 2011 Wiley Periodicals, Inc.
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