染色体易位
核型
髓系白血病
荧光原位杂交
生物
表型
融合基因
断点
髓样
基因
细胞遗传学
白血病
染色体
遗传学
癌症研究
分子生物学
作者
Claudio Panarello,Cristina Rosanda,Cristina Morerio
摘要
Abstract The cryptic translocation t(5;11)(q35;p15.5), which creates a NSD1‐NUP98 fusion gene, has been associated with a deletion of the long arm of chromosome 5, del(5q), in pediatric acute myeloid leukemia (AML) patients with differentiated phenotype. We screened five pediatric cases of AML with apparently normal karyotype by use of fluorescence in situ hybridization analysis and detected one case with early myeloid phenotype and poor clinical outcome, but with the same breakpoints and no del(5q). These findings point to the involvement of t(5;11) as an early event in leukemogenesis. Screening for this translocation in AML patients with apparently normal karyotype at onset is recommended. © 2002 Wiley‐Liss, Inc.
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