Department of Laboratory Medicine and Genetics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Leuk Res. 2012 Apr;36(4):418-21. doi: 10.1016/j.leukres.2011.12.021. Epub 2012 Feb 5.
The present study was performed to provide direct evidence on copy number changes during progression from chronic phase (CP) to blastic phase (BP) in chronic myeloid leukemia (CML) through a longitudinal follow-up study. Matched CP and BP samples in three patients were analyzed using high-resolution array comparative genomic hybridization (aCGH) chips. During blastic transformation, loss of large genomic segments including 6q14.1-q22.31, chromosome 7 and 9p13.2-p21.3 were noted. Furthermore, small-sized copy number changes involving cancer-associated genes were observed. In addition, we identified a novel fusion gene consisted of PAX5 and MLLT3 (AF9). It is likely that blastic transformation of CML is a multi-step process associated accumulation of several genomic events which may largely overlap with those found in acute leukemias.
本研究通过纵向随访研究,提供了在慢性髓性白血病(CML)从慢性期(CP)向急变期(BP)进展过程中拷贝数变化的直接证据。使用高分辨率 array 比较基因组杂交(aCGH)芯片分析了三例患者的 CP 和 BP 匹配样本。在急变转化过程中,观察到包括 6q14.1-q22.31、7 号染色体和 9p13.2-p21.3 在内的大片段基因组缺失,以及涉及癌相关基因的小片段拷贝数变化。此外,我们鉴定了一个由 PAX5 和 MLLT3(AF9)组成的新融合基因。CML 的急变转化可能是一个多步骤过程,涉及多个基因组事件的累积,这些事件可能与急性白血病中发现的事件有很大重叠。