Shimoyama Manabu, Yamamoto Katsuya, Nishikawa Shinichiro, Minagawa Kentaro, Katayama Yoshio, Matsui Toshimitsu
Hematology/Oncology, Department of Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, Japan.
Cancer Genet Cytogenet. 2009 Oct;194(1):38-43. doi: 10.1016/j.cancergencyto.2009.04.019.
Isodicentric chromosome 21, idic(21)(p11.2), is a rare but recurrent cytogenetic aberration in acute lymphoblastic leukemia. We describe here a novel case of acute myeloid leukemia (AML) with double idic(21)(p11.2). A 35-year-old man was diagnosed as having de novo AML with multilineage dysplasia because of 30% myeloperoxidase-positive blasts and trilineage dysplasia in the bone marrow. Surface marker analysis revealed that the blasts were positive for CD7, CD13, CD33, CD34, and HLA-DR. Chromosome analysis and spectral karyotyping showed 47,XY,+21,idic(21)(p11.2)x2, leading to pentasomy 21q. Fluorescence in situ hybridization demonstrated two RUNX1 signals on the idic(21)(p11.2), resulting in a total of five RUNX1 signals in metaphase spreads and interphase nuclei. These results suggest that the idic(21)(p11.2) could be implicated also in the pathogenesis of AML through amplification of genes including RUNX1 located on 21q.
等臂双着丝粒21号染色体,idic(21)(p11.2),是急性淋巴细胞白血病中一种罕见但反复出现的细胞遗传学异常。我们在此描述一例伴有双idic(21)(p11.2)的急性髓系白血病(AML)新病例。一名35岁男性因骨髓中30%的髓过氧化物酶阳性原始细胞和三系发育异常被诊断为伴有多系发育异常的初发AML。表面标志物分析显示原始细胞CD7、CD13、CD33、CD34和HLA-DR呈阳性。染色体分析和光谱核型分析显示为47,XY,+21,idic(21)(p11.2)x2,导致21q五体性。荧光原位杂交显示在idic(21)(p11.2)上有两个RUNX1信号,在中期分裂相和间期核中总共产生五个RUNX1信号。这些结果表明,idic(21)(p11.2)也可能通过位于21q上的包括RUNX1在内的基因扩增参与AML的发病机制。