Kuchinskaya Ekaterina, Heyman Mats, Nordgren Ann, Schoumans Jacqueline, Staaf Johan, Borg Ake, Söderhäll Stefan, Grandér Dan, Nordenskjöld Magnus, Blennow Elisabeth
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Br J Haematol. 2008 Mar;140(5):572-7. doi: 10.1111/j.1365-2141.2007.06917.x.
A tiling path 33K BAC array was used to study 28 children with acute lymphoblastic leukaemia (ALL) who had normal or failed G-banded karyotypes. Twenty-two patients (79%) had a total of 135 copy number alterations (CNA) (69 gains and 66 losses); most of these patients showed CNA that were below the resolution of G-banding. Molecular cytogenetic and array comparative genomic hybridization results enabled the division of B-precursor ALL patients into five groups: high hyperdiploidy, intrachromosomal amplification of 21q, ETV6/RUNX1 rearrangement, others and no CNA. Apart from a shared deletion of 9p21.3, T-ALL patients had additional small CNA, with no region in common.
使用一个平铺路径33K BAC阵列来研究28例急性淋巴细胞白血病(ALL)患儿,这些患儿的G带核型正常或异常。22例患者(79%)共有135个拷贝数改变(CNA)(69个增益和66个缺失);这些患者中的大多数显示出低于G带分辨率的CNA。分子细胞遗传学和阵列比较基因组杂交结果使得B前体ALL患者能够分为五组:高超二倍体、21q染色体内部扩增、ETV6/RUNX1重排、其他组和无CNA组。除了9p21.3的共同缺失外,T-ALL患者还有额外的小CNA,没有共同区域。