Chromosomal imbalances in adult T-cell leukemia revealed by comparative genomic hybridization: gains at 14q32 and 2p16-22 in cell lines
Chromosomal imbalances in adult T-cell leukemia revealed by comparative genomic hybridization: gains at 14q32 and 2p16-22 in cell lines
复制标题
DOI：
10.1007/s100380050178
复制
发表时间：
1999-01-01
影响因子：
3.5
通讯作者：
Inazawa, J
中科院分区：
文献类型：
--
作者：
Ariyama, Y;Mori, T;Inazawa, J
比较基因组杂交被用来确定染色体不平衡的8个细胞系和12个血液样本的成人T细胞白血病/淋巴瘤（ATL）患者。细胞系中最常过度表达的染色体是2 p（6例）、7 q（4例）和14 q（4例），最小共同区域分别位于2 p16 -22、7 q21 -36和14 q32。仅在7个临床样本中检测到明显的不平衡。染色体14 q32和2 p16 -22分别含有TCL 1和转录因子HTLF（人T细胞白血病病毒增强因子）。FISH分析显示，TCL 1并不与TCRA并列，尽管14 q32扩增，但我们在任何ATL细胞系中均未检测到TCL 1的表达。此外，HTLF的表达没有升高的ATL细胞系轴承增殖的2 p。这些结果表明，染色体区域2 p16 -22和14 q32港口基因以外的HTLF和TCL 1参与细胞永生化或在ATL的发病机制。
Comparative genomic hybridization was used to identify chromosomal imbalances in eight cell lines and 12 blood samples from patients with adult T-cell leukemia/lymphoma (ATL). The chromosomes most often over-represented in the cell lines were 2p (6 cases), 7q (4 cases), and 14q (4 cases), with minimal common regions at 2p16-22, 7q21-36, and 14q32, respectively. Distinct imbalances were detected in only 7 of the clinical samples. Chromosomes 14q32 and 2p16-22 harbor TCL1 and a transcription factor, HTLF (human T-cell leukemia virus enhancer factor), respectively. FISH analysis revealed that TCL1 did not juxtapose to TCRA, and we detected no expression of TCL1 in any of the ATL cell lines despite the 14q32 amplifications. Moreover, expression of HTLF was not elevated in the ATL cell lines bearing multiplication of 2p. These results suggest that chromosomal regions 2p16-22 and 14q32 harbor genes other than HTLF and TCL1 that are involved in cellular immortalization or in the pathogenesis of ATL.