Characterization of the human myeloid leukemia‐derived cell line GF‐D8 by multiplex fluorescence in situ hybridization, subtelomeric probes, and comparative genomic hybridization
Characterization of the human myeloid leukemia‐derived cell line GF‐D8 by multiplex fluorescence in situ hybridization, subtelomeric probes, and comparative genomic hybridization
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通过多重荧光原位杂交、亚端粒探针和比较基因组杂交表征人骨髓性白血病来源的细胞系 GF-D8
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发表时间：
1999
期刊：
影响因子：
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通讯作者：
L. Kearney
中科院分区：
文献类型：
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作者：
S. Tosi;G. Giudici;A. Rambaldi;S. Scherer;P. Bray;Luke Dirscherl;A. Biondi;L. Kearney
人髓性白血病细胞系GF-D8由急性髓性白血病FAB亚型M1（AML-M1）患者的外周血原始细胞建立。染色体组型，这并没有显着改变了几年的文化，最初被描述为44，XY，-5，del（7 q），inv（7 q），add（8 q），add（11 q），del（12 p），-15，-17，+mar。随着荧光原位杂交（FISH）技术的出现，准确地描述这种复杂的染色体组型的前景变得可行。在本研究中，我们应用了24色全染色体染色，并使用基于过滤器的检测系统和多重FISH（M-FISH）专有软件分析了结果。这导致了核型的细化和迄今未被怀疑的染色体重排的鉴定。M-FISH鉴定了add（8 q）和add（11 q）以及小标记染色体的起源。del（7 q）和del（12 p）都被重新定义为不平衡易位，而一条明显正常的11号染色体被证明是t（11;17）。重要的是，del（12 p）被证明是der（12）t（7;12）。单色全染色体染色研究证实了这些发现，但也发现了原始M-FISH分析中未发现的隐藏t（Y;12）。然后，我们使用一套完整的染色体特异性亚端粒探针进行FISH筛选试验。这允许鉴定参与易位的p和q亚端粒区域，并指示8 q亚端粒区域的扩增。比较基因组杂交（CGH）揭示了一个高度不平衡的核型，因为缺失伴随着大多数易位，并确定扩增区域为8q22.3-qter和11 q21-qter。最后，传统的荧光原位杂交与着丝粒和独特的序列探针是必要的，以阐明所有的重排。Genes Chromosomes Cancer 24：213-221，1999.© 1999 Wiley利斯公司
The human myeloid leukemia cell line GF‐D8 was established from the peripheral blood blasts of a patient with acute myeloid leukemia FAB subtype M1 (AML‐M1). The karyotype, which has not changed significantly over several years of culture, was described initially as 44,XY,‐5,del(7q),inv(7q),add(8q),add(11q),del(12p),‐15,‐17,+mar. With the advent of multicolor fluorescence in situ hybridization (FISH) techniques, the prospect of accurately characterizing this complex karyotype became feasible. In the present study, we applied 24‐color whole‐chromosome painting and analyzed the results using a filter‐based detection system and proprietary software for multiplex FISH (M‐FISH). This resulted in the refinement of the karyotype and the identification of hitherto unsuspected chromosome rearrangements. M‐FISH identified the origin of the add(8q) and add(11q) as well as the small marker chromosome. Both the del(7q) and del(12p) were redefined as unbalanced translocations and an apparently normal chromosome 11 was shown to be t(11;17). Importantly, the del(12p) was shown to be a der(12)t(7;12). Single‐color whole‐chromosome painting studies confirmed these findings, but also identified a cryptic t(Y;12) not seen in the original M‐FISH analysis. We then carried out a FISH screening assay using a complete set of chromosome‐specific subtelomeric probes. This allowed the identification of p and q subtelomeric regions involved in the translocations and indicated amplification of the 8q subtelomeric region. Comparative genomic hybridization (CGH) revealed a highly unbalanced karyotype, as deletions accompanied the majority of translocations, and identified the regions of amplification as 8q22.3‐qter and 11q21‐qter. Finally, conventional FISH with centromeric and unique sequence probes was necessary to elucidate all of the rearrangements. Genes Chromosomes Cancer 24:213–221, 1999. © 1999 Wiley‐Liss, Inc.
恶性骨髓疾病中常见缺失的 7 号染色体区域的细胞遗传学和分子描绘。
影响因子：
20.3
作者：
LeBeau,MM;Espinosa3rd,R;Davis,EM;Eisenbart,JD;Larson,RA;Green,ED
通讯作者：
Green,ED
通过荧光原位杂交鉴定的血液恶性肿瘤中涉及带 12p13 的平衡重排断点的异质性：TEL (ETV6 ) 仅涉及一半。
影响因子：
20.3
作者：
Sato,Y;Bohlander,SK;Kobayashi,H;Reshmi,S;Suto,Y;Davis,EM;Espinosa,R;Hoopes,R;Montgomery,KT;Kucherlapati,RS;LeBeau,MM;Rowley,JD
通讯作者：
Rowley,JD
与倒位 16 相关的 16p 缺失的分子特征定义了白血病发生的关键融合。
影响因子：
20.3
作者：
Marlton,P;Claxton,DF;Liu,P;Estey,EH;Beran,M;LeBeau,M;Testa,JR;Collins,FS;Rowley,JD;Siciliano,MJ
通讯作者：
Siciliano,MJ