Lee C L, Lee S H, Ghose T, Fernandez L A, Colp P
Department of Microbiology, Dalhousie University, Halifax, Nova Scotia, Canada.
Cancer Genet Cytogenet. 1991 Jul 1;54(1):101-8. doi: 10.1016/0165-4608(91)90036-t.
In this study we described the isolation of a subclonal EBV-transformed human CLL B-cell line with retarded growth rate and metastatic potential from its clonal parent (D10-1), which was karyotyped: 46.XY.dup(1)(q11----q32). The subclone, designated D10-1C, was isolated by limiting dilution of D10-1 following selection in 8-azaguanine-supplemented medium. Chromosome analysis of D10-1C revealed a constitution of 47,XY, + 11.dup(1)(q11----q32). This is the first demonstration that partial trisomy 1q-associated growth advantage in human cancer cells can be retarded by the presence of an additional dose of chromosome 11. Human chromosome 11 had been shown to be responsible for the suppression of tumor development. Whether the same suppressor genes are involved in D10-1C remains to be elucidated. The procedure described here for the enrichment and isolation of a growth-retarded mutant from D10-1 may be applicable in other malignant cell systems.
在本研究中，我们描述了从其克隆亲本（D10-1）中分离出一株生长速率迟缓且具有转移潜能的亚克隆EBV转化人慢性淋巴细胞白血病B细胞系，其核型为：46，XY，dup(1)(q11----q32)。该亚克隆命名为D10-1C，是在添加8-氮杂鸟嘌呤的培养基中筛选后，通过对D10-1进行有限稀释分离得到的。对D10-1C的染色体分析显示其组成为47，XY，+ 11，dup(1)(q11----q32)。这首次证明了在人类癌细胞中，1q部分三体相关的生长优势可因额外剂量的11号染色体的存在而受到抑制。已表明人类11号染色体负责抑制肿瘤发展。D10-1C中是否涉及相同的抑癌基因仍有待阐明。本文所述的从D10-1中富集和分离生长迟缓突变体的方法可能适用于其他恶性细胞系统。
