Thompson F H, Taetle R, Trent J M, Liu Y, Massey-Brown K, Scott K M, Weinstein R S, Emerson J C, Alberts D S, Nelson M A
Arizona Cancer Center, College of Medicine, University of Arizona, Tucson, USA.
Cancer Genet Cytogenet. 1997 Jul 15;96(2):106-10. doi: 10.1016/s0165-4608(96)00307-x.
In a series of 128 karyotyped ovarian carcinomas, 42% of cases with chromosome 1 clonal structural abnormalities had breaks at band 1p36 (usually involving translocations of unknown material). Fluorescent in situ hybridization (FISH) studies using combinations of 1 centromere and 1p36.3-specific probes (16 cases) or 1 centromeric and 17 whole-chromosome paint probes (11 cases with 1p+) revealed a trend toward deletion of 1pter relative to 1 centromere (63%); intratumor heterogeneity; and the origin of 1p+ in 3/11 cases (27%) from chromosome 17 [t(1;17)(p36;?)]. The frequency of this specific breakpoint and its involvement in recurrent translocations suggest that these regions are loci for genes important in the pathogenesis of a subset of sporadic ovarian carcinomas.
在一系列128例已进行核型分析的卵巢癌中，42%染色体1存在克隆性结构异常的病例在1p36带出现断裂（通常涉及未知物质的易位）。使用1个着丝粒和1p36.3特异性探针组合（16例）或1个着丝粒和17个全染色体涂染探针（11例1p+）进行的荧光原位杂交（FISH）研究显示，相对于1个着丝粒，1pter有缺失的趋势（63%）；肿瘤内异质性；以及11例中的3例（27%）1p+起源于染色体17[t(1;17)(p36;?)]。这种特定断点的频率及其参与复发性易位表明，这些区域是散发性卵巢癌一部分发病机制中重要基因的位点。
