Tanner M M, Tirkkonen M, Kallioniemi A, Collins C, Stokke T, Karhu R, Kowbel D, Shadravan F, Hintz M, Kuo W L
Department of Laboratory Medicine, Tampere University Hospital, Finland.
Cancer Res. 1994 Aug 15;54(16):4257-60.
Studies by comparative genomic hybridization have indicated that a major new locus for DNA amplification in breast cancer is 20q13 and suggested that this genetic event is associated with aggressive clinical behavior. We used interphase fluorescence in situ hybridization with anonymous cosmid probes and gene-specific P1 clones to determine the minimal common region of increased copy number and to study involvement of known genes at 20q13. Based on high-level copy number increases (3 to 10-fold) found with one or more probes in 5 of 14 (35%) breast cancer cell lines and in 3 of 36 (8%) primary tumors, the critical region was narrowed to approximately 1.5 megabases at 20q13.2 defined by fractional length pter values 0.81-0.84. Previously known genes were excluded as candidates, implying that this chromosomal region harbors a novel oncogene that contributes to the malignant progression of breast cancer.
通过比较基因组杂交研究表明,乳腺癌中DNA扩增的一个主要新位点是20q13,并提示这一基因事件与侵袭性临床行为相关。我们使用间期荧光原位杂交技术,结合匿名黏粒探针和基因特异性P1克隆,来确定拷贝数增加的最小共同区域,并研究20q13上已知基因的参与情况。基于在14个乳腺癌细胞系中的5个(35%)以及36个原发性肿瘤中的3个(8%)中,使用一种或多种探针发现的高水平拷贝数增加(3至10倍),关键区域被缩小至20q13.2上约1.5兆碱基,由分数长度的端粒值0.81 - 0.84定义。先前已知的基因被排除作为候选基因,这意味着该染色体区域含有一个新的癌基因,它有助于乳腺癌的恶性进展。