Walker G J, Hayward N K, Falvey S, Cooksley W G
Queensland Institute of Medical Research, Herston, Australia.
Cancer Res. 1991 Aug 15;51(16):4367-70.
Loss of tumor suppressor genes is involved in the mechanism of tumorigenesis of many solid tumors. We tested 9 hepatitis B virus (HBV)-positive and 10 HBV-negative hepatocellular carcinomas for loss of somatic heterozygosity using 14 polymorphic probes mapping to chromosomes 4, 11, 13, and 17. Losses were found on all chromosome arms tested. The highest frequency of loss was observed at the D13S1 locus (67%) at band 13q12. Losses were also observed at three other loci on 13q. Twenty-one % of informative cases showed loss on 17p using the probe pYNZ22 which maps near the p53 locus. Losses on 4q were infrequent with 17% found at one locus and no loss at two others. The retinoblastoma gene and the locus on 17p were only inactivated in our HBV-negative tumors, although the numbers were too small for statistical significance. For all loci tested, we found no significant differences in the frequency of losses with HBV status, ethnic background, cirrhosis, grade of tumor, or presence of hemochromatosis.
肿瘤抑制基因的缺失参与了许多实体瘤的肿瘤发生机制。我们使用14个定位在4号、11号、13号和17号染色体上的多态性探针，对9例乙型肝炎病毒（HBV）阳性和10例HBV阴性肝细胞癌进行了体细胞杂合性缺失检测。在所有检测的染色体臂上均发现有缺失。在13q12带的D13S1位点观察到最高的缺失频率（67%）。在13q的其他三个位点也观察到缺失。使用定位在p53基因座附近的探针pYNZ22，21%的信息性病例在17p上显示缺失。4q上的缺失很少见，在一个位点发现17%的缺失，在另外两个位点未发现缺失。视网膜母细胞瘤基因和17p上的基因座仅在我们的HBV阴性肿瘤中失活，尽管数量太少，无统计学意义。对于所有检测的位点，我们发现缺失频率在HBV状态、种族背景、肝硬化、肿瘤分级或血色素沉着症的存在方面无显著差异。
