Loss of heterozygosity (LOH) at 17q and 14q in human lung cancers
Loss of heterozygosity (LOH) at 17q and 14q in human lung cancers
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DOI：
10.1038/sj.onc.1202230
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发表时间：
1998-12-10
期刊：
影响因子：
8
通讯作者：
Hiai, H
中科院分区：
文献类型：
--
作者：
Abujiang, P;Mori, TJ;Hiai, H
我们最近对乌拉坦诱导的小鼠SMXA RI株肺腺瘤的连锁研究发现了两个宿主抗性基因，Par1(11号染色体)和Par3(12号染色体)。根据小鼠和人的同步性，Par1和Par3的MAP位置对应于人的17q11-23和14q11-24。在这项研究中，我们检测了30例具有匹配的正常DNA的原发肺腺癌样本中这两个同源人类染色体区域的杂合性缺失(LOH)。利用15个高度多态的标记，分别在人类14号和17号染色体上发现了两个常见的缺失区。在17q21，在17个信息性肿瘤中，有9个(53%)在D17S588和D17S518之间出现杂合性缺失。另一方面，在14q11-12，在D14S261和D14S80之间的22个信息性肿瘤中，有7个(32%)显示了杂合性缺失。随后，我们检查了25例鳞状细胞癌(SQ)和24例小细胞癌(SCC)。在14q11-12，16个信息性SQ中有6个(38%)和12个信息性SCC中有5个(42%)出现LOH。相反，在17q11-23，15个信息性SQ中有1个(7%)和14个SCC中有2个(14%)出现LOH。因此，17q上的基因似乎选择性地影响腺癌，而14q上的另一个基因似乎选择性地影响三种类型的肺癌。这些观察结果表明，比较遗传学分析为研究人类肺癌发生的多因素过程中涉及的基因提供了一种很有前途的方法。
Our recent linkage study of urethane-induced pulmonary adenomas in SMXA RI strains of mouse revealed two host resistance genes, Par1 (chromosome 11) and Par3 (chromosome 12). The map positions of Par1 and Par3 correspond to human 17q11-23 and 14q11-24, based on synteny between mouse and human. In this study, we examined the loss of heterozygosity (LOH) in these two homologous human chromosomal regions in 30 primary lung adenocarcinoma samples with matched normal DNA. Using 15 highly polymorphic markers, two commonly deleted regions were identified on human chromosomes 14 and 17, respectively. At 17q21, nine (53%) of 17 informative tumors showed LOH between D17S588 and D17S518. On the other hand, at 14q11-12, seven (32%) of 22 informative tumors showed LOH at loci between D14S261 and D14S80. Subsequently, we examined 25 squamous cell carcinomas (SQ) and 24 small cell carcinomas (SCC). At 14q11-12, six (38%) of 16 informative SQ and five (42%) of 12 informative SCC showed LOH. In contrast, at 17q11-23, one (7%) of 15 informative SQ and two (14%) of 14 SCC showed LOH. Therefore, the gene on 17q seemed to affect selectively adenocarcinomas, whereas the other gene on 14q, all three types of lung carcinomas. These observations indicate that a comparative genetic analysis provides a promising approach to survey genes involved in multifactorial process of human lung carcinogenesis.