Liu Mira C P, Choong David Y H, Hooi Christine S F, Williams Louise H, Campbell Ian G
Cancer Genetics Laboratory, Victorian Breast Cancer Research Consortium, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Vic, Australia.
Cancer Lett. 2007 Mar 8;247(1):91-7. doi: 10.1016/j.canlet.2006.03.024. Epub 2006 Apr 27.
Chromosome 22q shows a high frequency of loss of heterozygosity (LOH) in ovarian cancers suggesting the existence of one or more important tumor suppressor genes (TSGs). The tissue inhibitor of metalloproteinase-3 (TIMP-3) is a plausible TSG candidate since it is often encompassed within these regions of LOH. TIMP-3 has not previously been investigated for somatic mutations or promoter hypermethylation in ovarian cancer. We analyzed 65 ovarian cancers for both somatic genetic mutations and TIMP-3 promoter hypermethylation. Screening of all coding exons of TIMP-3 did not reveal any somatic genetic mutations and only 1/65 showed TIMP-3 methylation. Our data indicate that inactivation of TIMP-3 by somatic mutation or promoter hypermethylation is rare in ovarian cancer.
22号染色体在卵巢癌中显示出较高的杂合性缺失（LOH）频率，这表明存在一个或多个重要的肿瘤抑制基因（TSG）。金属蛋白酶组织抑制剂-3（TIMP-3）是一个合理的TSG候选基因，因为它经常包含在这些LOH区域内。此前尚未对卵巢癌中的TIMP-3体细胞突变或启动子高甲基化进行研究。我们分析了65例卵巢癌的体细胞基因突变和TIMP-3启动子高甲基化情况。对TIMP-3所有编码外显子的筛查未发现任何体细胞基因突变，只有1/65显示TIMP-3甲基化。我们的数据表明，在卵巢癌中，体细胞突变或启动子高甲基化导致TIMP-3失活的情况很少见。
