目的探讨DCC基因表达缺失与卵巢恶性肿瘤发生、发展及临床病理特征的关系。方法应用逆转录聚合酶链反应（RT-PCR）技术、目的基因片段克隆测序的方法，证实正常卵巢组织中DCC基因的正常表达：并以β-肌动蛋白作为内对照，在10例正常卵巢组织、10例卵巢良性肿瘤组织、34例原发性卵巢恶性肿瘤组织中检测DCC基因表达缺失情况。结果正常卵巢组织中DCC基因表达缺失率为0%：卵巢良性肿瘤组织为20%：卵巢恶性肿瘤为56%（19/34），其中浆液性囊腺癌14例（14/18）、黏液性囊腺癌4例（4/11），两者比较，差异有显著意义（P<0.05）。卵巢恶性肿瘤临床分期Ⅲ～Ⅳ期的25例中，17例DCC基因表达缺失（68%）：组织学分级低分化10例中，9例DCC基因表达缺失（90%）：盆腹腔转移的28例中，17例DCC基因表达缺失。结论卵巢恶性肿瘤组织中，DCC基因呈表达缺失或低表达：临床分期Ⅲ～Ⅳ期、组织学分化程度低、有盆腹腔肿瘤转移的恶性肿瘤组织中，DCC基因表达缺失率增高。DCC基因表达缺失与卵巢恶性肿瘤的发生、发展及转移、浸润有关。

Matrix metalloproteinases (MMPs) and their tissue inhibitors play important roles in the remodeling of extracellular matrix (ECM). MMP-26, also called endometase or matrilysin-2, is a novel member of the MMP family. The present study was to investigate the temporal and spatial expression of MMP-26 mRNA in mouse uterus during the estrous cycle and early pregnancy by using in situ hybridization and semi-quantitative RT-PCR. In this study, MMP-26 mRNA was found to be localized to the luminal and glandular epithelium at proestrus and estrus,and the expression level was decreased significantly from metestrus to dioestrus. During pre-implantation period, MMP-26 mRNA was predominantly expressed in luminal and glandular epithelium at much higher level;whereas it switched to stroma during peri-implantation period, and also appeared in the blastocysts and the implantation sites. The results suggested that MMP-26 might play a role in the cycling changes of mouse uterus during the estrous cycle and embryo implantation.