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为了解细胞在体外传代过程中以及在细胞离体诱导癌变过程中，遗传不稳定性及其规律，选择了１１个多态微卫星ＤＮＡ标记（ＭＳ），采用ＰＣＲ－聚丙烯酰胺凝胶电泳及银染技术对本室建立的永生性胃粘膜细胞系ＧＥＳ－１的不同代数（Ｐ８、Ｐ２１、Ｐ５８、Ｐ１００）及化学致癌剂转化的ＧＥＳ－１细胞系ＭＣ进行了ＭＳ的微卫星ＤＮＡ不稳定（ｍｉｃｒｏｓａｔｅｌｉｔｅｉｎｓｔａｂｉｌｉｔｙ，ＭＳＩ）及杂合性缺失（ｌｏｓｓｏｆｈｅｔｅｒｏｚｙｇｏｓｉｔｙ，ＬＯＨ）分析。结果发现，８代以前的细胞与正常细胞相比，有较高的ＭＳＩ和ＬＯＨ（４／１１），而从８代以后随传代时间延长降至１／１１，并基本稳定在这一频率。经过化学致癌剂处理的ＭＣ细胞并未出现显著增加的ＭＳＩ和ＬＯＨ。结果提示，胃粘膜细胞系中，高频率的ＭＳ突变（ＭＳＩ和ＬＯＨ）可能是ＳＶ４０整合到细胞基因组中的结果，与ＭＮＮＧ剂无关，细胞系建成后，具有相对稳定的遗传状态
In order to understand the process of cell passage in vitro and the genetic instability and its regularity in vitro induced canceration, 11 polymorphic microsatellite DNA markers (MS) were selected and analyzed by PCR-polyacrylamide gel electrophoresis and Silver staining technique was used to detect the microsatellite DNA instability of MS in different generations (P8, P21, P58, P100) of immortalized gastric mucosal cell line GES-1 and GES-1 cell line MC transformed with chemical carcinogens micrositeliteinstability, MSI) and loss of heterozygosity (LOH) analysis. As a result, it was found that MSCs and LOHs (4/11) had higher MSI and LOH (4/11) compared with normal cells, but decreased to 1/11 with passage time from the 8th passage, and basically stabilized at this frequency. MC cells treated with chemical carcinogens showed no significant increase in MSI and LOH. The results suggest that the high frequency of MS mutations (MSI and LOH) in gastric mucosal cell lines may be the result of SV40 integration into the cell genome, has nothing to do with MNNG agents, the cell line has a relatively stable genetic state