To investigate chromosome aberrations and their role in the genesis and development of primary gastric cancer. Methods: An improved, direct chromosome preparation from solid tumors was adopted for G-banding analysis followed by FISH on decolored G-banding chromosomes so that chromosome aberrations could be confirmed at DNA level. Results: A total of 28 primary gastric cancer specimens were studies. Case 1 and case 2 had simple chromosome numerical changes: 49, XY, +2, +8, +9 and 48, +8, +20, respectively. All but case 1 and 2 had complicated chromosome abnormalities. Chromosome structural of frequent occurrence involved del (7q)(21/26), (delOp)(14/26), del (lp)(ll/26) and del (17p)(10/26). The chromosome abnormalities could be simple and complicated. In former, numerical changes involving 1 to 3 chromosome could be observed. Trisomies 8 and 9 might represent a ytogenetic subgroup of primary gastric cancer. In the later, the del (7q) was the most consistent aberration. 7q32-qter was the commonly lost segment. Conclusion: Numerical and structural alterations of chromosomes are present in primary gastric cancer. Del (7q) is one of the structural change characteristic of primary gastric cancer. In the 7q32qter fragment, a tumor suppressor gene probably exists and it may have close relation to the genesis and progression of gastric cancer.

Genetically modified mice with spontaneous development of mammary carcinoma provide a powerful tool to study the efficacy of tumor vaccines, since they mimic breast cancer development in humans We used a transgenic murine model expressing poly-omavirus middle T oncogene and mucin I tumor-associated Ag to determine the prevenfive effect of a dendrific/tumor fusion cell vaccine. The MMT (a transgenic murine model) mice developed mammary carcinoma between the ages of 65-108 days with 100% penetrance. No spontaneous CTL were detected. However, prophylacfic vaccinafion of MMT mice with dendrific/tumor fusion cells induced polyclonal CTL activity against spontaneous mammary carcinoma cells and rendered 57-61% of the mice free of the disease at the end of experiment (180 days). Furthermore, the level of CTL activity was maintained with mulfiple vaccinafions. The antitumor immunity induced by vaccination with dendrific/tumor fusion cells reacted differently to injected tumor cells and autochthonous tumor. Whereas the injected tumor cells were rejected, the autochthonous tumor evaded the atiack and was allowed to grow. Collecfively these results indicate that prophylactic vaccinafion with dendrific/tumor fusion cells confers sufficient antfiumor immunity to counter the tumorigenesis of potent oncogenic products The findings in the present study are highly relevant to cancers in humans.

用改良的直接法分析了16例原发性胃癌的细胞遗传学改变，其染色体变化可分为简单型和复杂型两种。简单型只涉及1～3条染色体改变，以染色体三体为主，其中8号和9号染色体三体可能构成胃癌的一个细胞遗传学亚型。复杂型涉及较多的染色体数目和结构异常，经常出现的结构异常为7q-、3p-和1p-，其中7q-为本研究中最一致的结构异常，可能是原发性胃癌的特征性染色体改变之一。

目的检测原发性胃癌的染色体畸变，分析这些变化在胃癌发生和发展中的作用。方法用改良的实体瘤染色体直接制备法，对28例原发性胃癌染色体进行G显带分析，在此基础上建立了一种G显带后脱色，再进行荧光原位杂交(Hs H)的方法m分子水平上证实染色体DNA的变化。结果病例1，2具有简单染色体数目改变，核型分别为49，XY，+2，+8，+9和47，XX，+8，+20。其余26例原发性胃癌的染色体改变复杂，常见的染色体结构异常包括，7q-(21/26)、3p-(14/26)、1p-(11/26)和17p-(10/26)。结论原发性胃癌的染色体改变可分为两种类型：简单型只涉及1～3条染色体 数目改变，8号和9号染色体三体可能构成胃癌的一个细胞遗传学亚型，复杂型涉及较多染色体数目和结构畸变，7q-为最一致的结构异常，可认为是原发性胃癌特征性染色体结构改变之一，7q32-qter区域可能含有一个与胃癌发生和发展密切相关的抑癌基因。

肿瘤起源的染色体学说已经得到广泛证实。染色体变化可以改变某些关键基因的功能，导致细胞过量增殖，最终形成肿瘤。在慢性粒细胞性白血病中，t（9；22）形成一种嵌合DNA，即22号染色体“-bcr”区域与9号染色体c-abl癌基因融合，融合后的c-abl基因编码一种p210嵌合蛋白，此蛋白质具有自动催化酪氨酸酶活性，体外实验使幼稚造血细胞发生恶性转化。因此，肿瘤细胞染色体分析，对寻找肿瘤相关基因有着重要的意义。