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。

CD8+ CTL are the predominant tumoricidal effector cells. We find, however, that MHC class I-deficient mice depleted of CD8+ Tcells are able to mount an effective antitumor immunity after immunization with fused dendritic/tumor cells. Such immunity appears to be mediated by the generation of phenotypic and functional CD8+ CTL through CD4+ to CD8+ conversion, which we have demonstrated at the single cell level. CD4+ to CD8+ conversion depends on effective in vivo activation and is promoted by CD4+ T cell proliferation. The effectiveness of this process is shown by the generation of antitumor immunity through adoptive transfer of primed CD4+ Tcells to provide protection against tumor cell challenge and to eliminate established pulmonary metastases.

Direct chromo some analysis and FISH were performed on twelve prinary gastric carcinom as. Two of them had sinple chromosome changes: 48, XX, +8, +20, and 49, XY, +2, +8, +9, and tile others had complicated chromo some changes, which inchldesmuch more numerical and structural chro-inosome aberrations. Frequent structural changes in the complicated types involved chromosome 7, 3, 1, 5 and 12 etc. The del 7qwas noted in eight cases. The del (3p) and del (lp) were noted in six and five cases, respectively. The results plovide some mportant clues for isolation of the genes related to gastric cancer.

Comparative genomic hybridization (CGH) has been applied to detect recurrent chromosome al-terations in 62 primary gastric carcinomas. Several nomandom chromosomal changes, including gains of 8q (31 cases, 50%), 20q (29 cases, 47%) with a minimum gain region at 20q11.2 q12,13q (21 cases, 34%) with a minimum gain region at 13q22, and 3q (19 cases, 31%) were commonly ob-served. The regions most frequently lost included: 19p (23 cases, 37%), 17p (21 cases, 33%), and lp (14 cases, 23%). High copy number gain (DNA sequence amplification) was detected in 6 cases. Amplification of 8@3<124.2 and 20q11.2 q12 were observed in 3 cases. Gain of 20q and loss of 19p were confirmed by fluorescence in situ hybridization using corresponding bacterial artificial chromosomes (BAC) clones fiom those regions. The gain and loss of chromosomal regions idenfl-fled in this study provide candidate regions involved in gastric tumorigenesis.

目的应用一种能快速、准确识别胃癌标记染色体来源的技术，以提高对胃癌细胞复杂染色体畸变辨认的能力。方法采用改良的G显带染色体标本脱色后进行荧光原位杂交 (fluorescence in situ hybridization, FISH)，分别对胃癌系SGC-7901的两条标记染色体 (1和M 2) 和一例原发性胃癌的标记染色体 (M3) 进行分析。结果 显示了M 1、M2和M3有复杂的染色体结构畸变：del(7)(p15)/del(7)(q22); t(1; 3)(p11; q11)和del(7)(q32)。结论 该方法具有信号强、背景低和重复性好等优点，在识别胃癌染色体复杂结构改变中具有重要的作用。

The tmnom-associated antigen mucin 1 (MUCI) is a mnltifimctional protein involved in protection of muckous membranes, signal transduction, and mOdulation of the immume system. More than 70% of cancers overexpress MUCI, making MUC 1 a potential target for immnnotber apy. In the present study, MUCI transgenic mice were crossed with syngeneic strains that express the polyomavirus middle-T oncogene (PyMT) diiven by the mouse mammary tumour virus promoter long teminal repeat (MMTV-LTR). The resultant breed (MMT mice) developed spontaneous MUCI expressing mammary cmcinomas with 100% penetrance at 8-15 weeks of age. As fOund in buman breast cancer, the mammary carcinoma in MMT mice arose in multiple stages, Immumization with fusions of dendritic cells and MUC 1-positive tumour cells (PC/MUC1) induced MUCI specific immune responses that blocked or delayed the development of sponta neons breast carcinomas, in contrast, there was no delay of tumour development in MMT mice immmunized with in-adiated MC38/MUCI tumonr cells. The efficacy of fusion cells was closely correlated with the timing of initial immmlization, immumization with FC/MUCI initiated in MMT mice at<1, 1-2 and 2-3 months of age rendered 33, 5 and 0% of mice free of remora, respectively, up to 6 months. Whereas mice immunized in the later stage of tumour development succumbed to their disease, immunization resulted in control of tumour progression and prolongation of life. These results indicate that immunization with FC/MUC1 can generate an anti-MUCI response that is sufficient to delay the development of spontaneous mammary carcinomas and control tumour progression in MMT mice.