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.

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。

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.

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。

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.