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.

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.

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.

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。

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.