We used gene targeting in mice to insert a His 6 -tagged mouse c-Myc cDNA, MycHis , head to head into the mouse immunoglobulin heavy-chain locus, Igh, just 5V of the intronic enhancer, EA. The insertion of Myc His mimicked both the human t(8;14)(q24;q32) translocation that results in the activation of MYC in human endemic Burkitt lymphomas and the homologous mouse T(12;15) translocation that deregulates Myc in certain mouse plasmacytomas. Beginning at the age of 6 months, MycHis transgenic mice developed Bcell and plasma neoplasms, such as IgM + lymphoblastic B-cell lymphomas, Bcl-6 + diffuse large B-cell lymphomas, and CD138 + plasmacytomas, with an overall incidence of 68% by 21 months. Molecular studies of lymphoblastic B-cell lymphoma, the most prevalent neoplasm (50% of all tumors), showed that the lymphomas were clonal, overexpressed Myc His , and exhibited the P2 to P1 promoter shift in Myc expression, a hallmark of MYC/Myc deregulation in human endemic Burkitt lymphoma and mouse plasmacytoma. Only 1 (6.3%) of 16 lymphoblastic B-cell lymphomas contained a BL-typical point mutation in the amino-terminal transactivation domain of Myc His , suggesting that most of these tumors are derived from naive, pregerminal center B cells. Twelve (46%) of 26 lymphoblastic B-cell lymphomas exhibited changes in the p19ArfMdm2-p53 tumor suppressor axis, an important pathway for Myc-dependent apoptosis. We conclude that Myc His insertion into Igh predictably induces B-cell and plasma-cell tumors in mice, providing a valuable mouse model for understanding the transformation-inducing consequences of the MYC/Mycactivating endemic Burkitt lymphoma t(8;14)/plasmacytoma T(12;15) translocation. (Cancer Res 2005; 65(4): 1306-15)

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Allergenicity of genetically-modified (GM) soybean was evaluated in male Sprague Dawley rats. To confirm the GM soybean used in this study, the polymerase chain reaction (PCR) was performed using the chromosomal DNA of soybeans. The PCR result provided the clear discrimination of genetically-modified (GM) soybeans. To evaluate the allergenicity of GM soybean and non-GM control one, the soybean homogenate was sensitized subcutaneously 3 times a week for 3 weeks. The doses of soybean were 0, 2 and 20 mg/kg in the protein basis. A week after the last sensitization, antisera were recovered from individual animals. When the sera were injected intradermally on the clipped back of unsensitized rats with various dilutions, followed by a challenge with 20 mg/kg of soybean homogenate containing 1% Evans blue, no sign of passive cutaneous anaphylaxis reaction was detected. In addition, when the sera were treated in the cultures of peritoneal mast cells, the increase of histamine release by anti-(GM soybean) sera was not observed when compared to that by anti-(non-GM soybean) sera. The present results indicate that the GM soybean might not act as a strong allergen in male Sprague Dawley rats.

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