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Genetics Division, [Y. H., H. O., O. K., H. S., T. S., M. T.], Virology Division [T. M., K. S.], National Cancer Center Research Institute, and Hematology-Oncology and Medical Oncology Division, National Cancer Center Hospital [K. T.], 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104, Japan
We recently reported the isolation of the K-sam complementary DNA (cDNA), which was amplified preferentially in poorly differentiated types of stomach cancer and codes for one of the heparin-binding growth factor or fibroblast growth factor (FGF) receptor families. The K-sam-related gene, N-sam (NCC-IT-cell-derived sam), was isolated by screening of the cDNA libraries of human immature teratoma cells, NCC-IT. Sequence analysis of the N-sam cDNAs showed that N-sam encodes a human FGF receptor, the FLG protein. N-sam was expressed in lymphocytic leukemia/lymphoma cells, predominantly in the thymic T-cell phenotype. In a T-cell leukemia line, MOLT3, N-sam mRNA expression was markedly enhanced by 12-O-tetradecanoylphorbol-13-acetate treatment and was also up-regulated by basic FGF exposure. These results indicate that N-sam expression is regulated during T-cell ontogeny and modulated by its putative ligand exposure. The results also suggested that interaction between immature T-cell and marrow or thymic interstitial cells might be mediated by N-sam and basic FGF stored in the extracellular matrix of stromal cells.
1 This work was supported in part by a Grant-in-Aid for the Comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health and Welfare and by Grants-in-Aid for Cancer Research from the Ministry of Health and Welfare and from the Ministry of Education, Science, and Culture. Y. H., H. O., T. Y., and O. K. were awardees of a Research Resident Fellowship from the Foundation for Promotion of Cancer Research.
2 To whom requests for reprints should be addressed.
Received 12/12/91. Accepted 4/ 6/92.
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