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Radiobiology Division, National Cancer Center Research Institute, Chuo-ku, Tokyo 104 [H. I., K. S., M. O.], and Department of Pediatrics, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113 [Y. H.], Japan
The t(16;21)(p11;q22) translocation is a recurrent chromosomal abnormality found in several types of myeloid leukemia. We have previously demonstrated that the breakpoints of this translocation are clustered in a specific intron of the ERG gene on chromosome 21, which has recently been reported to be involved in Ewing's sarcoma. We show here that the TLS/FUS gene on chromosome 16 is fused with the ERG gene to produce the TLS/FUS-ERG chimeric transcript by this translocation. The TLS/FUS gene has been identified as a translocated gene in myxoid liposarcoma by the t(12;16)(q13;p11) translocation and encodes an RNA-binding protein that is highly homologous to the product of the EWS gene involved in Ewing's sarcoma. Thus, the TLS/FUS-ERG gene fusion in t(16;21) leukemia is predicted to produce a protein that is very similar to the EWS-ERG chimeric protein responsible for Ewing's sarcoma.
1 This work was supported in part by a Grant-in-Aid for Comprehensive 10-year Strategy for Cancer Control, a Research Grant on Aging and Health from the Ministry of Health and Welfare; Grants-in-Aid for Creative Basic Research (Human Genome Program), Cancer Research, and Scientific Research on Priority Areas from the Ministry of Education, Science, and Culture; and a grant from the Special Coordination Funds for Promotion of Science and Technology from the Science and Technology Agency of Japan.
2 To whom requests for reprints should be addressed.
Received 3/10/94. Accepted 4/21/94.
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