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[Cancer Research 59, 4261-4265, September 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 4261-4265, September 1, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

AF17q25, a Putative Septin Family Gene, Fuses the MLL Gene in Acute Myeloid Leukemia with t(11;17)(q23;q25)1

Tomohiko Taki, Hiroaki Ohnishi, Kenji Shinohara, Masahiro Sako, Fumio Bessho, Masayoshi Yanagisawa and Yasuhide Hayashi2

Department of Pediatrics, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-8655 [T. T., H. O., F. B., M. Y., Y. H.]; Division of Hematology, Yamaguchi Prefecture Central Hospital, Hofu, Yamaguchi 747-8511 [K. S.]; and Department of Pediatrics, Osaka City General Hospital, Miyakojima-ku, Osaka 543-0021 [M. S.], Japan

The t(11;17) has been described in patients with acute myeloid leukemia (AML), and the AF17 gene was previously cloned as a fusion partner of the MLL gene in t(11;17)(q23;q21)-AML. We analyzed one patient with de novo AML and one with therapy-related AML with t(11;17)(q23;q25) and identified the AF17q25 gene on chromosome 17q25, a putative septin family gene, fused with MLL. AF17q25 encoded at least three kinds of proteins [type I (568 a.a.), type II (594 a.a.), and type III (574 a.a.)] that contained two kinds of different amino acid sequences at the COOH terminus. The MLL-AF17q25 fusion transcript consisted of type I AF17q25 transcript. The AF17q25 protein is homologous to septin family proteins, including H5, NEDD5, CDC10, and hCDCrel, which is one of the fusion partners of MLL in t(11;22)(q23;q11)-AML. These results suggest that AF17q25 and hCDCrel might define a new septin family particularly involved in the pathogenesis of 11q23-associated leukemia.




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Copyright © 1999 by the American Association for Cancer Research.