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Adenoviral E1A-Associated Protein p300 Is Involved in Acute Myeloid Leukemia With t(11; 22)(q23; q13)
Kohmei Ida,
Issay Kitabayashi,
Tomohiko Taki,
Masafumi Taniwaki,
Keiko Noro,
Masao Yamamoto,
Misao Ohki, and
Yasuhide Hayashi
From the Department of Pediatrics, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan; the Radiobiology Division, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan; the 3rd Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, Japan; and the Department of Pediatrics, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.
p300, which was originally cloned as a nuclear binding target of the adenovirus E1A oncoprotein, forms a family with cyclic-AMP response element binding protein (CREB)-binding protein (CBP). p300/CBP are considered to be transcriptional coactivators that connect the basal transcriptional machinery to various DNA-binding transcriptional factors. p300/CBP are implicated in both cell differentiation and regulation of cell-cycle. We identify here that the p300 gene is fused to the MLL gene and that in-frame MLL-p300 fusion protein is generated in acute myeloid leukemia (AML) with t(11; 22)(q23; q13). These findings suggest that the basis for the leukemogenesis of t(11; 22)-AML is the inability of p300 to regulate cell-cycle and cell differentiation after fusion with MLL.
Blood, Vol. 90 No. 12 (December 15), 1997:
pp. 4699-4704
© 1997 by The American Society of Hematology.
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