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Blood, 15 April 2004, Vol. 103, No. 8, pp. 3185-3191. Prepublished online as a Blood First Edition Paper on December 11, 2003; DOI 10.1182/blood-2003-09-3022. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-09-3022v1 103/8/3185    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Matsunaga, T. Articles by Kurosawa, H. Search for Related Content PubMed PubMed Citation Articles by Matsunaga, T. Articles by Kurosawa, H. Related Collections Apoptosis Cell Adhesion and Motility Signal Transduction Gene Expression Hemostasis, Thrombosis, and Vascular Biology Immunobiology Neoplasia Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Regulation of annexin II by cytokine-initiated signaling pathways and E2A-HLF oncoprotein Takayuki Matsunaga, Toshiya Inaba, Hirotaka Matsui, Mayuko Okuya, Atsushi Miyajima, Takeshi Inukai, Tetsunori Funabiki, Mikiya Endo, A. Thomas Look, and Hidemitsu Kurosawa From the Division of Hematology, Department of Pediatrics, Dokkyo University School of Medicine, Tochigi, Japan; Department of Molecular Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Japan; Institute of Molecular and Cellular Bioscience, University of Tokyo, Japan; Department of Pediatrics, School of Medicine, University of Yamanashi, Japan; Department of Pediatrics, Yokohama City University, Japan; Department of Pediatrics, Iwate Medical University, Japan; and Pediatric Oncology Department, Dana-Farber Cancer Institute, Boston, MA. In pro-B cell acute lymphoblastic leukemia (ALL), expression of the E2A-HLF fusion gene as a result of t(17;19)(q22;p13) is associated with poor prognosis, hypercalcemia, and hemorrhagic complications. We previously reported that the E2A-HLF fusion protein protects interleukin-3 (IL-3)–dependent lymphoid cells from apoptosis caused by cytokine starvation. Here, we report that annexin II, a surface phospholipid-binding protein and one of the proposed causes of the hemorrhagic complications of acute promyelocytic leukemia (APL), is also implicated in t(17;19)+ ALL. Annexin II was expressed at high levels in APL cells and in each of 4 t(17;19)+ leukemia cell lines, and annexin II expression was induced by enforced expression of E2A-HLF in leukemia cells. In IL-3–dependent cells, we found that annexin II expression was regulated by IL-3 mainly by Ras pathways, including Ras/phosphatidylinositol 3-kinase pathways. Moreover, E2A-HLF increased annexin II expression in IL-3–dependent cells in the absence of the cytokine. These findings indicate that E2A-HLF induces annexin II by substituting for cytokines that activate downstream pathways of Ras. (Blood. 2004;103:3185-3191) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: "Annexing" acute leukemias Kevin S. Smith Blood 2004 103: 2869-2870. [Full Text] [PDF] This article has been cited by other articles: T. Inukai, T. Inaba, J. Dang, R. Kuribara, K. Ozawa, A. Miyajima, W. Wu, A. T. Look, Y. Arinobu, H. Iwasaki, et al. TEF, an antiapoptotic bZIP transcription factor related to the oncogenic E2A-HLF chimera, inhibits cell growth by down-regulating expression of the common {beta} chain of cytokine receptors Blood, June 1, 2005; 105(11): 4437 - 4444. [Abstract] [Full Text] [PDF]

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