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 Blood, 1 January 2009, Vol. 113, No. 1, pp. 66-74.
Prepublished online as a Blood First Edition Paper on September 26, 2008; DOI 10.1182/blood-2008-06-164889.

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IMMUNOBIOLOGY

Aurora-A kinase: a novel target of cellular immunotherapy for leukemia

Toshiki Ochi1, Hiroshi Fujiwara1, Koichiro Suemori1, Taichi Azuma1, Yoshihiro Yakushijin2, Takaaki Hato3, Kiyotaka Kuzushima4, and Masaki Yasukawa1,5

1 Department of Bioregulatory Medicine, 2 Cancer Center, and 3 Division of Blood Transfusion and Cell Therapy, Ehime University Graduate School of Medicine, Toon; 4 Division of Immunology, Aichi Cancer Center, Nagoya; and 5 Center for Regenerative Medicine, Ehime University Graduate School of Medicine, Toon, Japan

Aurora-A kinase (Aur-A) is a member of the serine/threonine kinase family that regulates the cell division process, and has recently been implicated in tumorigenesis. In this study, we identified an antigenic 9–amino-acid epitope (Aur-A207-215: YLILEYAPL) derived from Aur-A capable of generating leukemia-reactive cytotoxic T lymphocytes (CTLs) in the context of HLA-A*0201. The synthetic peptide of this epitope appeared to be capable of binding to HLA-A*2402 as well as HLA-A*0201 molecules. Leukemia cell lines and freshly isolated leukemia cells, particularly chronic myelogenous leukemia (CML) cells, appeared to express Aur-A abundantly. Aur-A–specific CTLs were able to lyse human leukemia cell lines and freshly isolated leukemia cells, but not normal cells, in an HLA-A*0201–restricted manner. Importantly, Aur-A–specific CTLs were able to lyse CD34+ CML progenitor cells but did not show any cytotoxicity against normal CD34+ hematopoietic stem cells. The tetramer assay revealed that the Aur-A207-215 epitope–specific CTL precursors are present in peripheral blood of HLA-A*0201–positive and HLA-A*2402–positive patients with leukemia, but not in healthy individuals. Our results indicate that cellular immunotherapy targeting Aur-A is a promising strategy for treatment of leukemia.


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