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 Blood, 15 January 2006, Vol. 107, No. 2, pp. 698-707.
Prepublished online as a Blood First Edition Paper on September 15, 2005; DOI 10.1182/blood-2005-03-1278.

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NEOPLASIA

Induction of tumor arrest and differentiation with prolonged survival by intermittent hypoxia in a mouse model of acute myeloid leukemia

Wei Liu, Meng Guo, Ya-Bei Xu, Dao Li, Zhao-Nian Zhou, Ying-Li Wu, Zhu Chen, Scott C. Kogan, and Guo-Qiang Chen

From the Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education of China, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine (SJU-SM; formerly Shanghai Second Medical University); Health Science Institute and Laboratory of Hypoxia Physiology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences; and Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco, CA.

We showed previously that mild real hypoxia and hypoxia-mimetic agents induced in vitro cell differentiation of acute myeloid leukemia (AML). We here investigate the in vivo effects of intermittent hypoxia on syngenic grafts of leukemic blasts in a PML-RAR{alpha} transgenic mouse model of AML. For intermittent hypoxia, leukemic mice were housed in a hypoxia chamber equivalent to an altitude of 6000 m for 18 hours every consecutive day. The results show that intermittent hypoxia significantly prolongs the survival of the leukemic mice that received transplants, although it fails to cure the disease. By histologic and cytologic analyses, intermittent hypoxia is shown to inhibit the infiltration of leukemic blasts in peripheral blood, bone marrow, spleen, and liver without apoptosis induction. More intriguingly, intermittent hypoxia also induces leukemic cells to undergo differentiation with progressive increase of hypoxia-inducible factor-1{alpha} protein, as evidenced by morphologic criteria of maturating myeloid cells and increased expression of mouse myeloid cell differentiation–related antigens Gr-1 and Mac-1. Taken together, this study represents the first attempt to characterize the in vivo effects of hypoxia on an AML mouse model. Additional investigations may uncover ways to mimic the differentiative effects of hypoxia in a manner that will benefit human patients with AML.


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