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IBB POSTECH

Faculty

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Lab : Tumor Microenvironment Laboratory
Office : +82-54-279-2353 / Lab : +82-54-279-0615
Homepage : cvbl.postech.ac.kr
E-Mail :

Profile

2004 : Ph.D. University of Auckland, Auckland 
2003-2008 : Postdoctoral Fellow, Department of Radiation Oncology, Stanford University School of Medicine
2008-2011 : Research Associate, Department of Radiation Oncology, Stanford University School of Medicine 

Research Interests

We aim to understand the role of myeloid cells (monocytes and macrophages) in the progression of hypoxic (low oxygen tension) inflammatory diseases including cancer and cardiovascular diseases. In particular, we are interested in determining the function of hypoxia-inducible factor-1 (HIF-1) in myeloid cells during the disease progression. Myeloid cells play a critical role in initiation, progression, and exacerbation of the diseases. Furthermore, hypoxic sensing by these cells is known to be essential for mediating inflammatory responses (such as in bacterial infection). However, it is currently unknown how HIF-1, the major transcription factor stabilized under hypoxic conditions, in myeloid cells may modulate the disease progression, in which chronic accumulation of subtle changes in hypoxia and inflammatory microenvironment may overall govern the disease progression. Hence, by using the genetically manipulated mouse model we seek to understand how myeloid cells under the control of HIF-1 may modulate the disease process. With our research, we hope to identify novel therapeutic targets to combat these diseases more effectively in patients.

Selected Publications

1. Ahn, G.O., Tseng, D. Liao, C.H., Dorie, M.J., Czechowicz, A., and Brown, J.M. (2010) Inhibition of Mac-1 (CD11b/CD18) enhances tumor response to radiation by reducing myeloid cell recruitment. Proc. Natl. Acad. Sci. U.S.A. 107, 8363-8368 Highlighted in: Qualls J.E. and Murray P.J. (2010) A double agent in cancer: Stopping macrophages wounds tumors. Nat. Med. 16, 863-864

2. Milbank, J., Stevenson, R., Ware, D., Chang, J., Tercel, M., Ahn, G.O., Wilson, W.R., Denny, W.A. (2009) Synthesis and evaluation of stable bidentate metal complexes of 1-(chloromethyl)-5-hydroxy-3-(5,6,7-trimethoxyindol-2-ylcarbonyl)-2,3-dihydro-1H-pyrrolo[3,2-f]quinoline (seco-6-azaCBI-TMI) as hypoxia selective cytotoxins. J. Med. Chem. 52, 6822-6834

3. Ahn, G.O., and Brown, J.M. (2008) Matrix metalloproteinase-9 is required for tumor vasculogenesis but not angiogenesis: Role of bone marrow-derived myelomonocytic cells. Cancer Cell 13, 193-205 (Impact factor 25) Previewed in: Seandel, M., Butler, J., Lyden, D., and Rafii, S. (2008) A catalytic role for proangiogenic marrow-derived cells in tumor neovascularization. Cancer Cell 13, 181-183 Featured article in: Vascular Biology Publications Alert by North American Vascular Biology Organization, United States

4. Ahn, G.O., Botting, K.J., Patterson, A.V., Ware, D.C., Tercel, M., and Wilson, W.R. (2006) Radiolytic and cellular reduction of a novel hypoxia-activated cobalt(III) prodrug of a chloromethylbenzindoline DNA minor groove alkylator. Biochem. Pharmacol. 71, 1683-1694

5. Ahn, G.O., Ware, D.C., Denny, W.A., and Wilson, W.R. (2004) Optimization of the auxiliary ligand shell of cobalt(III)(8-hydroxyquinoline) complexes as model hypoxia-selective radiation-activated prodrugs. Radiat. Res. 162, 315-325