Blount, M.M. Mack, C.M. Wehr, J.T. MacGregor, R.A. cinogenesis, depending upon the experimental system [36] . Hiatt, G. Wang, S.N. Wickramasinghe, R.B. Everson, B.N. Ames, Folate deiency causes uracil misincorporation into human DNA and chromosome breakage: implications for cancer and neuronal damage, Proc. Natl. Acad. Sci. U.S.A. 94 (1997) 3290?295. Acknowledgements [14] A.H. Borchers, K.A. Kennedy, J.A. Straw, Inhibition of DNA excision repair by methotrexate in Chinese hamster ovary cells Carboplatin Supported by grants from the American Institute for Cancer Research (02A002) and the Department of following exposure to ultraviolet irradiation or ethylmethanesul- fonate, Cancer Res. 50 (1990)786?789. [15] S.-W. Choi, Y.-I. Kim, J.N. Weitzel, J.B. Mason, Folate depletion Defense (DAMD17-01-1-0440). We thank Dr. Pamela impairs DNA excision repair in the colon of the rat, Gut 43 (1998)

Vacek for reviewing the manuscript and Dr. Leona Sam- 93?9. son for the gift of the Aag null breeder mice. [16] S.J. James, A.G. Basnakian, B.J. Miller, In vitro folate deiency induces deoxynucleotide pool imbalance, apoptosis, and muta- genesis in Chinese hamster ovary cells, Cancer Res. 54 (1994) References 5075?080. [17] R.F. Branda, M. Hacker, A. Lafayette, E. Nigels, L. Sullivan, J.A. [1] R.F. Branda, S.J. Naud, E.M. Brooks, Z. Chen, H. Muss, Effect of vitamin B12, folate, and dietary supplements on breast carcinoma chemotherapy-induced mucositis and neutropenia, Cancer01 (2004)058?064. [2] G.H. Clamon, R. Feld, W.K. Evans, S. Weiner, B.S. Kramer, L.L. Linninger, L.B. Gardner, E.C. Wolfe, W.D. DeWys, F.A. Hoff- man, Serum folate and Vitamin B12 levels in patients with small cell lung cancer, Cancer 53 (1984) 306?10. [3] A.C. Anthony,  Carboplatin Paraplatin Megaloblastic anemias, in: R. Hoffman, E.J. Benz, S.J. Shattil, B. Furie, H.J. Cohen (Eds.), Hematology: Basic Prin- ciples and Practice, Churchill Livingstone, New York,991, pp. 392?22. [4] R.F. Branda, D.B. Blickensderfer, Folate deiency increases genetic damage caused by alkylating agents and -irradiation in Chinese hamster ovary cells, Cancer Res. 53 (1993) 5401?408. [5] S. Melnyk, M. Pogribna

B.J. Miller, A.G. Basnakian, I.P. Pogribny, S.J. James, Uracil misincorporation, DNA strand breaks, and gene ampliation are associated with tumorigenic cell transformation in folate deient/repleted Chinese hamster ovary cells, Cancer Lett.46 (1999) 35?4. Nicklas, J.P. Oeill, Nutritional folate deiency augments the in vivo mutagenic and lymphocytotoxic activities of alkylating agents, Environ. Mol. Mutagen. 32 (1998) 33?8. [18] R.F. Branda, J.P. Oeill, E.M. Brooks, L.M. Trombley, J.A. Nicklas, The effect of folate deiency on the cytotoxic and mutagenic responses to ethyl methanesulfonate in human lym- phoblastoid cell lines that differ in P53 status, Mutat. Res. 473 (2001) 51?1. [19] R.F. Branda, J.P. Oeill, L.M. Sullivan, R.J. Albertini, Factors inencing mutation at the hprt locus in T-lymphocytes; women treated for breast cancer, Cancer Res. 51 (1991) 6603?607. [20] R.F. Branda, A.R. Lafayette, J.P. Oeill, J.A. Nicklas, The effect of folate deiency on the hprt mutational  Carboplatin DNA/RNA inhibitor spectrum in Chi- nese hamster ovary cells treated with monofunctional alkylating agents, Mutat. Res. 427 (1999) 79?7. [21] C.W. Op het Veld, M.Z. Zdzienicka, H. Vrieling, P.H.M. Lohman, A.A. van Zeeland, Molecular analysis of ethyl methanesulfonate- induced mutations at the hprt gene in the ethyl methanesulfonate- sensitive Chinese hamster cell line EM-C11 and its parental line CHO9, Cancer Res. 54 (1994) 3001?006. 5 Proceedings of the 46th Annual ASTRO Meeting S357 2031 Telomerase as a Molecular Target for7-AAG: Exploiting the Tumor to Improve

Therapeutic Index 1 1 Radiation Oncology, Washington University School of Laramide orogeny Medicine, Saint Louis, MO Purpose/Objective: Telomerase overexpression is a commonly identi ?ed trait of many solid tumors and thought to convey resistance to anticancer agents, suggesting telomerase as a potential molecular target. As such, it seem