Research Focus

The research objective of the lab is to understand the relationship between the structures of lesions formed in the genome by DNA damaging agents and the specific biological endpoints of mutation, cancer, and cell death. The goal of our work on carcinogenesis is to probe the molecular etiology of human cancer. Our parallel studies on antitumor drugs focus upon uncovering the mechanism of action of existing drugs. Based upon that understanding, we design novel compounds that could be useful for the treatment of cancer. more...

Selected Publications

Delaney, J.C., Henderson, P.T., Helquist, S.A., Morales, J.C., Essigmann, J.M., and E.T. Kool. High-fidelity in vivo replication of DNA base shape mimics lacking the ability to form Watson-Crick hydrogen bonds. Proc. Natl. Acad. Sci. (USA). 100: 4469-4473 (2003).

Henderson, P.T., Delaney, J.C., Muller, J.G., Neeley, W.L., Tannenbaum, S.R., Burrows, C.J. and J.M. Essigmann. The Hydantoin Lesions Formed from Oxidation of 7,8-Dihydro-8-oxoguanine are Potent Sources of Replication Errors in Vivo. Biochemistry (Accelerated Communication), In press.

Smela, M.E., Hamm, M.L., Harris, C.M., Harris, T.M. and J.M. Essigmann. The aflatoxin B1 formamidopyrimidine adduct has a mutational signature that matches that observed in human hepatocellular carcinoma. Proc. Natl. Acad. Sci. (USA) 99:6655-6660 (2002).

Zdraveski, Z.Z., Mello, J.A., Farinelli, C.K., Essigmann, J.M. and M.G. Marinus. MutS preferentially recognizes cisplatin- over oxaliplatin- modified DNA. J.Biol. Chem., 277: 1255-1260 (2002).

Henderson, P.T., Delaney, J.C., Gu, F., Tannenbaum, S.R. and J.M. Essigmann. Oxidation of 7,8-dihydro-8-oxoguanine affords lesions that are potent sources of G to T transversions in vivo. Biochemistry, 41: 914-921 (2002).

Mitra, K., Marquis, J.C., Hillier, S.M., Rye, P.T., Zayas, B., Lee, A.S., Essigmann, J.M., and R.G. Croy. A rationally designed genotoxin that selectively destroys estrogen receptor-positive breast cancer cells. J. Amer. Chem. Soc., 124: 1862-1863 (2002).

Delaney, J.C. and J. M. Essigmann. Effect of sequence context on O6-methylguanine repair and replication in vivo. Biochemistry, 40: 14968?14975 (2001).

Smela, M.E., Currier, S.S., Bailey, E.A. and J.M. Essigmann. The chemistry and biology of aflatoxin B1: From mutational spectrometry to carcinogenesis. Carcinogenesis 22: 535-545 (2001).

Kartalou, M. and J.M. Essigmann. Recognition of cisplatin adducts by cellular proteins. Mutation Research 478: 1-21 (2001).

Kartalou, M. and J.M. Essigmann. Mechanisms of resistance to cisplatin. Mutation Research, 478: 23-43 (2001).

Kartalou, M., Samson, L.D. and J.M. Essigmann. Cisplatin adducts inhibit 1,N6-ethenoadenine repair by interacting with the human 3-methyladenine DNA glycosylase. Biochemistry, 39: 8032-8038 (2000).

Zdraveski, Z.Z., Mello, J.A., Marinus, M.G. and J.M. Essigmann. Multiple pathways of recombination define cellular responses to cisplatin. Chem. and Biol. 7: 39-50 (2000).

Loeb, L.A., Essigmann, J.M., Kazazi, F, Zhang, J, and J.I. Mullins. Lethal mutagenesis of HIV with mutagenic nucleoside analogs. Proc. Natl. Acad. Sci. (USA), 96: 1492-1497 (1999).

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