Research Program: Carcinogenesis & Chemoprevention
Research Associate, Professor, and Associate Director, Hormel Institute

ambode@hi.umn.edu
507-437-9615 — office
507-437-9615 — lab
Preferred method of contact: e-mail

Dr. Bode received her Ph.D. from the University of Oregon in Applied Physiology. She conducted postdoctoral training in the laboratory of Dr. Robert Nordlie at the University of North Dakota School of Medicine in the Department of Biochemistry. She was an associate professor of Physiology at UND before she joined the Hormel Institute, University of Minnesota in 1999 in Molecular and Cellular Biology and is currently associate director of the Institute.

Research Interests

Carcinogenesis is a multistage process consisting of initiation, promotion, and progression stages and each stage may be a possible target for chemopreventive agents. A significant outcome of these investigations on the elucidation of molecular and cellular mechanisms is the explication of signal transduction pathways induced by tumor promoters in cancer development. The current belief today is that cancer may be prevented or treated by targeting specific cancer genes, signaling proteins and transcription factors. The molecular mechanisms explaining how normal cells undergo neoplastic transformation induced by tumor promoters are rapidly being clarified. Accumulating research evidence suggests that many of dietary factors, including tea compounds, may be used alone or in combination with traditional chemotherapeutic agents to prevent or treat cancer. The potential advantage of many natural or dietary compounds seems to focus on their potent anticancer activity combined with low toxicity and very few adverse side effects. Our work focuses on studying not only the effects but also identifying the molecular and cellular targets of various dietary factors on signal transduction pathways involved in neoplastic cell transformation and carcinogenesis.

Selected Publications

Bode AM, Dong Z. Cancer prevention by food factors through targeting signal transduction pathways. Nutrition 2004;20:89-94.

Bode AM, Dong Z. Targeting signal transduction pathways by chemopreventive agents. Mutat Res 2004;555:33-51.

Bode AM, Dong Z. Post-translational modification of p53 in tumorigenesis. Na Rev Cancer 2004;4:793-805.

Bode AM, Dong Z. Inducible covalent posttranslational modification of histone H3. Sci STKE 2005; 2005(281):re4.

Bode AM, Dong Z. Signal transduction pathways in cancer development and as targets for cancer prevention. Prog Nucleic Acid Res Mol Biol 2005;79:237-297.

Cho YY, He Z, Zhang Y, Choi HS, Zhu F, Choi BY, Kang BS, Ma WY, Bode AM, Dong Z. The p53 protein is a novel substrate of ribosomal S6 kinase 2 and a critical intermediary for ribosomal S6 kinase 2 and histone H3 interaction. Cancer Res. 2005;65:3596-603.

Choi BY, Choi HS, Ko K, Cho YY, Zhu F, Kang BS, Ermakova SP, Ma WY, Bode AM, Dong Z. The tumor suppressor p16(INK4a) prevents cell transformation through inhibition of c-Jun phosphorylation and AP-1 activity. Nat Struct Mol Biol. 2005;12:699-707.

Bode AM, Dong, Z. Molecular and cellular targets. Mol Carcinog. 2006;45:422-430.

Dong Z, Bode AM. The role of histone H3 phosphorylation (Ser10 and Ser28) in cell growth and cell transformation. Mol Carcinog. 2006;45:416-21.

Ermakova SP, Kang BS, Choi BY, Choi HS, Schuster TF, Ma WY, Bode AM, Dong Z. (-)-Epigallocatechin gallate overcomes resistance to etoposide-induced cell death by targeting the molecular chaperone glucose-regulated protein 78. Cancer Res 2006;66(18):9260-9.

Lu C, Zhu F, Cho YY, Tang F, Zykova T, Ma WY, Bode AM, Dong Z. Cell apoptosis: requirement of H2AX in DNA ladder formation, but not for the activation of caspase-3. Mol Cell 2006;23:121-32.

Zhu F, Choi BY, Ma WY, Zhao Z, Zhang Y, Cho YY, Choi HS, Imamoto A, Bode AM, Dong Z. COOH-terminal Src kinase-mediated c-Jun phosphorylation promotes c-Jun degradation and inhibits cell transformation. Cancer Res 2006;66:5729-36.

Zykova TA, Zhu F, Lu C, Higgins L, Tatsumi Y, Abe Y, Bode AM, Dong Z. Lymphokine-activated killer T-cell-originated protein kinase phosphorylation of histone H2AX prevents arsenite-induced apoptosis in RPMI7951 melanoma cells. Clin Cancer Res 2006;12:6884-93.

Bode AM, Dong Z. The enigmatic effects of caffeine in cell cycle and cancer. Cancer Lett, 2007;247:26-39.

Bode AM, Dong Z. The functional contrariety of JNK. Mol Carcinog. 2007;46:591-8. Review.

Cho YY, Yao K, Kim HG, Kang BS, Zheng D, Bode AM, Dong Z. Ribosomal S6 kinase 2 is a key regulator in tumor promoter induced cell transformation. Cancer Res. 2007;67:8104-12.

Oh SM, Zhu F, Cho YY, Lee KW, Kang BS, Kim HG, Zykova T, Bode AM, Dong Z. T-lymphokine-activated killer cell-originated protein kinase functions as a positive regulator of c-Jun-NH2-kinase 1 signaling and H-Ras-induced cell transformation. Cancer Res. 2007;67:5186-94.

Zhu F, Zykova TA, Kang BS, Wang Z, Ebeling MC, Abe Y, Ma WY, Bode AM, Dong Z. Bidirectional signals transduced by TOPK-ERK interaction increase tumorigenesis of HCT116 colorectal cancer cells. Gastroenterology 2007;133:219-31.

Choi HS, Kang BS, Shim JH, Cho YY, Choi BY, Bode AM, Dong Z. Cot, a novel kinase of histone H3, induces cellular transformation through up-regulation of c-fos transcriptional activity. Faseb J 2008;22:113-26.

Malakhova M, Tereshko V, Lee SY, Yao K, Cho YY, Bode A, Dong Z. Structural basis for activation of the autoinhibitory C-terminal kinase domain of p90 RSK2. Nat Struct Mol Biol. 2008;15:112-3.