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Cliff Wang - Assistant Professor

Office: Keck 251
Phone: (650) 721-1351
FAX: (650) 725-7294
E-Mail: cliff.wang@stanford.edu
Admin. Associate: Roosmery Yang, (650) 736-1807

Highest Degree

Ph.D., University of California, Berkeley, 2000

Major Honors and Awards

NIH Post-doctoral Fellowship, 2002-2004
Leukemia Research Foundation Fellowship, 2001

Research Area

Women born with a mutation in the gene BRCA-1 have up to an 80% chance of developing breast cancer in their lifetime. Yet cancer in these women is not a certainty and this one gene alone does not cause breast cancer; otherwise, girls would develop breast cancer almost immediately after birth. It is generally believed that multiple genes must be activated or inactivated to cause cancer. In the case of the inherited BRCA-1 mutation, other mutations likely must occur during a woman’s lifetime before she develops breast cancer. The requirement for multiple genes has been well demonstrated in fibroblast cells. Over-expression of the oncogene Ras alone does not lead to the transformation of human fibroblasts, but in the right context the combined over-expression of Ras and TERT, and inactivation of p53 and pRB does transform the cells.

Often times when it is observed that the expression of two or more genes leads to a new phenotype, these genes are said to cooperate. Of course the characteristics and degree of a cooperating relationship can vary. When two oncogenes together lead to immortalization of a cell, is the contribution of these two genes a sum of the individual activities of these genes? Or does the observed cooperation involve a synergy where the genes activated together drive cell proliferation at a level greater than the sum of their individual contributions?

Our goals are to identify oncogenes and tumor suppressor genes, quantify gene cooperation, and elucidate the mechanisms that govern the cooperation. One method we are using to identify genes is retroviral mutagenesis. Because retroviruses can cause tumors by activating or inactivating multiple genes, the identification of multiple retroviral integration sites within a single tumor allows us to identify candidate combinations of cooperating cancer genes. We are also devising methods to measure the degree of cooperation amongst a set of cancer genes and determine how cooperation affects cell phenotypes, e.g. cell proliferation, mutagenesis, senescence, and gene silencing. To perform these experiments we are engineering systems for inducible gene expression, constitutive promoter libraries, and reporter genes to measure genome instability. We hope that our research will lead to new technologies to diagnose and stratify cancer patients, and allow us to engineer systems for the evaluation of therapeutics.

Several Recent Publications

Wang, C.L., Wang, B., Channa, N., Li, L., Bartha, G., and Wabl, M. (2006) Activation of an oncogenic microRNA cistron via provirus integration into the intron. Proc Natl Acad Sci U S A 103, 18680-18684
Wang, C. L., Yang, D.Y., and Wabl, M. (2006) Slow, stochastic transgene repression with properties of a timer. Genome Biol 7, R47
Wang, C. L., and Wabl, M. (2005) Hypermutation rate normalized by chronological time. J Immunol 174, 5650-5654
Wang, C. L., and Wabl, M. (2005) Mutational activity in cell line WEHI-231. Immunogenetics 56, 849-853
Wang, C. L., Yang, D.Y., and Wabl, M. (2004) In vivo mutagenesis by somatic hypermutation. Protein Eng Des Sel 17, 659-664
Wang, C. L., and Wabl, M. (2004) DNA acrobats of the Ig class switch. J Immunol 172, 5815-5821.
Wang, C. L., and Wabl, M. (2004) Precise Dosage of an Endogenous Mutagen in the Immune System. Cell Cycle 3, 983-985.
Wang, C. L., Harper, R. A., and Wabl, M. (2004) Genome-wide somatic hypermutation. Proc Natl Acad Sci U S A 101, 7352-7356.
Wang, C. L., Hodgson, J. G., Malek, T., Pedersen, F. S., and Wabl, M. (2004) A murine leukemia virus with Cre-LoxP excisible coding sequences allowing superinfection, transgene delivery, and generation of host genomic deletions. Retrovirology 1, 5.
Wang, C.L., Ozuna, S.C., Clark, D.S., and Keasling, J.D. (2002) A Deep-Sea Hydrothermal Vent Isolate, Pseudomonas aeruginosa CW961, Requires Thiosulfate for Cadmium Tolerance and Precipitation. Biotech Letters 24, 637-641.
Wang, C. L., Lum, A. M., Ozuna, S. C., Clark, D. S., and Keasling, J. D. (2001) Aerobic sulfide production and cadmium precipitation by Escherichia coli expressing the Treponema denticola cysteine desulfhydrase gene. Appl Microbiol Biotechnol 56, 425-430.
Wang, C.L., Clark, D.S., and Keasling, J.D. (2001) Analysis of an Engineered Sulfate Reduction Pathway and Cadmium Precipitation on the Cell Surface. Biotech Bioeng 75, 285-291.
Wang, C. L., Maratukulam, P. D., Lum, A. M., Clark, D. S., and Keasling, J. D. (2000) Metabolic engineering of an aerobic sulfate reduction pathway and its application to precipitation of cadmium on the cell surface. Appl Environ Microbiol 66, 4497-4502.
Wang, C. L., Michels, P. C., Dawson, S. C., Kitisakkul, S., Baross, J. A., Keasling, J. D., and Clark, D. S. (1997) Cadmium removal by a new strain of Pseudomonas aeruginosa in aerobic culture. Appl Environ Microbiol 63, 4075-4078.

Current Students

Graduate Student, Jonathan Vroom, Ryan Peacock, and Josh Ferreira.