Research Profile: Gareth Bond, Ph.D., LICR Oxford Branch
Dr. Gareth Bond
Dr. Gareth Bond joined the Oxford Branch as an Assistant Member on January 15 and moved to the UK from the USA, where he formerly held a position at the Institute for Advanced Study (IAS) in Princeton, New Jersey. He is currently recruiting both PhD students and postdoctoral fellows as he builds up a research group to study how variations in the human genetic code contribute to the onset and progression of cancer.
Dr. Bond grew up in the USA and Germany, but pursued most of his graduate training in the USA. He earned his PhD with distinction in the laboratories of Drs. James Manley and Carol Prives at Columbia University in New York, and subsequently held a post-doctoral position in the laboratory of Dr. Arnold Levine, first at Rockefeller University and then at the Cancer Institute of New Jersey. He has been a Member at the Simons Center for Systems Biology at the IAS since 2005, and is eager to develop his research program within the LICR community. “Becoming part of a global Institute, with exciting basic and clinical research programs to collaborate with and contribute to, was one of the primary reasons for my initial interest in this position. Much of my research to date has been made possible by strong collaborations with both basic and clinical research programs throughout the US and Europe. I am excited that by joining the Ludwig this approach can continue and be expanded upon."
Dr. Bond aims to identify genetic variations that increase cancer risk, promote the progression and metastasis of tumors, and undermine chances of survival. Subsequently, he will investigate how these variations perpetuate disease at the molecular level. “The task of identifying functional genetic variants,” he says, “is complicated by the extremely large size of the human genome and the relative abundance of variations in the genetic code found between individuals. To overcome this, my approach is to focus on biologically relevant pathways that are likely to be involved in disease causation and progression.”
In particular, Dr. Bond is focusing on genes that make up the p53 signaling pathway as they are known to be central both in reducing cancer frequency and in mediating the response of conventional cancer treatments such as chemo- and radiotherapy. The p53 pathway is activated in cells to protect the genome’s integrity when the DNA is damaged, or when oncogenes (genes that can transform normal cells into tumor cells) are activated. Once triggered, the pathway suppresses the formation of tumors; either by preventing cells from dividing and inducing DNA repair mechanisms or, alternatively, by prompting cell death.
Dr. Bond will integrate computational, molecular, cellular, and genetic approaches to study widespread genetic variations that impede with the p53 pathway and with other, interacting pathways. He hopes that his work in the long term will clarify how genetic inheritance contributes to susceptibility of cancer and disease progression; knowledge that is likely to expose potential strategies for prevention and treatment of cancer diseases. “I hope that this research can contribute to one of Ludwig’s key interests, namely to identify and characterize the therapeutic utility of scientific discoveries.”
To find out more about available positions in Dr. Bond’s laboratory, send an email to Gareth Bond
Suggested Reading
- Bond, G. L., and Levine, A. J. (2007). A single nucleotide polymorphism in the p53 pathway interacts with gender, environmental stresses and tumor genetics to influence cancer in humans. Oncogene 26, 1317-1323.
- Bond, G. L., Menin, C., Bertorelle, R., Alhopuro, P., Aaltonen, L. A., and Levine, A. J. (2006). MDM2 SNP309 accelerates colorectal tumour formation in women. J Med Genet 43, 950-952.
- Bond, G. L., Hirshfield, K. M., Kirchhoff, T., Alexe, G., Bond, E. E., Robins, H., Bartel, F., Taubert, H., Wuerl, P., Hait, W., Toppmeyer, D., Offit, K., and Levine, A. J. (2006). MDM2 SNP309 Accelerates Tumor Formation in a Gender-Specific and Hormone-Dependent Manner. Cancer Res 66, 5104-5110.
- Bond, G.L., Hu, W., and Levine, A. (2005) A Single Nucleotide Polymorphism in the MDM2 Gene: From a Molecular and Cellular Explanation to Clinical Impact. Cancer Research 65(13): 5481-5484.
- Bond, G.L., Hu, W., Bond, E.E., Robins, H., Lutzker, S., Arva, N., Bargonetti, J, Bartel, F.,Taubert, H., Wuerl, P., Onel, K., Linwah, Y., Hwang, S-J, Strong, L., Lozano,G., Levine, A. (2004) A Single Nucleotide Polymorphism in the MDM2 Promoter Attenuates the p53 Tumor Suppressor Pathway and Accelerates Tumor Formation in Humans. Cell (119): 591-602.