Gareth L. Bond, Ludwig Institute for Cancer Research, Oxford, UK
Gareth L.
Bond
Genomics, Tumor biology
Bio

I am molecular geneticist with a primary interest in understanding the effect of high-frequency genetic variants on human cancer.

Education
Postdoctoral Fellow of Professor Arnold J. Levine, Institute for Advanced Study, Princeton, New Jersey, USA, 2005-2007

Postdoctoral Fellow of Professor Arnold J. Levine, Cancer Institute of New Jersey, New Brunswick, New Jersey, USA, 2003-2005

Postdoctoral Fellow of Professor Arnold J. Levine, The Rockefeller University, New York, New York, USA, 2001-2003

PhD with distinction with Professors James Manley and Carol Prives, Columbia University, Department of Biological Sciences, New York, New York, 2001

First Degree equivalent in Biological Sciences, Christian Albrechts Universitaet zu Kiel, Kiel, Germany, 1994


Achievements

Nuffield Department of Medicine Scientific Leadership Award, University of Oxford, 2007

PhD awarded with distinction, Columbia University, New York, New York, USA, 2001

John S. Newberry Prize: The most promising student of the year in the field of vertebrate zoology, Columbia University, 2000

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Gareth L. Bond lab

Our goals are to better understand the contribution of heritable genetics to human cancer and use this information to more accurately predict an individual’s cancer risk, progression and response to therapies, as well as uncover novel therapeutic interventions.

Gareth L. Bond, Ludwig Institute for Cancer Research, Oxford, UK
Gareth L.
Bond
Genomics, Tumor biology
Bio

I am molecular geneticist with a primary interest in understanding the effect of high-frequency genetic variants on human cancer.

Education
Postdoctoral Fellow of Professor Arnold J. Levine, Institute for Advanced Study, Princeton, New Jersey, USA, 2005-2007

Postdoctoral Fellow of Professor Arnold J. Levine, Cancer Institute of New Jersey, New Brunswick, New Jersey, USA, 2003-2005

Postdoctoral Fellow of Professor Arnold J. Levine, The Rockefeller University, New York, New York, USA, 2001-2003

PhD with distinction with Professors James Manley and Carol Prives, Columbia University, Department of Biological Sciences, New York, New York, 2001

First Degree equivalent in Biological Sciences, Christian Albrechts Universitaet zu Kiel, Kiel, Germany, 1994


Achievements

Nuffield Department of Medicine Scientific Leadership Award, University of Oxford, 2007

PhD awarded with distinction, Columbia University, New York, New York, USA, 2001

John S. Newberry Prize: The most promising student of the year in the field of vertebrate zoology, Columbia University, 2000

Read More

TEAM

Elisabeth
Bond
Bio
Juliet
Hewitt
Bio
Emmanouela
Repapi
Bio
Jorge
Zeron
Bio
Anna
Grawenda
Bio
Elleke
Peterse
Bio
Ross
Worrall
Bio

RESEARCH AREAS

There are tremendous differences among individuals in their risk of developing cancer, their disease progression and their responses to therapy.  This heterogeneity is a major obstacle in designing uniformly effective prevention, screening and treatment strategies and is a driving force behind the large effort to personalize them.  The long-term goals of my laboratory are to contribute to this effort through the study of commonly inherited genetic variants.  We are focusing on exploring their influence on to serve as easily accessible and measurable biomarkers in the clinic: identifying those at increased risk of developing cancer and worsened prognosis.

Our field has been very successful in identifying commonly inherited genetic variants, such as single nucleotide polymorphisms (SNPs), which associate with disease. More than one thousand SNPs have been shown to significantly associate with human cancer to date. Despite these findings, major challenges remain in translating these associations into clinical applications. For example, discerning both the responsible, causal SNP from the many linked nonfunctional SNPs and the molecular mechanism connecting the variant to disease have proven extremely challenging. These uncertainties have limited our ability to integrate SNP biomarkers into the proper context for use in the clinic. My laboratory proposes to address these challenges with a focus on the identification and analysis of functional, cancer-associated SNPs residing in well-defined cancer signaling pathways.  Our ultimate goal is to create functional genetic maps of these common variants, enabling us to increase their predictive and prognostic value through the integration of single SNPs into networks of functional SNPs, in the correct cellular and clinical context.

We have begun our work in the well-defined p53 tumor suppressor network: a good model system to begin to assess the potential impact of SNPs on cancer for many reasons.  Other genetic variations in the pathway, such as low-frequency inherited mutations and common somatic mutations, are already used as critical biomarkers in patient-stratification strategies in the clinic, which can help both to inform our studies and to serve as a point of integration.  Moreover, these genetic variations have been shown to affect cancer risk, progression and response to therapies of many cancers. Therefore, identified functional SNPs in this pathway could affect many types of cancers, and help us to understand and intervene in all stages of the disease.

PUBLICATIONS

Zeron-Medina J, Wang X, Repapi E, Campbell MR, Su D, Castro-Giner F, Davies B, Peterse EF, Sacilotto N, Walker GJ, Terzian T, Tomlinson IP, Box NF, Meinshausen N, De Val S, Bell DA, Bond GL. (2013)  A Polymorphic p53 Response Element in KIT Ligand Influences Cancer Risk and Has Undergone Natural Selection. Cell. 2013 Oct 10;155(2):410-22. doi: 10.1016/j.cell.2013.09.017.

Grochola L.F., A.J., Zeron-Medina, J., Repapi, E., Finlayson, A.E., Cai, Y., Atwal, G.S., and Bond, G.L. (2012).  The Inheritance of p53.  p53 in the Clinics. Springer Science and Business Media, New York, p. 25-46

Post, S.P., Quintas-Cardama, A., Pant, V., Iwakuma, T., Hamir, A., Jackson, J.G., Maccio, D.R., Bond, G.L., Johnson, D.G., Levine, A.J., Lozano, G. (2010). A high-frequency regulatory polymorphism in the p53 pathway accelerates tumor development. Cancer Cell 18, 220-230

Vazquez, A., Grochola, L.F., Bond, E.E., Levine, A.J., Taubert, H., Muller, T.H., Wurl, P., and Bond, G.L. (2010). Chemosensitivity Profiles Identify Polymorphisms in the p53 Network Genes 14-3-3{tau} and CD44 That Affect Sarcoma Incidence and Survival. Cancer Research 70, 172-80.

Atwal, G. S., Kirchhoff, T., Bond, E. E., Montagna, M., Menin, C., Bertorelle, R., Scaini, M. C., Bartel, F., Bohnke, A., Pempe, C., Gradhand, E., Hauptmann, S., Offit, K., Levine, A. J., and Bond, G. L. (2009). Altered tumor formation and evolutionary selection of genetic variants in the human MDM4 oncogene. Proc Natl Acad Sci USA 106, 10236-10241.

Vazquez, A., Bond, E. E., Levine, A. J., and Bond, G. L. (2008). The genetics of the p53 pathway, apoptosis and cancer therapy. Nat Rev Drug Discov 7, 979-987.