UK MEG Prize Winners

David H Phillips

David PhillipsDavid H Phillips obtained his degree in Chemistry from Oxford University and his PhD in Biochemistry from the University of London. He obtained his post-doctoral training in the laboratories of James and Elizabeth Miller (McArdle Laboratory for Cancer Research, University of Wisconsin, Madison) and of Philip Hanawalt (Stanford University). On returning to the UK he joined the Institute of Cancer Research. In 2011 he moved to King’s College London, where he is Professor of Environmental Carcinogenesis.

David Phillips’s unique contribution to biomedical science over several decades is in the detection, characterisation and biological consequences of DNA damage. He has an international reputation in the field of environmental carcinogenesis and his research has advanced understanding of the role of environmental factors in the aetiology of cancer. This has been through innovative mechanistic studies on the metabolic activation of chemical carcinogens leading to the formation of DNA adducts, an early critical event in the carcinogenic process, and also in pioneering methods for the detection of adducts in human tissues as a validated biomarker in molecular epidemiology and a major component of the emerging field of “exposomics”.
He was the first to demonstrate that chemical modification of a proto-oncogene with an environmental carcinogen led to its mutation and activation to an oncogene. He has pioneered the characterisation of DNA adducts as a means of identifying mechanisms of action of carcinogens such as polycyclic aromatic hydrocarbons and tamoxifen, showing the latter to be a genotoxic carcinogen in rodents but a non-genotoxic carcinogen in humans. He has made major contributions to understanding the harmful effects of tobacco by detecting smoking-related DNA damage in smokers’ lung, and also in other human tissues including cervix and breast in studies that predated the epidemiological evidence that smoking causes cervical and breast cancer. The same approaches have led to the major discovery of aristolochic acid as a human carcinogen.

His wider commitment to medical science and public engagement is demonstrated by his advocacy for tobacco control, his chairing the government advisory Committee on Carcinogenicity and by his serving on many international committees evaluating carcinogenic risks to humans. He is past President of the UK Environmental Mutagen Society and has tirelessly promoted the careers of young scientists. He is also editor of a scientific journal, Mutagenesis.

Christopher Paul Wild

Chris WildChristopher Paul Wild obtained his PhD in 1984 from the University of Manchester, UK while working on the production of monoclonal antibodies to detect low levels of methylated DNA bases. He was awarded a post-doctoral fellowship from the International Agency for Research on Cancer (IARC) to work in Lyon, France and subsequently a UK Royal Society European Exchange Fellowship to spend a year at the Netherlands Cancer Institute in Amsterdam.

In 1987 he rejoined IARC as a staff scientist and later became Chief of the Unit of Environmental Carcinogenesis. In 1996 he was appointed to the Chair of Molecular Epidemiology at the University of Leeds, was Head of the Centre for Epidemiology and Biostatistics and became Director of the Leeds Institute of Genetics, Health and Therapeutics in December 2005.

Dr Wild was elected Director of IARC, the specialized cancer agency of the World Health Organization, from 1st January 2009 and was subsequently re-elected for a second five-year term of office. While at the Agency he has pursued a strategy of cancer research for cancer prevention, with activities structured around core areas of: describing the occurrence of cancer; elucidating the causes; and evaluating preventive interventions and their implementation in national cancer control programmes. He has also placed emphasis on training the next generation of cancer researchers worldwide.

Dr Wild’s main research interest is to understand the interplay between environmental and genetic risk factors in the causation of human cancer. He has particularly sought to apply biomarkers in population-based studies in relation to liver and oesophageal cancers. His work on mycotoxins has resulted in the development of novel exposure biomarkers for aflatoxins, fumonisins and deoxynivalenol. The work on aflatoxins led to the first observations that these potent carcinogens also cause growth impairment in young children in sub-Saharan Africa. In 2005 he proposed the concept of the exposome in order to draw attention to the need for improved exposure assessment to elucidate the causes of human cancer.

Further details can be found on the IARC website: and

Peter B Farmer

Peter FarmerPeter B Farmer’s University education was in Oxford where he received a BA and a DPhil in Chemistry.  After a year as a post-doctoral fellow in the Albert Einstein Medical Center in Philadelphia, he worked at the Chester Beatty Research Institute, Institute of Cancer Research, London for 7 years. In 1978 he moved to the MRC Toxicology Unit in Carshalton, and moved with the Unit to Leicester in 1993. From 2002 to the end of 2012 (when he retired to an Emeritus Professorship) he worked in the University of Leicester where he was Professor of Cancer Biomarkers in the Department of Cancer Studies and Molecular Medicine.

Peter Farmer’s initial research interest was in the mechanism of action of anticancer drugs and carcinogens, and in particular their metabolism and the reactions of active metabolites with target sites in DNA. The greater understanding of the nature of these interactions led to the possibility of developing biomarkers of exposure and effect of carcinogens, which could be used to guide the use of preventive measures aimed at reducing carcinogenesis in humans. It was this strategy that Peter Farmer pursued throughout his career. The crucial factor was the design of sufficiently sensitive and selective biomarkers that would be applicable to large-scale human molecular epidemiological studies. For example his group developed and validated state of the art analytical methodology for the determination of carcinogen adducts with proteins and DNA. The analysis of DNA adducts focused on the use of mass spectrometry (notably LC-MS/MS), although 32P-postlabelling, immunoassay, HPLC and accelerator mass spectrometry were also employed.  The interaction of reactive oxygen species with DNA was a further major area of research, and in later years the applicability of 'omics' methodology to develop biomarkers of exposure and effect was also explored.

The development of these biomarkers made an important contribution to molecular epidemiological studies on environmental and life-style factors that were thought to play a major role in the causation of cancer and other chronic diseases. Potential carcinogenic agents from environmental air pollution and dietary factors were major areas of Peter Farmer’s studies, along with investigations of the nature and source of endogenous DNA damage, and the influence of dietary chemopreventive agents on genotoxic damage.  

Peter Farmer published over 330 papers in peer reviewed journals and books, and was heavily involved in student training, including the supervision of 20 PhD students. He was much involved in large-scale research collaborations, particularly those funded by EC, to further the molecular epidemiological studies. He was also very active in a large number of committees in UK and abroad advising on carcinogenic risks to humans, including the Committee on Mutagenicity, of which he was Chairman. He is a past President of the UK Environmental Mutagen Society.

Marc Gunter

Marc GunterI am appointed Reader in Cancer Epidemiology and Prevention at Imperial College London. My research is focused on understanding the role of metabolic and hormonal pathways in cancer development and prognosis. Specifically I am interested in insulin signaling and related pathways, their dysregulation in metabolic disease and how these impact on carcinogenesis. My research has, for example, demonstrated a substantial role for hyperinsulinaemia in postmenopausal breast cancer development that is independent of oestrogen and that insulin is a major pathway underlying the obesity-breast cancer relation. The role of metabolic pathways in colorectal cancer development is also a major focus for my research group and we have ongoing studies employing metabolomic profiling and hormonal signaling characterization in prospective studies with incident colorectal cancer cases. My research also encompasses studies of cancer progression with a view to identifying biomarkers of metastases and recurrence. For example, we are currently investigating the role of insulin, insulin-like growth factor and steroid hormones and high stage endometrial cancer recurrence in a large, well-characterised cohort of uterine cancer patients that employs both serologic testing and tissue-based analyses.

I am an investigator in the European Prospective Investigation into Cancer and Nutrition (EPIC) and I have also worked extensively within the Women’s Health Initiative (WHI) and the Prostate Lung Colorectum and Ovarian Cancer Screening Trial (PLCO). In addition, I employ smaller-scale clinical studies and trials to investigate the impact of cancer risk factors on biological mechanisms in non-malignant and tumour tissues. Further, I lead a number of large consortial efforts such as the diabetes and cancer initiative, nested within the NCI Cohort Consortium, which aims to further knowledge on the role of diabetes in cancer development and survival using epidemiologic and molecular tools. In addition to my research activities, I also co-direct the Imperial College MSc in Epidemiology and lead the training program for the MRC-PHE Centre for Environment and Health.


  • American Association for Cancer Research (AACR)
  • UK Molecular Epidemiology Group
  • Royal Society of Medicine
  • Editor for Cancer Research

Links to Institutes Home Pages

Selected Recent Publications

    1. Gunter MJ, Wang T, Cushman M, Xue X, Wassertheil-Smoller S, Strickler HD, Rohan TE, Manson JE, McTiernan A, Kaplan RC, Scherer PE, Chlebowski RT, Snetselaar L, Wang D, Ho GYF. Circulating Adipokines and Inflammatory Markers and Postmenopausal Breast Cancer Risk. J National Cancer Institute 2015 (In Press).
    2. Murphy N, Strickler HD, Stanczyk FZ, Xue X, Wassertheil-Smoller S, Rohan TE, Ho GYF, Anderson GL, Potter JD, Gunter MJ. A Prospective Evaluation of Endogenous Sex Hormone Levels and Colorectal Cancer Risk in Postmenopausal Women. J National Cancer Institute 2015 (In Press)
    3. Merritt MA, Tzoulaki I, Tworoger SS, De Vivo I, Hankinson SE, Fernandes J, Tsilidis KK, Weiderpass E, Tjønneland A, Petersen KE, Dahm CC, Overvad K, Dossus L, Boutron-Ruault MC, Fagherazzi G, Fortner RT, Kaaks R, Aleksandrova K, Boeing H, Trichopoulou A, Bamia C, Trichopoulos D, Palli D, Grioni S, Tumino R, Sacerdote C, Mattiello A, Bueno-de-Mesquita HB, Onland-Moret NC, Peeters PH, Gram IT, Skeie G, Quirós JR, Duell EJ, Sánchez MJ, Salmerón D, Barricarte A, Chamosa S, Ericson U, Sonestedt E, Nilsson LM, Idahl A, Khaw KT, Wareham N, Travis RC, Rinaldi S, Romieu I, Patel CJ, Riboli E, Gunter MJ. Investigation of dietary factors and endometrial cancer risk using a nutrient-wide association study approach in the EPIC and Nurses' Health Study (NHS) and NHSII. Cancer Epidemiol Biomarkers Prev. 2015 Feb;24(2):466-71.
    4. Gunter MJ, Xie X, Xue X, Kabat GC, Rohan TE, Wassertheil-Smoller S, Ho GY, Wylie-Rosett J, Greco T, Yu H, Beasley J, Strickler HD. Breast cancer risk in metabolically healthy but overweight postmenopausal women. Cancer Res. 2015 Jan 15;75(2):270-4.
    5. Catsburg C, Gunter MJ, Chen C, Cote ML, Kabat GC, Nassir R, Tinker L, Wactawski-Wende J, Page DL, Rohan TE. Insulin, estrogen, inflammatory markers, and risk of benign proliferative breast disease. Cancer Res. 2014 Jun 15;74(12):3248-58.
    6. Xue X, Kim MY, Gaudet MM, Park Y, Heo M, Hollenbeck AR, Strickler HD, Gunter MJ. A comparison of the polytomous logistic regression and joint cox proportional hazards models for evaluating multiple disease subtypes in prospective cohort studies. Cancer Epidemiol Biomarkers Prev. 2013 Feb;22(2):275-85.
    7. Cross AJ, Sinha R, Wood RJ, Xue X, Huang WY, Yeager M, Hayes RB, Gunter MJ. Iron homeostasis and distal colorectal adenoma risk in the prostate, lung, colorectal, and ovarian cancer screening trial. Cancer Prev Res (Phila). 2012 Sep;4(9):1465-75.
    8. The Endogenous Hormones and Breast Cancer Collaborative Group. “Insulin-like Growth Factor 1 (IGF1), IGF Binding Protein 3 (IGFBP3), and Breast Cancer Risk: Pooled Individual Data Analysis of 17 Prospective Studies.” The Lancet Oncology 11.6 (2011): 530–542.
    9. Zervoudakis A, Strickler HD, Park Y, Xue X, Hollenbeck A, Schatzkin A, Gunter MJ. Reproductive history and risk of colorectal cancer in postmenopausal women. J Natl Cancer Inst. 2011 May 18;103(10):826-34.
    10. Gunter MJ, Hoover DR, Yu H, Wassertheil-Smoller S, Rohan TE, Manson JE, Li J, Ho GY, Xue X, Anderson GL, Kaplan RC, Harris TG, Howard BV, Wylie-Rosett J, Burk RD, Strickler HD. Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women. J Natl Cancer Inst. 2009 Jan 7;101(1):48-60.
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