Carcinogenesis, Vol. 20, No. 8, 1387-1388,
August 1999
© 1999 Oxford University Press
Obituary
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Anthony Dipple, Executive Editor of Carcinogenesis and an international leader in the field of chemical carcinogenesis, died May 26, 1999, in Frederick, Maryland.
Born in Mansfield, UK, in 1940, Tony attended the University of Birmingham and received his PhD in Biological Chemistry in 1964 and, in recognition of his scientific accomplishment, a DSc in 1987. From 1964 to 1966 he was a Damon Runyon Postdoctoral Fellow and developed novel anticancer drugs in the laboratory of Charles Heidelberger at the McArdle Laboratory, University of Wisconsin. He then returned to England to initiate his research on the metabolic activation of polycyclic aromatic hydrocarbons and their DNA interactions with Philip D. Lawley and Peter Brooks at the Chester Beatty Research Institute, Institute for Cancer Research, London. These seminal studies demonstrated the requirement of metabolic activation in the formation of covalent DNA adducts by these carcinogens. In 1975, Tony moved to the, then newly established, cancer research laboratories at Fort Detrick in Frederick, Maryland. He held positions of increasing responsibility and was appointed to Director, Chemistry of Carcinogenesis Laboratory and Head, Molecular Aspects of Chemical Carcinogenesis Section, ABL-Basic Research Program, NCI–Frederick Cancer Research and Development Center.
Tony's studies of nucleoside adducts formed from the reactive bromomethylbenz[a]anthracenes led to the first crystal structure of a hydrocarbon–nucleoside adduct and the discovery that cellular repair of hydrocarbon–dAdo adducts in mammalian cells was faster than that for hydrocarbon–dGuo adducts. Tony was largely responsible for defining the molecular mechanism of metabolic activation of 7,12-dimethylbenz[a]anthracene (DMBA) and the characterization of DMBA–DNA adducts showed that this non-planar carcinogen reacts extensively with dAdo residues in DNA. This observation helped considerably to elucidate the role of DMBA in initiation of carcinogenesis, through mutagenesis of adenosine residues in ras proto-oncogenes. In addition to being a superb chemist, Tony adroitly utilized molecular and cellular biological approaches to investigate chemical carcinogenesis in cellular and animal models. He systematically investigated the mutagenic activities of the dihydrodiol epoxides of many hydrocarbon carcinogens and demonstrated that the DNA sequence context significantly affects the mutagenic potential of a given carcinogen–DNA adduct. Most recently, Tony and co-workers have shown that, although certain carcinogen-induced DNA damage can increase p53, the levels of the cyclin-dependent kinase inhibitor, p21waf1, are not increased sufficiently by p53 to cause a cell cycle arrest in G1. He proposed that the lack of a G1 arrest could increase the probability of a carcinogen–DNA adduct being converted to a mutagenic event during DNA synthesis.
In the late 1970s, Tony and Colin Garner founded the journal Carcinogenesis. Tony served as an Executive Editor of Carcinogenesis from its launch in January 1980 and nurtured it to maturity with his considerable intellect, sound judgement and hard work. He viewed this effort as a service to the scientific community. Tony's contributions to cancer research will continue to be amplified by his many trainees and collaborators and his substantial influence on the international community of biomedical scientists.
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