Michael B. Cook, Ph.D.
|Organization:||National Cancer InstituteDivision of Cancer Epidemiology & Genetics, Nutritional Epidemiology Branch|
|Address:||9609 Medical Center Drive Room 7E106|
Dr. Michael Blaise Cook earned his B.Sc. in genetics at the University of Nottingham, England, and, subsequently, a Ph.D. in epidemiology at the University of Leeds, England. Dr. Cook joined the HREB as a Visiting Postdoctoral Fellow in 2007 before becoming a Research Fellow in 2008 and then an Investigator in 2011. Dr. Cook’s research interests include the epidemiology of esophageal adenocarcinoma—specifically, sex differences and the effects of obesity in the natural history of this disease—as well as hormonal and genetic mechanisms of prostate carcinogenesis.
Esophageal adenocarcinoma is a highly fatal cancer—in the United States the five-year survival rate is 19%. Esophageal adenocarcinoma is considered to represent the end of a continuum of disease which initiates with severe gastroesophageal reflux, causing erosion of the native squamous stratified epithelium of the esophagus which may subsequently be re-epithelialized with an intestinal metaplasia containing goblet cells. This metaplasia is known as Barrett’s esophagus and increases the risk of esophageal adenocarcinoma by 10–30 times that of the general population. To elucidate the etiology of these distinct stages of esophageal carcinogenesis, Dr. Cook is utilizing classical and molecular epidemiologic approaches in his attempts to understand why as many as seven men for every woman develop this malignancy. Dr. Cook is pursuing hypotheses including sex steroid hormones, inflammatory cytokines, and metabolic syndrome, each of which shares associations with both sex and body mass index.
Dr. Cook is strategically attempting to overcome the shortcomings of some of the prior studies that have been conducted on the relationships between hormones and prostate cancer risk. As is now well understood, prostate-specific antigen (PSA) testing has resulted in overdiagnosis of prostate cancer, making it difficult to study “clinically-relevant” disease and elucidate risk factors that may have translational capacity. In addition, previous studies have often focused on parent/major hormones of the sex steroid biosynthesis pathway. In his attempts to overcome some of these limitations, Dr. Cook is focusing on aggressive disease and/or fatal prostate cancer as outcomes, as well as broadening the scope of hormone exposures assessed. Dr. Cook is also investigating germline and somatic genetics of this disease, and assessing how this may overlap with hormonal factors that may be associated with carcinogenic risk.