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The Metastasis Genetics Section (MGS) seeks to define how naturally occurring, hereditary variation present in the general population alters susceptibility to aggressive, fatal forms of prostate cancer, and why similar tumors can have highly divergent outcomes in different people or families.  It is estimated that over 220,000 males in the United States will be diagnosed with prostate cancer in 2015, making it the most common non-cutaneous cancer in men.  However, only approximately 13 percent of men diagnosed with prostate cancer will die as a direct result of this disease.  At the time of diagnosis, the tests available to physicians to identify the subset of men that will succumb to this disease are of limited accuracy, which means that prostate cancer is over-treated.    

The aim of the MGS is to clarify the molecular mechanisms of aggressive prostate cancer, in order to more clearly understand why only a relatively small proportion of men die from this exceedingly common disease.  Mouse models of prostate cancer are used to define specific genetic differences that make certain people more susceptible to fatal forms of this disease. Through selective breeding, genetic changes that cause prostate cancer are introduced into mice of different strains, akin to races or families in humans. Differences in the growth rate of the primary tumor and spread of the tumor to distant organs (metastasis) are then measured in each of these different mouse strains.  Through the use of these approaches, the section has been able to identify multiple genes, called modifier genes, in the mouse genome that drive the development of more aggressive forms of prostate cancer. 

They then explore the role of these candidate modifier genes in aggressive prostate cancer by comparing these genes to genes suspected of playing a role in human prostate cancer patients. This is initially explored by examining candidate gene single nucleotide polymorphisms in human prostate candidate populations, and candidate gene expression levels in human prostate tumors.  Following this screening process, the functions of the highest priority candidate genes are investigated in human prostate cancer cell lines and clinical tissue specimens.


Dr. Crawford obtained his M.B. Ch.B. degree (M.D. equivalent) from the University of Liverpool, United Kingdom, in 1998 and his Ph.D. from the University of Louisville, in 2004.  Dr. Crawford's current work reflects his longstanding interest in the influence of germline variation on human disease.  He served as Price Fellow for Surgical Research in the Department of Surgery at the University of Louisville from 2001 to 2004.  There, he used molecular epidemiological techniques to characterize the influence of the germline on the development of inflammatory bowel disease. 

Following this, he performed his postdoctoral fellowship in the laboratory of Kent Hunter, Ph.D., National Cancer Institute, Bethesda, Maryland, from 2004 to 2009.  His studies concentrated on the influence of germline variation on breast cancer metastasis, where he identified germline regulators of metastasis-associated extracellular matrix (ECM) genes, which are frequently dysregulated in both mouse mammary tumors and human breast carcinomas prone to metastasis.  Expression correlation analysis identified seven candidate genes with expression highly correlated to that of metastasis predictive ECM genes.   He has be a tenure-track investigator in the National Human Genome Research Institute since September 2009. 

Dr. Crawford has won a number of awards and honors, including an American Association for Cancer Research Scholar-in-Training award in 2007.

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Last Reviewed: January 6, 2016