Christopher A. Haiman, ScD
Professor of Population and Public Health Sciences; AFLAC Chair in Cancer Research

Christopher A. Haiman ScD is a professor in the Department of Population and Public Health Sciences and the USC Norris Comprehensive Cancer Center. He came to the Keck School of Medicine of USC in 2000 as a post-doctoral fellow under Brian Henderson MD and became a faculty member in 2003. His major research focus is in the genetic basis of cancer in minority populations. He is currently leading a number of large genetic studies on the prostate, including the African Ancestry Prostate Cancer GWAS Consortium (AAPC, PI) and the ELLIPSE U19 GAME-ON project (co-PI).

What initially attracted you to study genetic epidemiology?

I have always had an interest in genetics from the standpoint of understanding inherited susceptibility to disease. At UC Berkeley, I pursued a degree in molecular biology with an emphasis in genetics. Not fond of the many hours required at the bench, I set my sights on medical school or in becoming a genetic counselor. In the ‘90s, there was a strong perception that phenotypic differences within and between populations may stem from inherited differences — and the Human Genome Project was born. This concept that genetics could have an important impact — beyond individuals but perhaps to populations — was eye-opening and drew me to public health and epidemiology. A focus in epidemiology provided the scientific framework and career path to integrate my interest in genetics with population-based health research.

Much of your research is in genetic risk factors for breast and prostate cancer in minority populations. What influenced your decision to focus in this area?

My long-standing interest in these common hormone-related cancers is based on my training in chronic disease epidemiology as well as interest in understanding how genetic risk factors may underlie cancer susceptibility and contribute to racial and ethnic differences in risk. These cancers, in particular prostate cancer, display wide variation in cancer incidence across racial and ethnic populations. To date, the vast majority of research focused on genetic susceptibility to common cancers has been conducted in populations of European ancestry. While these efforts have been successful, we cannot assume that all genetic factors and biological insights in breast and prostate cancer will be identified through studies conducted solely in populations of European ancestry. My research has focused on establishing large-scale genetic studies of these cancers in populations of African and Latino ancestry, which have revealed susceptibility alleles that are population-specific, and may contribute to population differences in risk. One example is a variation at the 8q24 risk region, which harbors multiple alleles that are only found in men of African ancestry. Ongoing multiethnic efforts are crucial, as such discoveries, over the coming years, may play a significant role in shaping preventive and therapeutic strategies.

On what other areas of research have you collaborated and how have these collaborations advanced or influenced your own research?

I have also worked in many large consortia studying the genetic basis for other common phenotypes and diseases, including obesity and type 2 diabetes that vary in prevalence across populations. One study in particular, a genome-wide association study of diabetes in Latinos (SIGMA Consortium), has provided novel and important insight into the genetic underpinnings of Type 2 diabetes risk in this population. The majority of common human genetic variation globally is present in African populations as the result of population history and human migration patterns out of Africa. Through our genome-wide search we identified a variant in the SLC16A11 gene that has a very unusual frequency pattern across population. The higher disease risk version of the gene is common in Native American populations, largely absent in African populations and rare in Europeans. Through collaborations with Swedish evolutionary geneticist Svante Pääbo, PhD, analyses revealed that the higher disease risk version of the SLC16A11 gene was introduced into modern humans through mixing with Neanderthals, which is not uncommon — approximately 1 to 2 percent of genetic sequences present in all modern day humans outside of Africa were inherited from Neanderthals. This is the first example, to our knowledge, of a common disease risk locus being transmitted from Neanderthals and presents a new avenue for exploring inherited disease risk for other common complex diseases.

What do you think will be the next big advances in your field and what do you think the Keck School of Medicine of USC can do to position itself to be a leader in this area?

The next big advance will be to conduct whole-genome sequencing in very large numbers of samples to investigate the contribution of rare forms of variation in disease susceptibility. While data generation will be limited to established genome centers and industry, bioinformatic demands will be daunting. Thus, establishing bioinformatic capabilities at Keck School of Medicine will be essential. Also, with the immense diversity of the catchment area of the affiliated Keck hospitals, establishing infrastructure for biobanking and electronic medical records for research should be considered, as it would position Keck as a leader in genetic (and non-genetic) initiatives to study diseases and health disparities of importance to the Los Angeles population.

What advice would you give to junior faculty about being competitive in getting grant funding?

My advice would be not to get discouraged. Grants are getting funded; you just need to have a good idea. Make sure to involve your mentor and other faculty members as sage advice is often needed to get it under the pay line. And most importantly, apply frequently. You won’t get a bite if you don’t have many lines in the water!