Boston in the second week of November was dark, rainy and cold. Despite such unwelcoming weather, hundreds of cancer researchers from a variety of disciplines met in the city to present and discuss new findings in cancer prevention.

As a UBRP student, I work in the Arizona Cancer Center satellite clinic of Dr. Iman Hakim, on two clinical trials looking at tea as a chemopreventive agent for lung carcinogenesis. I completed a cross-sectional study of participants utilizing the baseline (pre-intervention) data, including population characteristics and biomarkers. In September, I submitted an abstract of the research to the American Association for Cancer Research Frontiers in Cancer Prevention Research Conference.

I arrived at the conference in time for the first plenary session and the hors d'oeuvres that followed. Professionals from around the world and from a variety of institutions were there. I met researchers from Iran, India, and Maine, from Harvard and from the NIH.

The following two and one-half days were filled with plenary, educational, and concurrent sessions on a variety of cancer research topics, from preventing tobacco use with a Public Health approach to cancer immunoediting.

Many of the presentations focused on the mechanisms of cancer development. Steven M. Dubinett (UCLA) spoke about inflammation and immunity in lung tumorigenesis, but what he says about lung cancer is true for all cancers: "Successful lung cancer chemoprevention will require identification of appropriately targeted effective agents with acceptable toxicity profiles. Identification of molecular pathways critical to lung carcinogenesis advances development of targeted therapies for prevention."

Another theme that consistently emerged is the high interest that researchers have in the relationship between inflammation and cancer. This is particularly relevant as the rate of obesity in the population is increasing at a rapid rate, and obesity is associated with chronic inflammation.

Monday and Tuesday evenings included one poster session each, consisting of 225 and 230 posters, respectively. The amount of research presented in posters and in talks was staggering. Despite the incredible volume of information available, there was nearly a constant stream of people inquiring about the research area covered in my poster, which was very encouraging. I met at least one potential collaborator, who is working on a gene that codes for a tobacco carcinogen-detoxifying enzyme, which is different between males and females. She suggested that this could possibly explain our findings, that DNA oxidative damage is higher among females. Even if this does not explain the difference, the question of why females have more oxidative damage is an intriguing one.

The preparations for the conference were challenging but I found the opportunity to participate highly rewarding. I gratefully acknowledge support from HHMI (52003749) and from the National Institute of Health and the Department of Defense.

Our cross-sectional study looked at population characteristics, such as age, gender, lung function, smoking status and history, as well as biomarkers including catalase (CAT), sodium oxide dismutase (SOD), and 8-hydroxydeoxyguanosine (8-OHdG) among older smoker and former smoker study participants. We compiled the data and analyzed it using the statistics program STATA to perform linear regression. 8-OHdG is a commonly used marker of DNA damage, and is measured in the urine. CAT and SOD are antioxidant enzymes found in the blood. We expected to find some relationship between oxidative DNA damage and antioxidant enzymes. Our most significant results show females having a higher level of oxidative damage and lower levels of CAT than males.

Laura Goodman, UBRPer, Dr. Iman Hakim's lab, Public Health