Thank you to Erik Anderson, Co-Chairman & CEO of Topgolf® and to the entire Topgolf team for promoting a healthy lifestyle by supporting programs and research in the Center for Energy Balance in Cancer Prevention and Survivorship. Topgolf’s fundraising efforts in July of 2017 raised $50,000 for the Center.
Learn more about the Topgolf partnership.
Going Gym Free with Hosts Marc & Beth and Guest Karen Basen-Engquist
Blog Talk Radio
Karen Basen-Engquist, Ph.D., professor of Behavioral Science and director of the Center for Energy Balance in Cancer Prevention and Survivorship was a featured guest on the "Let's Talk! Going Gym Free Show" with Marc and Beth. Listen now
The National Cancer Institute is providing data for researchers to develop novel analytic approaches for quantifying physical activity and dietary exposures
This data is available to all qualified investigators for studies of physical activity and nutrition. Interested investigators can request access to IDATA Study via the Cancer Data Access System.
Research Spotlight: Getting to Know Imad Shureiqi, M.D., M.S.
“From my early clinical training in medical school, I saw how people suffered from cancer, and I always wished I could help them. There is a global effort toward a cure, but the need remains great, even today.”
Dr. Imad Shureiqi has dedicated his life’s work to contribute to ending this never-ending disease, and has focused much of his research on colon cancer, which remains prevalent in industrialized countries like the U.S. “Colon cancer evolves in a progressive manner, from polyps, as pre-malignant lesions to cancer. Removing the early-stage polyps is commonly a missed opportunity, as people do not like colonoscopies, which allow polyp detection. We assume either genetics or one’s environment drive cancer, but both are likely to play a role in colon cancer. Diet, obesity, intestinal microbial flora and chronic inflammation are likely to influence colon cancer development. For example, chronic bowl inflammatory diseases such as ulcerative colitis significantly increase the risk of colon cancer,” he proclaims.
A hands-on physician scientist, Dr. Shureiqi earned his MD in Medicine at Damascus University. He completed his Residency in Internal Medicine as well as his Fellowship in Medical Hematology at State University of New York at Buffalo. He completed another Fellowship in Medical Oncology at the University of Michigan in Ann Arbor, where he began working on gastrointestinal and colon cancers. Here he also earned his M.S. in Clinical Trial Design and Statistical Analysis. He was recruited to M.D. Anderson in 1999, where he has served as an Assistant Professor and later as an Associate Professor, Departments of Clinical Cancer Prevention, Division of Cancer Prevention and Population Sciences and Gastrointestinal Medical Oncology, Division of Cancer Medicine.
Dr. Shureiqi has been widely recognized and honored for his peer-reviewed research, academic leadership and publications, and has served as the principal investigator for a host of protocols on colon cancer and the many molecules which impact its expression and progression. He has focused much of his work on how linoleic acid, the 15-LOX-1 enzyme, and the PPAR-delta gene interact to impact colon cancer.
“In simple terms, we think that diet plays a very important role in colon cancer, so I’ve done a lot of work studying the potential role of lipids and particularly unsaturated omega 6 fatty acids such as linoleic acid in colon cancer. The life span of a colon cell averages seven days, after which cells undergo programmed cell death (apoptosis) to prevent the accumulation of cells that have corruptive DNA which mutates into cancer. Colon cells, in contrast, do not undergo apoptosis, and thus these cells can form tumors. This ability of colon cancer cells to escape apoptosis is thought to be important to colon cancer development. Through our work in our laboratory, we demonstrated that a key enzyme that metabolizes linoleic acid, 15-lipoxygenase-1 (15-LOX-1), is lost in colon cancer cells and that 15-LOX-1 loss is linked to the cancer cells’ ability to escape apoptosis. We later showed that 15-LOX-1 exerts these effects by suppressing the activity of PPAR-delta. Our current research efforts are focused on developing drugs that target these genes.”
“There is a dichotomy regarding body weight and cancer in some individuals; it is not always a linear relationship, as many think,” he explains. “There is possibly a higher risk if you are either too thin, or too heavy. We are doing genetic mouse models to determine the influence of the PPAR-delta gene in cancer evolution. When the PPAR gene is experimentally genetically deleted, mice become fat, and if you activate it, the mice become lean. Yet even when the mice look slim and fit, they are often developing cancer. We need to continue exploring the relationship of weight to cancer, and I welcome opportunities to collaborate with like-minded researchers on how the important PPAR-delta gene controls body weight and impacts energy balance and cancer development.”