Q&A with Colorectal Surgeon and Researcher Emina Huang, MD

When colorectal surgeon and researcher Emina Huang, MD, joined Cleveland Clinic’s staff in August 2013, she brought along two five-year NIH R01 grants with remaining funding totaling $1.5 million. The monies support her groundbreaking research into the pathogenesis of inflammatory associated colorectal cancer.

Q: What is the premise behind your work?

The relationship between chronic inflammation and cancer development is well-known, but the cellular and molecular mechanisms underlying this relationship are not well-understood. We suspect that increased levels of the inflammation-causing protein interleukin-8 (IL-8) may be partly to blame for increased rates of colon cancer in patients with ulcerative colitis. Our long-term goal is to clarify the link between inflammation and cancer in general, and to prevent colitis-associated cancer (CAC) in particular.

Q: Discuss the role of colonic stem cell niche in oncogenesis

In this project, we are examining the contribution of the microenvironment to inflammatory- associated cancer. Our immediate objective is to determine the roles of genetic defects, cancer stem cells and stromal fibroblasts in the generation of colon cancer-initiating cells. Our central hypothesis is that these three factors are key to CAC development. Proving this hypothesis will facilitate the development of novel strategies to prevent CAC and substantially improve our ability to predict which patients will progress to malignancy.

Q: Explain your work with IL-8 in colitis-associated tumor initiation

Up to 18 percent of patients with chronic ulcerative colitis develop colorectal cancer. This project focuses on why epithelial cells make IL-8, and what effect the protein has on the development of cancer. Is it creating the angiogenic switch by making VEGF downstream and usurping the local vessels to feed itself? If IL-8 is the culprit in cancer formation, we can focus on finding ways to regulate its function to prevent inflammation-associated cancer, and specifically, colorectal cancer. Our approach is innovative, because we have unique tools, including colitis-derived colon cancer-initiating cells (CCICs), and are using CCICs from sporadic colorectal cancer for comparison. Our central hypothesis is that IL-8 signaling is required for the colitis-to-cancer transition. Once we understand the contribution and mechanism by which IL-8 promotes tumor initiation, we will be able to develop ways to interfere with the progression from benign colitis to malignant cancer.

Q: Are you working with any other researchers at Cleveland Clinic?

Several of my colleagues are studying colitis-associated cancer, but from different angles. Others are studying inflammatory bowel disease or colorectal cancer. We will be discussing ways to dovetail our research in order to more quickly gain an understanding of the mechanisms that promote the development of colorectal cancer and develop novel ways to prevent this devastating disease.

Dr. Huang can be reached at 216.445.4631 or huange2@ccf.org.