The Harold E. Eisenberg Foundation

Annual Program Book 2018-2019

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Page 23 of 103

22 Philanthropy In Action Gastrointestinal Cancer Research Q&A with Research Scholar Dr. Sumagin 2017-18 Harold E. Eisenberg Scholar Award Recipient Ronen Sumagin, PhD How are you using the funds received from the Harold E. Eisenberg Foundation? The funds received through the Eisenberg Foundation were used to partially support a laboratory technician who helps with experimental procedures, and for purchases of essential reagents used in the study. Our work is aimed at understanding how chronic inflammation and tissue injury, as seen in inflammatory bowel diseases, contribute to increased incidence of colorectal cancer. We assert that understanding the early mechanistic contributions of chronic inflammation to initiating malignancy will provide us with novel approaches to identify pre- malignant lesions that will advance to invasive cancer, as well as help us to devise novel therapeutic approaches to treat such cancers. We anticipate that understanding how tissue injury contributes to cancer can benefit up to one in four cancer patients. Do you have any results to share, or unique contributions that you would like to mention that resulted from the Research Scholar Award? During the past year, we have made significant advances on the proposed studies. We are excited to report that we have identified several potential molecules that can be used as prognostic biomarkers for inflammation induced colorectal cancer. We found that the loss of these molecules in colon tissue is associated with genomic instability (increased mutations rate) leading to cancer. We confirmed this in a mouse model of inflammation and cancer, as well as in a small cohort of human patients. We plan to expand this in the future. Did any of your findings spark any new or novel hypothesis or avenues of study that you might like to follow in the future? These findings prompted us to hypothesize that injury-induced genomic instability and mutations will be the reason for inactivation of tumor suppressor genes, which are important factors contributing to cancer development. Thus, we started an exciting new project and have promising preliminary results, suggesting that during injury immune cells cause specific genetic deletions in one of the key tumor suppressor genes (TP53) to stop its activity, leading to cancer. We now plan to define (map and sequence) these specific deletions in patients with inflammatory bowel diseases and correlate this with patients that have progressed to cancer, with a goal of using them in the future as predictive markers. "I would like to thank the Harold E. Eisenberg Foundation for the important philanthropic work they are doing to support gastrointestinal cancer research. As the available federal funding from national institutes is limited and highly competitive, securing funds to execute novel and groundbreaking projects becomes more and more difficult. Personally, being a junior investigator, where my team and I are still developing our research program, obtaining national funding for new ideas with limited preliminary data is even harder. Thus, support from foundations, such as the Harold E. Eisenberg Foundation, is invaluable to developing these ideas to a stage where we can apply for larger grants in the future." – Ronen Sumagin, PhD

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