Dr. Boman’s work also showed that survivin expression is upregulated in ApcMin/+ mice in association with Tcf4 activation and intestinal tumorigenesis. In addition, Dr. Boman’s work reported that stem cell overproduction results from increased symmetric stem cell division. Our recent research findings led to the discovery that ALDH1 is a marker for colonic stem cells and allows tracking of stem cell overpopulation during colon cancer development and isolation of cancer stem cells.

Dr. Boman’s overall hypothesis is “APC mutations that drive growth of colon cancers do so by causing stem cell overpopulation.” Dr. Boman recently published a novel model that provides a mechanism that explains how APC regulates crypt fission and, when mutant, how APC leads to abnormal crypt fission, colonic stem cell overpopulation and adenoma development.

Dr. Boman has been involved in research on APC and GI tumorigenesis for over 20 years and have vast expertise in quantitative immunohistochemical mapping of cell populations in mouse and human intestinal crypts as well as efficacy studies of chemopreventive agents using Apc Min mice. While Dr. Boman has significant experience as a laboratory chief investigating the molecular and cellular etiology of colon cancer, he is also a clinical investigator and has been integrally involved in translational efforts at all levels to advance the discoveries of cancer research to the benefit of oncology patients.

Dr. Boman served as the national princiapl investigator of the NSABP colon cancer statin prevention trial to investigate the efficacy of rosuvastatin in preventing adenomas. In addition, he has made numerous contributions to the field through publications, presentations, as a patient advocate, and service as a member on many NIH committees and study sections.