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285Bruce M. Boman, MD, PhD, MS, FACP(267) 303-9241brucemboman@gmail.comCenter for Translational Cancer Research, The Helen F. Graham Cancer Center and Research InstituteCenter for Translational Cancer Research, The Helen F. Graham Cancer Center and Research Institute<ul><li>BISC 625 - Cancer Biology (guest lecturer)</li><li> CHEG 660 Systems Biology (guest lecturer)<br></li></ul><p>The main focus of my laboratory research is to understand molecular mechanisms that mediate development of colorectal cancer (CRC). CRC is the second-leading cause of cancer deaths both in the US and worldwide. The goal is to identify mechanisms that will lead to the development of new more effective, potentially even curative or preventive, treatments for colon cancer.</p><p>I have over 20 years’ experience as a laboratory chief investigating the molecular and cellular etiology of colon cancer. I am also a clinical investigator and have been integrally involved in translational efforts at all levels to advance the discoveries of cancer research to the benefit of oncology patients. In addition, I have made numerous contributions to the field through publications (>150), presentations, as a patient advocate, and service as a member on many NIH committees and study sections.<br></p><p><span style="text-decoration:underline;">Cancer Stem Cells</span>. Based on the emerging paradigm in oncology, effective agents will need to target cancer stem cells because malignant stem cells become overpopulated within tumors that drives cancer growth. Our recent research findings led to the discovery that aldehyde dehydrogenase (ALDH) is a specific marker for colonic stem cells and allows tracking of stem cell overpopulation during colon cancer development. Additionally, we showed that stem cell overproduction results from increased symmetric stem cell division. The test for ALDH also gives us the technology to isolate cancer stem cells from colon cancers. Our lead scientific paper that reported this finding was published in the most widely distributed cancer journal in the world, Cancer Research, and it has been widely cited (over 400 times) in the scientific literature. </p><p> <span style="text-decoration:underline;">APC Tumor Suppressor Gene</span>. My laboratory also investigates the adenomatous polyposis coli (APC) gene which is the most common (~90%) occurring mutation in colorectal cancers. Several lines of scientific evidence demonstrate that APC mutations. We were the first research team to report that mutation in the APC gene leads to stem cell overpopulation during colon tumorigenesis. Unfortunately, we do not currently have any systemic drugs that target APC or colon cancer stem cells. Thus, our translational research goal is to design novel agents that target APC in order to develop cancer stem cell-based treatments for cancer patients.</p><p>Our further studies focused on the specific molecular mechanisms that become dysregulated in cancer cells due to APC mutation. We showed that the APC protein acts, via a gene transcription factor (TCF4), to normally down-regulate expression of survivin which is a protein that functions to prevent cells from undergoing programmed cell death. However, when APC becomes mutant, this leads to increased expression of survivin in colon tumor cells and protects them from being killed by cancer drugs. We also showed that survivin expression is upregulated in APC mutant mice in association with Tcf4 activation and intestinal tumorigenesis. </p><p> <span style="text-decoration:underline;">HOX Genes</span>. HOX genes encode an evolutionarily conserved set of transcription factors that control how the phenotype of an organism becomes organized during development based on its genetic makeup. For example, in bilaterian-type animals, HOX genes are organized in gene clusters that encode anatomic segment identity, that is, whether the embryo will form with bilateral symmetry with a head (anterior), tail (posterior), back (dorsal), and belly (ventral). Although HOX genes are known to regulate stem cell (SC) differentiation and HOX genes are dysregulated in cancer, the mechanisms by which dysregulation of HOX genes in stem cells causes cancer development is not fully understood. Hence, we have been studying how dysregulation of HOX expression contributes to CRC development.</p><p><span style="text-decoration:underline;">Retinoid acid signaling</span>. Because aberrant dysregulation acid (RA) signaling alters cell proliferation and differentiation that might contribute to CRC progression and because ALDH is a key enzyme in the RA signaling pathway, we are studying RA signaling in normal and malignant colon stem cells. RA signaling is mediated by two nuclear retinoic receptor subtypes: the retinoic acid receptor (RAR) and the retinoic X receptor (RXR). We discovered that retinoid receptors RXR and RAR are selectively expressed in ALDH+ stem cells, which indicates RA signaling mainly occurs via ALDH+ stem cells, which provides a mechanism to selectively target cancer stem cells. Our goal is to determine how RA signaling regulates stem cell dynamics and how to translate research findings to CRC initiation and progression.<br></p>

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