Bruce M. Boman, M.D., Ph.D., M.S.P.H., FACP

Research Interests

With the advent of recent and exciting new opportunities in the study of regulatory pathways, mutations, and colon carcinogenesis, I am interested in the signaling pathways, including molecular and cellular mechanisms of crypt homeostasis in the large intestine as well as the investigation of the stem cell origin of colorectal cancer (CRC). I am particularly interested in small genetic elements, called microRNAs, which are involved in the genesis of colon tumors, with the ultimate goal of identifying new therapeutic targets. MicroRNAs were discovered only a few years ago and are now known to be major genetic control elements that turn on and off gene expression. Many of these small regulators play a key role in driving normal cells to become cancerous. A second interest is in cancer stem cells, especially those of the colon. Another major research focus involves characterizing normal and malignant colonic stem cells in order to understand their role in the origin of colon cancer. Using specific markers that recognize colonic stem cells, our laboratory can identify and isolate colon cancer stem cells. Research on cancer stem cells holds great promise in developing new diagnostic markers and curative treatments for advanced forms of this deadly malignancy. A third research focus is in use of mathematical modeling to study kinetic mechanisms that lead to development of stem cell overpopulation that drives tumor growth. This research uses a systems biology approach to integrate kinetic models, microarray expression profiling, proteomics, bioinformatics and signaling pathway analyses to identify molecular and cellular mechanisms involved in normal colonic epithelial homeostasis and how dysregulation of these mechanisms contribute to the development of colon cancer.

Current Projects

• Delaware Idea Network of Biomedical Research Excellence (INBRE), microRNA Expression in Colon Cancer Stem Cells
• Program Project Grant with Thomas Jefferson University (pending), Homeostasis and Dysregulation of the Intestinal Tract and Cancer.
• NIH, Screening Pretest for Hereditary Non-polyposis Colon Cancer (HNPCC).
• Statin Polyp Prevention Trial in Participants with Resected Colon Cancer, NSABP, (NCI approved concept statement) including biologic correlative markers on stem cells and gene polymorphisms

Selected Publications

• Boman BM, Fields JZ, Cavanaugh KL, Guetter A, Runquist OA. How dysregulated colonic crypt dynamics cause stem cell overpopulation and initiate colon cancer. Cancer Res. 2008;68(9):3304–3313.
• Boman BM, Wicha MS, Fields JZ, Runquist OA. Symmetric division of cancer stem cells--a key mechanism in tumor growth that should be targeted in future therapeutic approaches. Clin Pharmacol Ther. 2007;81(6):893–898.
• Patel BB, Li X-M, Dixon MP, et al. Searchable high-resolution 2D gel proteome of the human colon crypt. J Proteome Res. 2007;6(6):2232–2238.
• Lipkin SM, Boman BM, Offit K. Hereditary colorectal cancer: New advances and the integration of molecular testing into clinical practice. J Clin Oncol. 2006;42(ASCO Educational Supplement):64–66.
• Boman BM, Walters R, Fields JZ, et al. Colonic crypt changes during adenoma development in familial adenomatous polyposis: immunohistochemical evidence for expansion of the crypt base cell population. Am J Pathol. 2004;165(5):1489–1498.
• Charara M, Edmonston TB, Burkholder S, et al. Microsatellite status and cell cycle associated markers in rectal cancer patients undergoing a combined regimen of 5-FU and CPT-11 chemotherapy and radiotherapy. Anticancer Res. 2004;24(5b):3161–3167.
• Fields JZ, Gao Z, Gao Z, et al. Immunoassay for wild-type protein in lymphocytes predicts germline mutations in patients at risk for hereditary colorectal cancer. J Lab Clin Med. 2004;143(1):59–66.
• Forsyth NR, Morales CP, Damle S, et al. Spontaneous immortalization of clinically normal colon-derived fibroblasts from a familial adenomatous polyposis patient. Neoplasia. 2004;6(3):258–265.
• Li X-M, Patel BB, Blagoi EL, et al. Analyzing alkaline proteins in human colon crypt proteome. J Proteome Res. 2004;3(4):821–833.
• Stoyanova R, Clapper ML, Bellacosa A, et al. Altered gene expression in phenotypically normal renal cells from carriers of tumor suppressor gene mutations. Cancer Biol Ther. 2004;3(12):1313–1321.
• Stoyanova R, Upson JJ, Patriotis C, et al. Use of RNA amplification in the optimal characterization of global gene expression using cDNA microarrays. J Cell Physiol. 2004;201(3):359–365.
• Upson JJ, Stoyanova R, Cooper HS, et al. Optimized procedures for microarray analysis of histological specimens processed by laser capture microdissection. J Cell Physiol. 2004;201(3):366–373.
• Zhang T, Fields JZ, Ehrlich SM, Boman BM. The chemopreventive agent sulindac attenuates expression of the antiapoptotic protein survivin in colorectal carcinoma cells. J Pharmacol Exp Ther. 2004;308(2):434–437.
• Cutler NS, Graves-Deal R, LaFleur BJ, et al. Stromal production of prostacyclin confers an antiapoptotic effect to colonic epithelial cells. Cancer Res. 2003;63(8):1748–1751.
• Boman BM, Fields JZ, Bonham-Carter O, Runquist OA. Computer modeling implicates stem cell overproduction in colon cancer initiation. Cancer Res. 2001;61(23):8408–8411.
• Zhang T, Otevrel T, Gao Z, et al. Evidence that APC regulates survivin expression: a possible mechanism contributing to the stem cell origin of colon cancer. Cancer Res. 2001;61(24):8664–8667.