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Last Updated: 2/26/2007
| Robert S. Sandler, M.D., M.P.H.
Professor |  |
Research Interests
Dr. Robert Sandler is an internist/gastroenterologist with research interests in colon cancer etiology, screening and prevention, and intermediate markers of colon cancer risk. He is the principal investigator of the North Carolina Colon Cancer Study, a population-based, case-control study exploring environmental, lifestyle and medical factors that might explain diverging black-white incidence and mortality trends for colorectal cancer. He is principal investigator for an NCI-funded investigation to study rectal mucosal proliferation and recently served as study chair of a multicenter chemoprevention clinical trial testing whether aspirin can prevent colorectal adenomas in patients who have undergone curative resection for e colorectal cancer. He is the principal investigator for the North Carolina Colorectal Cancer Care Outcomes Research and Surveillance (CanCORS) study, an NCI initiative to investigate the impact of processes of cancer care on outcomes. He is also an investigator for multicenter cooperative trials of calcium and aspirin/folate prevention of neoplastic polyps. He directs an NIH-funded training grant in digestive disease epidemiology and the NIH-funded UNC Center for Gastrointestinal Biology and Disease. He is the vice president of the American Gastroenterological Association and a member of the National Commission on Digestive Diseases.
Recent Accomplishments and Honors
It has been known for some time that NSAIDs decrease the risk of colorectal neoplasia. There has also been the widespread belief that there is an increase in proliferation in the normal mucosa of patients with adenomas – a field effect. In previous work, Robert Sandler and his colleagues have shown no evidence of a field effect for proliferation. However, research recently published in Gastroenterology, showed a strong field effect for apoptosis. Specifically patients with the lowest tertile of apoptosis were almost 90% less likely to have adenomas when compared to those in the highest tertile. Importantly, there was no association between apoptosis and the use of NSAIDs. Based on the results of prior studies that show an anti-apoptotic effect of aspirin, the authors presume that aspirin has effects on transformed cells, but not on normal mucosa. The results are important because they suggest that NSAIDs do not operate through an apoptotic mechanism in the normal mucosa, and because they suggest that apoptosis could prove to be a useful surrogate endpoint biomarker for chemoprevention trials.
In a paper published in the New England Journal of Medicine, we reported the results of a randomized controlled trial of aspirin vs. placebo to prevent colorectal adenomas in individuals with prior cancer. The study showed that patients randomized to 325 mg of aspirin were 35% less likely to develop adenomas. The mean number of adenomas was lower and the time to adenoma development was delayed in the aspirin group.
Publications
1. Sandler RS, Halabi S, Baron JA, Budinger S, Paskett E, Keresztes R, Petrelli N, Pipas JM, Karp DD, Loprinzi CL, Steinbach G, Schilsky R A Randomized Trial Aspirin to Prevent Colorectal Adenomas in Patients with Previous Colorectal Cancer. Results of CALGB study 9270. New England Journal of Medicine 2003;348:883-90
2. Baron JA, Cole B, Sandler RS, Haile R, Ahnen D, Bresalier R, McKeown-Eyssen G, Summers R, Rothstein R, Burke C, Snover D, Church TR, Allen JI, Beach M, Beck G, Bond J, Greenberg ER, Marcon N, Mott L, Pearson L, Saibil R, van Stolk R. A randomized trial of aspirin to prevent colorectal adenomas. New England Journal of Medicine 2003;348:891-9.
3. Miller EA, Keku TO, Satia JA, Martin CR, Galanko JA, Sandler RS. Calcium, vitamin D, and apoptosis in the rectal epithelium. Cancer Epidemiology Biomarkers and Prevention 2005;14:525-28.
4. Bresalier RS, Sandler RS, Quan H, Bolognese JA, Oxenius B, Horgan K, Lines C, Riddell R, Morton D, Lanas A, Konstam M, Baron JA. Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. New England Journal of Medicine 2005;352:1092-1102.
5. Eaton AM, Sandler RS, Carethers JM, Millikan RC, Galanko J, Keku TO. 5,10 Methylenetetrahydrofolate reductase 677 and 1298 polymorphisms, folate intake, and microsatellite instability in colon cancer. Cancer Epidemiology Biomarkers and Prevention 2005;14:2023-9.
6. Sansbury LB, Millikan RC Schroeder J, Moorman PG, North K, Sandler RS. Use of Nonsteroidal Anti-inflammatory Drugs and Risk of Colon Cancer in a Population-based, Case-control study of African Americans and Whites. American Journal of Epidemiology, 2005;162:548-58.
7. Sansbury LB, Millikan RC, Schroeder JC, North KE, Moorman PG, Keku T, deCotret AR, Player J, Sandler RS. Cox-2 polymorphism, use of nonsteroidal anti-inflammatory drugs and risk of colon cancer in African Americans. Cancer Causes and Control 2006;17:257-66..
8. Baron JA, Sandler RS, Bresalier RS, Quan H, Riddell R, Lanas A, Bolognese JA, Oxenius B, Horgan K, Loftus S, Morton D. A randomized trial of rofecoxib for the chemoprevention of colorectal adenomas. Gastroenterology 2006;131:1674-82.
E-mail: rsandler@med.unc.edu
Telephone: (919) 966-0090
FAX: (919) 966-9185
Address: 4157 Bioinformatics Bldg, CB #7555 Chapel Hill, NC 27599-7555
