Authors
- Saddler, Delores MSN, RN, CGRN
- Greenwald, Beverly PhD, MSN, CNS, RN
Article Content
Colorectal cancer (CRC) is the number two cause of cancer deaths in the United States, for both men and women (AHCPR, 2003). About 151,000 Americans are diagnosed and over 57,000 die each year from CRC (Jemal et al., 2004). One risk factor for CRC that has been heavily studied is inflammation. A personal history of inflammatory bowel disease, for instance, has been associated with an increased risk for CRC (ACS, 2003). Numerous studies have reported the protective effect from CRC of nonsteroidal anti-inflammatories (NSAIDS) and aspirin (Baron et al., 2003;Gann, Manson, Glynn, Buring, & Hennekens, 1993;Greenberg, Baron, Freeman, Mandel, & Haile, 1993;Sandler, Galanko, Murray, Helm, & Woosley, 1998;Sandler et al., 2003).
Recently, one study indicated a possible link between C-reactive protein (CRP), a marker for inflammation, and CRC. C-reactive protein was first discovered in 1930 (Pasche & Serhan, 2004) and is a protein produced in the liver during episodes of acute inflammation (NIH, 2002). Local inflammation and tissue injury may signal the liver to produce and release CRP into the bloodstream (Pasche & Serhan). Specifically, CRP is made in response to interleukin-6 (IL-6) (Erlanger, Platz, Rifai, & Helzlsouer, 2004). C-reactive protein's most important role is to interact with the complement system (NIH). C-reactive protein may bind to damaged cell tissues and components and may act as an opsonin, which helps prepare the cellular debris for phagocytosis and elimination by macrophages and leukocytes (Pasche & Serhan).
Erlinger et al. (2004) investigated the possibility that CRP, as a marker for inflammation, could help identify people at risk for the development of CRC. The subjects of their prospective study were participants of Washington County, Maryland's CLUE II cohort, established in May 1989 (baseline). Blood was drawn at baseline and stored at -70 degrees C. A linkage with the Washington County Cancer Registry and Maryland State Cancer Registry was used to determine which subjects were diagnosed with CRC during a period of up to 11 years after baseline (Erlinger et al., 2004).
A total of 172 subjects developed CRC. Of these 172 subjects, 131 had colon cancer and 41 had rectal cancer. For each CRC case, 1 or 2 case matched controls were found. C-reactive protein concentrations in the frozen samples for each case and control were then measured in duplicate (Erlinger et al., 2004).
Among the significant findings were that the risk of developing CRC increased with the concentration of CRP present at baseline. Those with the higher CRP (top 25%) had twice the risk of CRC compared with those with lower CRP (bottom 25%). The increased risk was more highly associated with colon cancer than rectal cancer. Results were similar in men and women.
Their findings are consistent with other studies which suggest that inflammation may increase the risk of colon cancer (Erlinger et al., 2004).
Additional studies need to be done to confirm the results of this study. One implication from this study may be regarding prevention strategies, as CRP levels may be reduced by weight loss and smoking cessation. Further analysis of the association between CRP, anti-inflammatory agents, and colon cancer may lead to the confirmation of elevated CRP as a risk factor (Erlinger et al., 2004).
References
Agency for Health Care Policy and Research. (2003). Retrieved December 30, 2003, from http://www.apcpr.gov/clinic/colorsum.htm[Context Link]
American Cancer Society (2003). Retrieved July 31, 2003, from http://www.cancer.org/docroot/CRI/content/CRI_2_4_3X_Can_colon_and_rectum_cancer[Context Link]
Baron, J. A. Cole, B. F., Sandler, R. S., Haile, R. W., Ahnen, D., Bresalier, R., McKeown-Eyssen, G., Summers, R. W., Rothstein, R., Burke, C. A., Snover, D. C., Church, T. R., Allen, J. I., Beach, M., Beck, G. J., Bond, J. H., Byers, T., Greenberg, E. R., Mandel, J. S., Marcon, N., Mott, L. A., Pearson, L., Saibil, F., & van Stolk, R. U. (2003). A randomized trial of aspirin to prevent colorectal adenomas. New England Journal of Medicine, 348 (10), 891-899. [Context Link]
Erlinger, T. P., Platz, E. A., Rifai, N., & Helzlsouer, K. J. (2004). C-reactive protein and the risk of incident colorectal cancer. Journal of the American Medical Association, 291 (5), 585-590. [Context Link]
Gann, P. H. Manson, J. E., Glynn, R. J., Buring, J. E., & Hennekens, C. H. (1993). Low-dose aspirin and incidence of colorectal tumors in a randomized trial. Journal of the National Cancer Institute, 85 (15), 1220-1224. [Context Link]
Greenberg, E. R., Baron, J. A., Freeman, D. H., Mandel, J. S., & Haile, R. (1993). Reduced risk of large-bowel adenomas among aspirin users: The Polyp Prevention Study Group. Journal of the National Cancer Institute, 85, (11), 912-916. [Context Link]
Jemal, A., Tiwari, R. C., Murray, T., Ghafoor, A., Samuels, A., Ward, E., Feuer, E. J., & Thun, M. (2004). Cancer statistics 2004. CA: A Cancer Journal for Clinicians, 54 (1), 8-29. [Context Link]
National Institute of Health. (2002). Retrieved April 14, 2004, from http://www.nlm.nih.gov/medlineplus/ency/article/003356.htm[Context Link]
Pasch, B., & Serhan, C. N. (2004). Is C-reative protein an inflammation opsonin that signals colon cancer risk?Journal of the American Medical Association, 291 (5), 623-624.
Sandler, R. S., Galanko, J. C., Murray, S. C., Helm, J. F., & Woosley, J. T. (1998). Aspirin and nonsteroidal anti-inflammatory agents and risk for colorectal adenomas. Gastroenterology, 114 (3), 441-447. [Context Link]
Sandler, R. S., Halabi, S., Baron, J. A., Budinger, S., Paskett, E., Keresztes, R., Petrelli, N., Pipas, J. M., Karp, D. D., Loprinzi, C. L., Steinbach, G., & Schilski, R. (2003). A randomized trial of aspirin to prevent colorectal adenomas in patients with previous colorectal cancer. New England Journal of Medicine, 348 (10), 883-890. [Context Link]