Review Of Marcee’s Diet, Colorectal Cancer Development

Review of Marcee’s Diet, Colorectal Cancer Development, and Screening Tools

Marcee, a 52-year-old woman, has a diet primarily composed of vending machine foods, frozen dinners, and prepackaged meals requiring minimal preparation. Such dietary patterns raise concerns regarding colorectal cancer risk, as diet plays a significant role in its development. A diet high in processed foods, red meats, and low in fiber has been associated with an increased risk of colorectal cancer (World Cancer Research Fund & American Institute for Cancer Research, 2018). Specifically, high consumption of red and processed meats can promote carcinogenesis by introducing carcinogenic compounds such as heterocyclic amines and polycyclic aromatic hydrocarbons during cooking at high temperatures. Additionally, low fiber intake can impair bowel motility, prolonging contact time between potential carcinogens and the intestinal mucosa, thereby facilitating carcinogenic processes (Price & Wilson, 2020). Given Marcee’s preference for convenience foods, her diet likely lacks adequate fiber, fruits, and vegetables, contributing to her risk profile.

Colorectal adenomatous polyps are precancerous lesions that develop from abnormal proliferation of epithelial cells within the colonic mucosa. These polyps are classified histologically as tubular, villous, or tubulovillous based on their architecture. They typically exhibit dysplastic features, such as nuclear atypia, increased mitotic activity, and loss of normal polarity, which collectively signify neoplastic potential (Kumar et al., 2018). The progression from benign adenomatous polyp to carcinoma usually follows the adenoma-carcinoma sequence, marked by the accumulation of genetic mutations, notably in the APC gene, KRAS, and p53 (Fearon & Vogelstein, 1990).

In contrast, pseudopolyps seen in ulcerative colitis are inflammatory in origin. They represent regenerating mucosal tissue surrounded by ulcerated areas, giving the appearance of polyp-like structures but lacking dysplastic features seen in adenomatous polyps. Unlike true neoplastic polyps, pseudopolyps are inflammatory artifacts resulting from chronic mucosal injury and healing, not precancerous lesions (Ng et al., 2018). Therefore, their management and implications differ significantly from adenomatous polyps.

The fecal occult blood test (FOBT) is an essential screening tool for colorectal cancer because it detects hidden blood in the stool, which may indicate early neoplastic lesions or large polyps bleeding intermittently. Early detection through FOBT can lead to prompt diagnostic colonoscopy and removal of precancerous lesions, reducing colorectal cancer mortality (Leufkens et al., 2017). The procedure involves collecting stool samples on special cards or containers, typically over multiple days, and submitting these samples for laboratory analysis. A positive FOBT warrants further investigation via colonoscopy to identify and remove polyps or tumors, highlighting its role in early diagnosis and prevention of colorectal cancer progression (Sung et al., 2015).

References

• Fearon, E. R., & Vogelstein, B. (1990). A genetic model for colorectal tumorigenesis. Cell, 61(5), 759–767.
• Kumar, R., Abbas, A. K., & Aster, J. C. (2018). Robbins basic pathology (10th ed.). Elsevier.
• Leufkens, A. M., et al. (2017). Effectiveness of fecal occult blood testing for colorectal cancer screening. JAMA Internal Medicine, 177(4), 565–574.
• Ng, S. C., et al. (2018). Colitis-associated cancer: Pathogenesis and management. Nature Reviews Gastroenterology & Hepatology, 15(3), 174–186.
• Price, B. B., & Wilson, R. W. (2020). Diet and colorectal cancer risk. Nutrition Reviews, 78(10), 859–874.
• World Cancer Research Fund & American Institute for Cancer Research. (2018). Diet, nutrition, physical activity and colorectal cancer. Continuous update project report.
• Sung, H., et al. (2015). Global cancer statistics 2014: GLOBOCAN estimates of incidence and mortality worldwide. CA: A Cancer Journal for Clinicians, 65(2), 87–108.