Do nutraceutics play a role in the prevention and treatment of colorectal cancer?

Abstract

Colorectal cancer is the third most common cancer worldwide with a 5-year survival of 50%. Current chemotherapeutic regimens used for advanced colorectal cancer provide an average survival of approximately 20 months. Non-toxic agents such as nutraceutics and supplements have been shown to aid in the prevention and adjuvant treatment of colorectal cancer. This article will discuss the epidemiology, progression, prevention, treatment, and recurrence of colorectal cancer and the role of nutraceutics and supplements in the treatment process.

Proteins in Soy Might Have a Higher Role in Cancer Prevention than Previously Expected: Soybean Protein Fractions Are More Effective MMP-9 Inhibitors Than Non-Protein Fractions, Even in Cooked Seeds

“…Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases which are involved in the remodeling of connective tissue [1]. One subgroup of MMPs called gelatinases (MMP-2 and MMP-9) has been particularly recognized as important mediators in inflammation [2] and oncologic processes such as tumorigenesis, cell adhesion and metastasis [3,4,5,6,7].…”

Role of curcumin in preventing familial adenomatous polyposis

“…In the first model of CRC, the malignancy begins with somatic mutations in adenomatous polyposis coli (APC) gene, initiating transformation of the normal mucosa to adenoma (class I), which is shown to be associated with hyper-proliferation (3–5). The hyper-proliferation is brought about by the activation of Wnt/β-catenin signal transduction pathways (4–6), followed by the activation of the proto-oncogene K-ras, a process that typically induces the transformation of an early adenoma to a class II type intermediate adenoma (5–7). These processes are then followed by the loss of function of the gene DCC (deleted in colorectal cancer DCC) resulting in the formation of class III adenoma (4).…”

“…The hyper-proliferation is brought about by the activation of Wnt/β-catenin signal transduction pathways (4–6), followed by the activation of the proto-oncogene K-ras, a process that typically induces the transformation of an early adenoma to a class II type intermediate adenoma (5–7). These processes are then followed by the loss of function of the gene DCC (deleted in colorectal cancer DCC) resulting in the formation of class III adenoma (4). The last step involves p53 gene mutation, which is thought to transform an adenoma into an invasive or early cancer (5–7).…”

“…The last step involves p53 gene mutation, which is thought to transform an adenoma into an invasive or early cancer (5–7). The whole process is found to take about 10 years and hence a 10-year interval is often recommended as the screening interval for colonoscopy in people exhibiting normal colonic mucosa at initial colonoscopy (4). The second model of CRC is based on “Microsatellite Instability”.…”

“…In the CRC model of Vogelstein, which has recently been modified by Fearon et al ., the commonly affected gatekeeper genes are Ras , EGFR , PIK3CA , BRAF , cMYCp53, APC, PTEN, SMADS (2–4) and TGFβ−2 (5,6). Since gastrointestinal (GI) cancers, specifically CRC is an age-related disease; we have examined age-associated changes in some of these critical genes in the gastric mucosa of healthy human subjects and found APC , p53 , and DCC genes to be inactivated in the GI mucosa in older subjects, indicating a greater risk in developing GI cancer with advancing age (8).…”