Showing posts with label colorectal cancer. Show all posts
Showing posts with label colorectal cancer. Show all posts

Saturday, February 6, 2010

Soy Shows Promise

An article featured in the December 15, 2009 issue of the journal Cancer Research reveals the discovery of a team at Children's Hospital & Research Center in Oakland, California of compounds occurring in soy that could help prevent and possibly treat colon cancer.

Children's Hospital Oakland Research Institute Cancer Center director Julie Saba, MD, PhD and her associates discovered that natural lipid molecules called sphingadienes may be responsible for some of the cancer-preventive benefits found for soy products. They first identified the compounds in fruit flies and found that they had the effect of inducing the death of mutant cells. The molecules were determined to be similar to sphingadienes that occur in soy sphingolipids.

When the researchers compared the effects of sphingadienes from flies or soy with those of another soy compound in experiments with cultured human colon cancer cells, sphingadienes were demonstrated to reduce cell viability dose and time-dependently by increasing apoptosis (programmed cell death) and autophagy, while the other soy compound was less effective. Nonmalignant human colon cells were shown to be less sensitive to sphingadienes' effects. In another experiment utilizing a mouse model of intestinal tumorigenesis, animals given sphingadienes averaged 35 percent fewer polyps (benign colon tumors that can become cancerous in humans), and polyps tended to be smaller compared to those detected in untreated animals.

"It's very exciting," enthused Dr Saba. "First, we are encouraged to find a natural molecule that could be consumed through soy products as a strategy to help prevent colon cancer. Second, this information is important because we can build on our understanding of the structure and metabolism of sphingadienes in terms of developing new drugs to treat people who already have colon cancer. Uncovering how sphingadienes exert their effects also helps us to find the most likely combinations of drugs that may work synergistically to eliminate cancer cells and mutant cells that could give rise to cancer."

"I would be comfortable recommending soy products as a change in the diet that could protect against cancer," she added. "The more that soy is studied, the more of these protective agents are found, so it's a very healthy diet choice."

Tuesday, September 1, 2009

Colorectal Cancer

Colorectal cancer develops through a process involving genetic change in the epithelial cells of the colon lining. The main factors that initiate colorectal cancer are consumption of cooked red meat (due to heterocyclic amines) (Gerhardsson de V et al 1991; Reddy S et al 1987), high intake of refined carbohydrates (Franceschi S et al 2001), poor vitamin and mineral intake, alcohol consumption, smoking, bile acids, fecal mutagens (DNA-damaging agents), fecal pH, and compromised detoxification enzymes (Winawer SJ et al 1992). An example of one important detoxification enzyme is N-acetyltransferase, which catalyzes the formation of DNA-damaging products from heterocyclic amines that form in cooked meats. Differences in the activity of this enzyme classify individuals as slow or fast acetylators. The level of red meat consumption in fast but not slow acetylators is associated with risk for colorectal cancer development (Welfare MR et al 1997).

In industrialized Western societies, both polyps and colon cancer occur more frequently due in part to diets low in fruits, vegetables, vegetable protein, and fiber (Satia-Aboutaj J et al 2003). Fecal mutagens are produced by certain diets such as those containing overcooked or burnt meat or fish. Increased intake of fiber, on the other hand, shortens the intestinal transit time, which in turn reduces the exposure of the colorectal lining to mutagens within the stool (Johansson G et al 1997).

Low folate intake, especially when combined with alcohol consumption and a low-protein diet, increases colorectal cancer risk (Kato I et al 1999). Dietary folate influences DNA methylation, synthesis, and repair. Abnormalities in these DNA processes enhance cancer development, particularly in rapidly growing tissues such as the colorectal mucosa (Lengauer C et al 1997; Feinberg AP et al 1983). Higher folate intake from either dietary sources or supplements may protect against the initiation of colorectal cancer (Giovannucci E 2002, 1998).