Colon cancer answer
A paper published online in the Journal of Biological Chemistry on September 8, 2004, explains why mutations in the adenomatous polyposis coli (APC) tumor suppressor gene cause the majority of cases of colon cancer. Researchers at the University of Utah's Huntsman Cancer Institute led by David Jones, PhD discovered that the gene controls the conversion of dietary vitamin A (retinol) into retinoic acid, which is necessary for normal cell growth in the lining of the intestines, without which colon cancer can develop.

The APC gene is mutated in individuals who have familial adenomatous polyposis, an inherited syndrome in which potentially thousands of precancerous polyps form in the colon, inevitably leading to colon cancer. Acquired mutations of the APC gene are also found in 85 percent of those with sporadic colon cancer.

The researchers blocked the APC gene in embryonic zebra fish, who share many genes with humans. They observed a lack of normal cells in the lining of their intestines, which was restored when the embryos were treated with retinoic acid.

Dr Jones commented, “For a long time, scientists believed they knew what the APC gene did – that it regulated cell growth and division – but now we know we've been missing a big piece of the picture... Implications of this study are far reaching. We have long suspected that vitamin A was helpful in preventing certain cancers, including colon cancer. With this new understanding, it may be possible to bypass a non-functioning APC gene by introducing retinoids as a form of chemoprevention, and thus control the undifferentiated and uncontrolled growth of colon cells that results in colon cancer."

If someone had the genetic defect, increasing dietary vitamin A would not overcome it, however, Dr Jones told Life Extension, “treatment with retinoic acid or retinoic acid derivatives might. “

Colorectal cancer
Several epidemiological investigations have demonstrated that a diet rich in carotenoids could prevent the development of precancerous and cancerous lesions of the digestive tract. Indeed, there are close and inverse correlations between the serum level of carotenoids and colorectal polyps with different histological grades. Serum levels of vitamin A were found to be significantly lower in all patients with polyps than in healthy controls. The lowest levels were found in patients with focal adenocarcinoma in the polyp. The low mean carotenoid levels in patients with adenocarcinoma in the polyp indicate that deficiency of carotenoids may be an important factor in the development of colorectal cancer (Rumi et al. 1999).

In a population-based case-control study of 105 cases of colorectal adenoma, serum concentrations of vitamin A were significantly inversely related to the risk of colorectal adenoma when cases were compared with the control group. The risk of developing colorectal adenomas was found to be reduced in those with high vitamin A levels (Breuer-Katschinski et al. 2001).

Retinol, retinoic acid, and beta-carotene (in nanomolar concentrations) block stimulation of protein kinase C (PKC), which when stimulated has been shown to increase tumor activity in the colon. It has been suggested that beta-carotene could be useful in the prevention and treatment of colorectal cancer (Kahl-Rainer et al. 1994), as beta-carotene has been shown to down-regulate growth factors which contribute towards proliferation of pre-malignant cells. Combined, vitamin A and vitamin D3 have been shown to inhibit tumor-induced angiogenesis (Majewski et al. 1996).

Convincing evidence is available showing that dietary calcium and vitamin D impede the development of colonic carcinogenesis (Lamprecht et al. 2001). Calcium supplementation and vitamin D both appear to have anti-neoplastic effects in the large bowel; they appear to act together to reduce the risk of colorectal adenoma recurrence (Grau et al. 2003). Additionally, dietary vitamin D3 impedes the neoplastic process in murine large intestine (Mokady et al. 2000) and vitamin D3 has demonstrated the ability to inhibit liver cancer cell growth (Alvarez-Dolado et al. 1999; Majewski et al. 1996).

https://www.lifeextension.com/protocols/cancer/colorectal

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If you have questions or comments concerning this issue or past issues of Life Extension Update, send them to ddye@lifeextension.com or call 954 766 8433 extension 7716.

For longer life,

Dayna Dye
Editor, Life Extension Update
ddye@lifeextension.com
LifeExtension.com
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954 766 8433 extension 7716

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