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Colon cancer answer
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. “
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).
Vitamin A (retinol) is a yellow, fat-soluble solid terpene alcohol obtained from some carotenoids by conversion in the liver, its storage organ. While carotenoids are widely distributed in such foods as green and yellow vegetables, retinol is not found in any vegetable sources, but is concentrated in egg yolks and the livers of many animals. Vitamin A, either from animal sources or synthesized in our own liver, is essential for growth and reproduction, maintaining healthy vision, and supporting protein synthesis and cell differentiation.
Vitamin A and its analogs have shown the ability to help maintain proper DNA function.
Calcium is a major essential mineral that is often inadequately supplied, inefficiently absorbed, or excreted faster than it is being assimilated. The citrate salt of calcium has been documented to be well absorbed and utilized by the body. Calcium is important in maintaining bone mineral density and in blocking the absorption into the bloodstream of free radical generating iron.
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