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| Life Extension
Update Exclusive 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. “
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| Protocol
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).
http://www.lef.org/protocols/prtcl-148.shtml
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Vitamin A (retinol) is a yellow, fat-soluble solid terpene alcohol
obtained from some carotenoids by conversion in the liver, its storage
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sources, but is concentrated in egg yolks and the livers of many
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or call 954 766 8433 extension 7716.
For longer life,
Dayna Dye
Editor, Life Extension Update
ddye@lifeextension.com
LifeExtension.com
1100 West Commercial Boulevard
Fort Lauderdale FL 33309
954 766 8433 extension 7716
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